You searched for subject:(Alzheimer s Disease).
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1.
Ben Sundra Ashok.
Biochemical markers in Alzheimer s disease;.
Degree: Biochemical, 2003, INFLIBNET
URL: http://shodhganga.inflibnet.ac.in/handle/10603/4579 
► Alzheimer?s disease (AD) is a severe neurodegenerative disease with a characteristic progressive decline in cognitive functions and dementia. It is believed that the majority of…
(more)
▼ Alzheimer?s disease (AD) is a severe
neurodegenerative disease with a characteristic progressive decline
in cognitive functions and dementia. It is believed that the
majority of all AD patients are affected by the sporadic form,
caused by the combined effects of several risk factors. Currently
there exists no simple test or biological markers that could detect
AD cases, and the definite diagnosis of AD is based on
histopathological evidence obtained from autopsy. This thesis deals
with the problem of finding reliable biochemical markers in the
peripheral venous blood. Increasing evidence suggests that abnormal
processing of amyloid precursor protein and oxidative stress may
play an important role in the pathogenesis of AD. The present study
characterizes the usefulness of systemic oxidative stress, platelet
amyloid precursor protein ratio, plasma and red blood cells beta
amyloid (Aand#946; 1-42) levels in the diagnosis of AD and to
monitor the progression of the disease. The biochemical markers
were quantified in the lymphocytes, red newlineblood cells,
platelets and plasma of probable/possible sporadic AD patients and
non demented age matched healthy controls. There was a significant
increase in reactive oxygen species (ROS) newlineproduction in
lymphocytes, coupled with increase in erythrocyte antioxidant
enzymatic activities of superoxide dismutase and glutathione
peroxidise in AD. In parallel to increase in ROS, measurement of
8-0HdG as an index of DNA damage revealed a significantly higher
level in AD. The present study also found that the plasma
glutathione redox system is also affected as reduced glutathione
(GSH) were significantly lower in AD; conversely oxidised
glutathione (GSSG) levels were significantly elevated and the
GSH/GSSG molar ratio was found to be low in AD The present study
also found a reduction in platelet APP ratio. The magnetitude of
the APP ratio reduction is proportional to the severity of the
cognitive loss in AD.
References p. i-xxii, Annexure
included
Advisors/Committee Members: Vasudevan D.
Subjects/Keywords: Alzheimer?s disease; Biochemical
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APA (6th Edition):
Ashok, B. S. (2003). Biochemical markers in Alzheimer s disease;. (Thesis). INFLIBNET. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/4579
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ashok, Ben Sundra. “Biochemical markers in Alzheimer s disease;.” 2003. Thesis, INFLIBNET. Accessed November 20, 2019.
http://shodhganga.inflibnet.ac.in/handle/10603/4579.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ashok, Ben Sundra. “Biochemical markers in Alzheimer s disease;.” 2003. Web. 20 Nov 2019.
Vancouver:
Ashok BS. Biochemical markers in Alzheimer s disease;. [Internet] [Thesis]. INFLIBNET; 2003. [cited 2019 Nov 20].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4579.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ashok BS. Biochemical markers in Alzheimer s disease;. [Thesis]. INFLIBNET; 2003. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4579
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Hong Kong University of Science and Technology
2.
Wu, Renfei.
Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease.
Degree: 2016, Hong Kong University of Science and Technology
URL: https://doi.org/10.14711/thesis-b1626356
;
http://repository.ust.hk/ir/bitstream/1783.1-87113/1/th_redirect.html
► Interleukin-33 (IL-33) is a relatively newly discovered member of the IL-1 family. It is regarded as an alarmin located in the nuclei of barrier cells…
(more)
▼ Interleukin-33 (IL-33) is a relatively newly discovered member of the IL-1 family. It is regarded as an alarmin located in the nuclei of barrier cells such as endothelial cells. Upon tissue damage or cell death, IL-33 is released into the extracellular space and initiates corresponding cascades in nearby cells for protective reactions. The role of IL-33 in immune responses is dichotomous, as both pro-inflammatory and anti-inflammatory properties have been reported under various conditions. While most of the literature focuses on IL-33 dynamics in the peripheral immune system, its function in the central nervous system (CNS) remains somewhat ambiguous. Our group previously found that the cognitive impairment in 12-month-old APP/PS1 mice, an animal model of Alzheimer’s disease (AD), was improved after a 2-day treatment with IL-33. This beneficial effect of IL-33 on neurodegenerative disease models prompted us to explore the underlying mechanism of IL-33 in AD model mice. Therefore, the transcriptome of mouse brains was analysed by oligonucleotide microarray, and 4 candidate genes were examined further. Herein, CD11c was characterized in APP/PS1 mice. CD11c protein overexpression was confirmed by immunofluorescence in the microglia-like cells of 7.5-month-old APP/PS1 mouse brains and compared to that in wild-type (WT) littermates. In addition, CD11c mRNA expression increased in parallel with AD pathogenesis, but not with aging in WT mice. These findings implicate a possible new contributory factor to AD progression as well as a possible mechanism of IL-33 signaling effects in the AD mouse model. In the future, we will investigate the origin of CD11c or CD11c+ cells in the AD mouse brain as well as the interaction of IL-33 with CD11c+ cells.
Subjects/Keywords: Interleukins; Alzheimer'; s disease
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APA (6th Edition):
Wu, R. (2016). Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease. (Thesis). Hong Kong University of Science and Technology. Retrieved from https://doi.org/10.14711/thesis-b1626356 ; http://repository.ust.hk/ir/bitstream/1783.1-87113/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wu, Renfei. “Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed November 20, 2019.
https://doi.org/10.14711/thesis-b1626356 ; http://repository.ust.hk/ir/bitstream/1783.1-87113/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Renfei. “Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease.” 2016. Web. 20 Nov 2019.
Vancouver:
Wu R. Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2019 Nov 20].
Available from: https://doi.org/10.14711/thesis-b1626356 ; http://repository.ust.hk/ir/bitstream/1783.1-87113/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu R. Effect of interleukin-33 on the transcriptome in a mouse model of Alzheimer's disease. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: https://doi.org/10.14711/thesis-b1626356 ; http://repository.ust.hk/ir/bitstream/1783.1-87113/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Georgia
3.
Wilks, Scott Eddie.
The relationship between private prayer and resiliency among Alzheimer's caregivers.
Degree: PhD, Social Work, 2004, University of Georgia
URL: http://purl.galileo.usg.edu/uga_etd/wilks_scott_e_200412_phd
► The purpose of the study was to understand the influence of private prayer, used as a coping method to caregiving burden, as a factor of…
(more)
▼ The purpose of the study was to understand the influence of private prayer, used as a coping method to caregiving burden, as a factor of resiliency among Alzheimer’
s caregivers. A cross-sectional research design was employed, surveying a sample of Alzheimer’
s caregivers (N=304) who attended caregiver support groups in the southeastern United States. Questionnaire items empirically measured a number of constructs, including perceived burden; use of private prayer as a coping method; frequency and importance of prayer; and perceived resiliency. Demographic characteristics of the sample were reported. Regression analysis evaluated the relationship between prayer and resiliency, controlling for demographic factors. Over three- fourths of the sample reported a high frequency of private prayer, and over 90% of those who prayed indicated importance to four general types of prayer. As hypothesized, results indicated a strong association and positive, significant relationship between the extent of prayer usage as a method of coping, and resiliency. Implications for social work practice and education are discussed.
Advisors/Committee Members: M. Elizabeth Vonk.
Subjects/Keywords: Alzheimer\'s disease
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APA (6th Edition):
Wilks, S. E. (2004). The relationship between private prayer and resiliency among Alzheimer's caregivers. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/wilks_scott_e_200412_phd
Chicago Manual of Style (16th Edition):
Wilks, Scott Eddie. “The relationship between private prayer and resiliency among Alzheimer's caregivers.” 2004. Doctoral Dissertation, University of Georgia. Accessed November 20, 2019.
http://purl.galileo.usg.edu/uga_etd/wilks_scott_e_200412_phd.
MLA Handbook (7th Edition):
Wilks, Scott Eddie. “The relationship between private prayer and resiliency among Alzheimer's caregivers.” 2004. Web. 20 Nov 2019.
Vancouver:
Wilks SE. The relationship between private prayer and resiliency among Alzheimer's caregivers. [Internet] [Doctoral dissertation]. University of Georgia; 2004. [cited 2019 Nov 20].
Available from: http://purl.galileo.usg.edu/uga_etd/wilks_scott_e_200412_phd.
Council of Science Editors:
Wilks SE. The relationship between private prayer and resiliency among Alzheimer's caregivers. [Doctoral Dissertation]. University of Georgia; 2004. Available from: http://purl.galileo.usg.edu/uga_etd/wilks_scott_e_200412_phd
University of Ontario Institute of Technology
4.
James, Chantal.
Prevalence and patterns of alcohol consumption among persons with dementia in Canada.
Degree: 2018, University of Ontario Institute of Technology
URL: http://hdl.handle.net/10155/970
► Aim: To identify the prevalence of alcohol consumption and its impact on chronic disease, injury and hospital stays in persons with dementia (PWD). Methods: Multivariate…
(more)
▼ Aim: To identify the prevalence of alcohol consumption and its impact on chronic
disease, injury and hospital stays in persons with dementia (PWD).
Methods: Multivariate analysis was conducted using data collected from a nationwide population-based survey, Canadian Community Health Survey (CCHS).
Results: PWD consume alcohol at comparable rates to persons without dementia. A reported 60% of PWD consume alcohol. Males more often reported alcohol consumption than females. Multivariate analysis showed PWD who consumed alcohol were less likely to report chronic conditions such as heart
disease (22% vs 30%) and diabetes (13% vs 24%) than their counterparts who abstained from consumption.
Conclusions: Lower rates of injury, hospital stays, and various chronic diseases demonstrates the importance of assessing alcohol consumption in PWD. A better understanding of drinking habits in PWD would allow for the development of recommendations and guidelines to alcohol consumption.
Advisors/Committee Members: Bartfay, Emma.
Subjects/Keywords: Alcohol consumption; Alzheimer???s disease; Dementia
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APA (6th Edition):
James, C. (2018). Prevalence and patterns of alcohol consumption among persons with dementia in Canada. (Thesis). University of Ontario Institute of Technology. Retrieved from http://hdl.handle.net/10155/970
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
James, Chantal. “Prevalence and patterns of alcohol consumption among persons with dementia in Canada.” 2018. Thesis, University of Ontario Institute of Technology. Accessed November 20, 2019.
http://hdl.handle.net/10155/970.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
James, Chantal. “Prevalence and patterns of alcohol consumption among persons with dementia in Canada.” 2018. Web. 20 Nov 2019.
Vancouver:
James C. Prevalence and patterns of alcohol consumption among persons with dementia in Canada. [Internet] [Thesis]. University of Ontario Institute of Technology; 2018. [cited 2019 Nov 20].
Available from: http://hdl.handle.net/10155/970.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
James C. Prevalence and patterns of alcohol consumption among persons with dementia in Canada. [Thesis]. University of Ontario Institute of Technology; 2018. Available from: http://hdl.handle.net/10155/970
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Southern California
5.
Jayaraman, Anusha.
Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways.
Degree: PhD, Neuroscience, 2010, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/375673/rec/2506
► The depletion of estrogen and progesterone in postmenopausal women is associated with increased risk for several disorders in the cardiovascular, skeletal and nervous system. To…
(more)
▼ The depletion of estrogen and progesterone in
postmenopausal women is associated with increased risk for several
disorders in the cardiovascular, skeletal and nervous system. To
reduce this risk, hormone therapy containing estrogens and a
synthetic progestagen has been used but with little success. For
example, the Women’
s Health Initiative clinical trial showed that
hormone therapy was associated with reduced incidence of hip
fractures associated with osteoporosis but unexpectedly increased
incidences of both stroke and dementia. The disparities between
basic research studies that demonstrate neuroprotective effects of
estrogen and progesterone and recent clinical findings that report
adverse neural effects of hormone therapy indicate the need for a
more complete understanding of estrogens and progesterone
interactions in brain and other tissues. One important issue that
is not well understood is how neural effects of estrogens are
affected by progestagens. Recent experimental evidence shows that
prolonged progesterone exposure often represses estradiol function.
The mechanism by which progesterone inhibits estrogen action in the
brain is unclear. We hypothesize that progesterone might oppose
estrogen activity by regulating the expression and or function of
estrogen receptors, ERα and ERβ, thereby affecting ER-dependent
transcriptional activity and E2-mediated neuroprotection. My thesis
work involved testing these hypotheses and in the following
chapters, I provide the experimental evidence for the same. Chapter
1 is a comprehensive introduction to a number of topics that are
relevant to my research area. Chapter 2 describes the effects of
progesterone on the expression of estrogen receptors both in
primary neuron cultures as well as in rat brains.; Chapter 3
describes the effect of progesterone regulation of estrogen
receptors on estrogen-mediated transcriptional activity and
neuroprotection against apoptotic factors primarily in cell-culture
and to some extent in organotypic cultures. Chapter 4 describes the
effects of estradiol and progesterone individually as well as
combined on the expression of β-amyloid degrading enzymes and the
accumulation of amyloid both in vitro and in vivo. In Chapter 5 we
look at the effects of progesterone on apoptotic pathways by itself
and in the presence of estradiol mainly in primary neurons. In
Chapter 6 I discuss the relevance of my research findings in the
context of neurobiology and translational research and predict the
potential outcomes of incorporating these findings in hormone
therapy against risk for neurodegenerative diseases such as
Alzheimer’
s disease.
Advisors/Committee Members: Pike, Christian J. (Committee Chair), Brinton, Roberta Diaz (Committee Member), Baudry, Michel (Committee Member), Rayudu, Gopalakrishna (Committee Member).
Subjects/Keywords: estrogen; progesterone; Alzheimer'; s disease; neuron
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APA ·
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APA (6th Edition):
Jayaraman, A. (2010). Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/375673/rec/2506
Chicago Manual of Style (16th Edition):
Jayaraman, Anusha. “Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways.” 2010. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/375673/rec/2506.
MLA Handbook (7th Edition):
Jayaraman, Anusha. “Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways.” 2010. Web. 20 Nov 2019.
Vancouver:
Jayaraman A. Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways. [Internet] [Doctoral dissertation]. University of Southern California; 2010. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/375673/rec/2506.
Council of Science Editors:
Jayaraman A. Estrogen and progesterone interactions in neurons:
implications for Alzheimer's disease-related pathways. [Doctoral Dissertation]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/375673/rec/2506
University of Southern California
6.
Yao, Jia.
Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics.
Degree: PhD, Molecular Pharmacology & Toxicology, 2010, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/317029/rec/2508
► Presented here are a collection of studies that build on our existing knowledge of estrogen actions on brain mitochondria. Previous studies from our lab as…
(more)
▼ Presented here are a collection of studies that build
on our existing knowledge of estrogen actions on brain
mitochondria. Previous studies from our lab as well as other
colleagues have demonstrated that estrogen (E2, 17β-estradiol) is
neuroprotective against neurotoxic insults including exposure to
glutamate and amyloid beta (Aβ) (Nilsen et al, 2006; Simpkins and
Dykens, 2007; Vina et al, 2007b). Further, the E2 induced
neuroprotective mechanisms converge on mitochondria (Brinton,
2008b; Nilsen and Diaz Brinton, 2003; Nilsen et al, 2007). In the
current research project, we have hypothesized that mitochondria,
particularly mitochondrial bioenergetics play a pivotal role in the
pathogenesis of age-related Alzheimer’
s disease (AD) whereas
estrogen proactively sustains and enhances mitochondrial function
that was compromised in aging and AD. To test our hypotheses, we
have conducted a combination of in vitro and in vivo analyses which
address four specific aims. Specific Aim 1 (Chapter 2) serves to
investigate the role of mitochondrial bioenergetic deficits in AD
pathogenesis using the triple transgenic Alzheimer’
s mouse model.
Specific Aim 2 (Chapter 3) serves to determine the impact of E2
deficiency on mitochondrial function and AD progression. Specific
Aim 3 (Chapter 4) seeks to investigate the underlying mechanism of
estrogen induced neuroprotection as well as to examine the role of
different estrogen receptors in estrogen action in the brain.
Specific Aim 4 (Chapter 5) focuses on the therapeutic implications
of the findings from the previous three aims and introduces a novel
therapeutic strategy targeting mitochondria for preventing AD
and/or delaying the progression of AD.; Data from these four
specific aims have demonstrated that: 1) Mitochondrial bioenergetic
deficit precedes Alzheimer’
s pathology in the 3xTgAD mouse model.
2) Loss of ovarian hormones either due to age-related reproductive
senescence or surgical ovariectomy (OVX) significantly exacerbates
mitochondrial dysfunction that occurs in aging or AD. 3) E2
treatment initiated at the time of OVX prevented the OVX-induced
mitochondrial deficits by sustaining mitochondrial bioenergetic
capacity, decreasing oxidative stress, and preventing mitochondrial
amyloid and ABAD induction. 4) Therapeutic strategies targeting
mitochondria could alter AD progression by manipulating brain
mitochondrial bioenergetic profile.; We believe that findings from
these studies will expand our understanding of the mechanism of AD
pathogenesis as well as the pharmacological pathway of estrogen
induced neuroprotection against AD. Our research will also enable
the development of novel therapeutics that target mitochondrial
bioenergetics for the prevention and treatment of AD and other
neurodegenerative diseases that could be partially attributed to
mitochondrial dysfunction.
Advisors/Committee Members: Brinton, Roberta Diaz (Committee Chair), Cadenas, Enrique (Committee Member), Alkana, Ronald (Committee Member), Baudry, Michel (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; estrogen; mitochondria; bioenergetics; therapeutics
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APA (6th Edition):
Yao, J. (2010). Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/317029/rec/2508
Chicago Manual of Style (16th Edition):
Yao, Jia. “Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics.” 2010. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/317029/rec/2508.
MLA Handbook (7th Edition):
Yao, Jia. “Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics.” 2010. Web. 20 Nov 2019.
Vancouver:
Yao J. Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics. [Internet] [Doctoral dissertation]. University of Southern California; 2010. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/317029/rec/2508.
Council of Science Editors:
Yao J. Estrogen regulation of bioenergetics and mitochondrial
function: implications for Alzheimer's disease risk and
therapeutics. [Doctoral Dissertation]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/317029/rec/2508
7.
Herrero Tuñas, Ana María.
¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
.
Degree: 2014, Universidad da Coruña
URL: http://hdl.handle.net/2183/14441
► [Resumen] Introducción: La depresión y la demencia repercuten negativamente en la calidad de vida de las personas mayores, además de generar un gran gasto sociosanitario.…
(more)
▼ [Resumen] Introducción: La depresión y la demencia repercuten negativamente en la calidad de vida de las personas mayores, además de generar un gran gasto sociosanitario. Los estudios llevados a cabo en los últimos años reconocen que existe relación entre ambos trastornos. Aclarar esta relación permitirá conocer si la depresión es un factor de riesgo para el posterior desarrollo de la demencia.
Material y métodos: Se realizó una búsqueda bibliográfica en diferentes bases de datos como Medline, Pscynfo, Isi Web Of Knowledge, Isi Web Of Science y PubMed, además de consultarse diversos libros. La búsqueda incluyó los términos depresión, demencia, prevalencia y personas mayores. Las publicaciones y estudios seleccionados están comprendidos entre los años 2000 y 2013. Todos los artículos seleccionados están incluidos en revistas científicas con clasificación Journal Citation Report (JCR).
Resultados: La mayoría de los estudios seleccionados para esta revisión, apoyan la hipótesis de que la depresión es un factor de riesgo para el desarrollo de demencia. A su vez, reconocen que existe una relación temporal entre ambos trastornos. Sólo dos de los estudios encontrados no apoyan dicha relación.
Conclusiones: Se ha encontrado que existe relación entre ambos trastornos y que la depresión se asocia con un mayor riesgo de desarrollar demencia.
Subjects/Keywords: Demencia;
Depresión;
Enfermedad de Alzheimer;
Prevalencia;
Personas mayores;
Dementia;
Depression;
Alzheimer`s disease;
Prevalence;
Elderly
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APA ·
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Manager
APA (6th Edition):
Herrero Tuñas, A. M. (2014). ¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
. (Masters Thesis). Universidad da Coruña. Retrieved from http://hdl.handle.net/2183/14441
Chicago Manual of Style (16th Edition):
Herrero Tuñas, Ana María. “¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
.” 2014. Masters Thesis, Universidad da Coruña. Accessed November 20, 2019.
http://hdl.handle.net/2183/14441.
MLA Handbook (7th Edition):
Herrero Tuñas, Ana María. “¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
.” 2014. Web. 20 Nov 2019.
Vancouver:
Herrero Tuñas AM. ¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
. [Internet] [Masters thesis]. Universidad da Coruña; 2014. [cited 2019 Nov 20].
Available from: http://hdl.handle.net/2183/14441.
Council of Science Editors:
Herrero Tuñas AM. ¿Es la depresión un factor de riesgo para el desarrollo de la demencia en las personas mayores?
. [Masters Thesis]. Universidad da Coruña; 2014. Available from: http://hdl.handle.net/2183/14441
8.
Castellano, Sabrina.
Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease.
Degree: 2015, Università degli Studi di Catania
URL: http://hdl.handle.net/10761/3789
► Psychometrics is the science of psychological measurement and is concerned with the objective measurement of skills and knowledge, abilities, attitudes, personality traits, and educational achievement.…
(more)
▼ Psychometrics is the science of psychological measurement and is concerned with the objective measurement of skills and knowledge, abilities, attitudes, personality traits, and educational achievement. Efficacy trials with antidepressant drugs often fail to demonstrate beneficial effects, even though efficacious treatments are investigated, due, among other factors, to the lack of sensitivity of psychometric tools.
Affective disorders and particularly major depressive disorders (MDD) have been recently identified as new risk factors for the development of mild cognitive impairment and Alzheimer s disease (AD).
According to this clinical continuum between depression, MCI and AD new strategies of neuropsychological assessments should be explored by using multiple psychometric tools able to detect both affective and cognitive symptoms from depression and MCI to early AD.
Aim of the present Doctorate Thesis is to discuss recent evidence on the role of psychometric tools in the diagnosis of MDD and AD and in the evaluation of pharmacological treatment, focusing on a new combination of psychometric tools useful to detect early cognitive deficits both in MDD patients and MCI patients with an high risk to convert into AD.
The results presented in the PhD Thesis have been published in two articles on peer-reviewed journals, whereas a third study has been recently submitted for publication.
My first study demonstrated the efficacy of omega-3 in depressed patients and was based on psychometric data obtained with Hamilton Depression Rating Scale (HDRS) in published clinical studies. Omega-3 were also effective on bipolar disorder, although the evidence was weakened by the exclusion of three studies conducted on patients with MDD or on patients with depressive symptoms in which a lack of rigor in patients selection may lead to the inclusion of both normal emotional states and subthreshold depressed subjects, eventually affecting the results.
The study, in addition, highlights a number of methodological criticisms that mainly concern the inclusion criteria that should be more rigid and based on the score to psychometric tests rather than solely on clinical diagnosis. Psychometric instruments, in fact, represent an essential tool not only for a better diagnostic or for evaluating the efficacy of a treatment, but also for use inclusion criteria more rigid in order to improve the methodology in efficacy studies.
In the second study we critically reviewed the current literature on biological and neuropsychological markers in amnestic MCI patients who are at high risk to develop AD. A major conclusion of this study was that it is possible to identify a combination of neuropsychological tools (MMSE, MoCA, Rey s Test, FAB) and validated biological markers essential for an early diagnosis of AD and also for monitoring the response to disease modifying therapies in amnestic MCI patients who are at high risk to develop AD.
In the third study presented in this doctorate thesis we have adopted a new strategy of psychometric evaluation…
Subjects/Keywords: Area 06 - Scienze mediche; Psychometrics, Major Depression, Alzheimer s disease, Pharmacology
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APA (6th Edition):
Castellano, S. (2015). Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease. (Thesis). Università degli Studi di Catania. Retrieved from http://hdl.handle.net/10761/3789
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Castellano, Sabrina. “Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease.” 2015. Thesis, Università degli Studi di Catania. Accessed November 20, 2019.
http://hdl.handle.net/10761/3789.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Castellano, Sabrina. “Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease.” 2015. Web. 20 Nov 2019.
Vancouver:
Castellano S. Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease. [Internet] [Thesis]. Università degli Studi di Catania; 2015. [cited 2019 Nov 20].
Available from: http://hdl.handle.net/10761/3789.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Castellano S. Role of psychometric tools in the diagnosis and pharmacological treatment of Major Depression and Alzheimer s disease. [Thesis]. Università degli Studi di Catania; 2015. Available from: http://hdl.handle.net/10761/3789
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
9.
Reddy, Jambula Mukunda.
Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -.
Degree: Chemistry, 2011, Jawaharlal Nehru Technological University
URL: http://shodhganga.inflibnet.ac.in/handle/10603/4564
► Chapter-I deals with the introduction to Alzheimer?s disease, biological importance of (-)-Galanthamine, Memantine and the previous synthetic approaches cited in the literature towards the synthesis…
(more)
▼ Chapter-I deals with the introduction to
Alzheimer?s disease, biological importance of (-)-Galanthamine,
Memantine and the previous synthetic approaches cited in the
literature towards the synthesis of racemic.Galanthamine 1. In
chapter-II, studies towards the total synthesis of (-) Galanthamine
and its hydro bromide salt is described, wherein a stereo selective
reduction of prochiral ketone using L-selectride followed by
diastereomeric separation using di-p-toluyl-D-tartaric acid.
Synthesis and characterization of Galanthamine process related
chiral impurities have been described in chapter-III. A detailed
study on polymorphism of Galanthamine amorphous and crystalline
forms is presented in chapter-IV. An improved, cost effective and
scalable process has been developed for Memantine hydrochloride.
CHAPTER-I This chapter deals with the introduction to Alzheimer?s
disease, biological importance of (-)-Galanthamine and the previous
synthetic approaches cited in the literature towards the synthesis
of racemic and (-) Galanthamine 1. CHAPTER-II This chapter
describes the studies towards the total synthesis of (-)
Galanthamine and its hydrobromide salt, through a stereo selective
reduction of prochiral ketone using L-selectride followed by
diasteromeric separation using p-diparatoluyl-D-tartaric acid.
CHAPTER- III Synthesis and characterization of Galanthamine process
related chiral impurities have been described in chapter-III.
Impurities are in pharmaceutical industry are the unwanted
chemicals that remain with the active pharmaceutical ingredients
(API?s) or developed during synthesis of API or in formulation.
Various regulatory authorities like ICH, USFDA, Canadian Drug and
Health agency are emphasizing on the purity requirements and the
identification of impurities in API?s. Formation of impurities due
to incomplete chemical reactions, Impurities originating from
impurities in the starting material of the
synthesis.
References given chapters wise
Advisors/Committee Members: Reddy, G Mahesh, Himabindu, V.
Subjects/Keywords: Alzheimer?s Disease; Galanthamine hydrobromide; Memantine hydrochloride; Chemistry
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APA (6th Edition):
Reddy, J. M. (2011). Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -. (Thesis). Jawaharlal Nehru Technological University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/4564
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Reddy, Jambula Mukunda. “Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -.” 2011. Thesis, Jawaharlal Nehru Technological University. Accessed November 20, 2019.
http://shodhganga.inflibnet.ac.in/handle/10603/4564.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Reddy, Jambula Mukunda. “Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -.” 2011. Web. 20 Nov 2019.
Vancouver:
Reddy JM. Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -. [Internet] [Thesis]. Jawaharlal Nehru Technological University; 2011. [cited 2019 Nov 20].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4564.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Reddy JM. Synthesis and characterization of (-)Galanthamine
hydrobromide and memantine hydrochloride as anti Alzheimers drugs
and their impurities; -. [Thesis]. Jawaharlal Nehru Technological University; 2011. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4564
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Canterbury
10.
Kristinsdottir, Svava.
A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease.
Degree: Mechanical Engineering, 2009, University of Canterbury
URL: http://hdl.handle.net/10092/3200
► The role of the cardiovascular system is is to deliver oxygen and nutrients via arteries to the tissues of the body and to remove their…
(more)
▼ The role of the cardiovascular system is is to deliver oxygen and nutrients via arteries to the tissues of the body and to remove their waste products through the venous system. Due to certain pathological processes, arteries can be damaged resulting in a reduction of well oxygenated nutrient rich blood delivered to the tissues. Chronic hypoperfusion to the brain has been related to Alzeimer„s disease (AD). AD primarily affects people over 55 years of age, with an average duration of 7-10 years, resulting in death. Currently there are 600 million people in the world aged 60 years and over. This figure is expected to double by 2025 and to reach 2 billions by 2050. Finding a cure for a neurodegenerative disease such as AD would herald a major breakthrough in medical care. Currently AD is being widely investigated, but in order to find a cure, the complete pathophysiology of AD needs to be understood. Physilogical modelling could play a significant role to further develop that understanding. The underlying cause for AD is debated although several genetic loci have been identified for AD. Scientists have also demonstrated a strong connection with cerebral hypoperfusion. This results in tissue oxygen and nutrition deprivation which is a possible causative factor in the development of AD. In this thesis a Simulation model (SM) has been built to produce an arterial tree which resembles a natureal arterial tree. The SM model is based on Schreiner et al´s Constrained Constructive Optimization (CCO) method. The SM model produces a binary tree by choosing a random point in a defined area, and connects it to an exising tree structure, each time forming a new bifurcation. This bifurcation is optimized using the target function total minimum volume of the tree. The main difference between the CCO and SM method is the handling of the constrained areas in which the binary trees are grown within. The CCO method inceases the constrained area each time a segment is added to the tree structure, resulting in
rescaling of the total tree each time. The SM tree utilizes a unit circle for the tree to grow in and uses a scaling factor to retrieve the real values of the tree segments as needed. Two trees were produced using the SM method, containing 250 (T250) and 2000 (T2000) terminals respectively. The segment Radii and length of the T2000 terminal tree was extracted and reorganized to fit the data structure of a zero-dimensional model developed by Alzaidi. This model was used to produce pressure and flow rate results for the T2000 tree. The relative perfusion of the infiltrated area in the T2000 tree was also calculated. This thesis shows a close resemblance between the SM tree and a true arterial tree, both visually and geometrically. The morphometric distribution of radii and length showed a good correlation between the SM tree and previous experimental research. The real values of radii and length found in the T2000 SM tree were found to be of larger radii and shorter length compared to previously reported values in the literature.…
Subjects/Keywords: A Computational Model; Arterial Structures; Alzheimer´s Disease
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MLA ·
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APA (6th Edition):
Kristinsdottir, S. (2009). A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease. (Thesis). University of Canterbury. Retrieved from http://hdl.handle.net/10092/3200
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kristinsdottir, Svava. “A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease.” 2009. Thesis, University of Canterbury. Accessed November 20, 2019.
http://hdl.handle.net/10092/3200.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kristinsdottir, Svava. “A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease.” 2009. Web. 20 Nov 2019.
Vancouver:
Kristinsdottir S. A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease. [Internet] [Thesis]. University of Canterbury; 2009. [cited 2019 Nov 20].
Available from: http://hdl.handle.net/10092/3200.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kristinsdottir S. A Computational Model of Arterial Structures: A Relationship to Alzheimer´s Disease. [Thesis]. University of Canterbury; 2009. Available from: http://hdl.handle.net/10092/3200
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Penn State University
11.
Srinivasan, Mahadevan.
A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA.
Degree: MS, Electrical Engineering, 2011, Penn State University
URL: https://etda.libraries.psu.edu/catalog/11947
► We studied several neural network architectures for predicting whether a patient will convert to Alzheimer's disease after being initially diagnosed with Mild Cognitive Impairment. The…
(more)
▼ We studied several neural network architectures for
predicting whether a patient will convert to Alzheimer's disease
after being initially diagnosed with Mild Cognitive Impairment. The
first architecture to be studied was what we call a Localized
Neuron Architecture which tries to learn the non-linear
relationship between the brain atrophy and the age of the patient.
Next, we studied how good the performance is when using a standard
multilayer perceptron architecture. We used the brain scan data of
the first visit only since the prediction is prognostic.
Furthermore, we observed how including the age of the patient when
the base line scan was taken would impact the performance. On a
previous study based on this data, a support vector machine (SVM)
was used to predict conversion. Here, we are using a neural network
in place of an SVM. Also, we are trying to predict when the
conversion will happen. The challenge is to train a neural network
of the correct size and correct structure such that the error in
predicting conversion and the standard deviation in the prediction
of time at which conversion takes place are minimal.
Subjects/Keywords: Alzheimer s disease; MCI; Conversion; Neural Network; MCI
to AD
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APA ·
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APA (6th Edition):
Srinivasan, M. (2011). A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA. (Masters Thesis). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/11947
Chicago Manual of Style (16th Edition):
Srinivasan, Mahadevan. “A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA.” 2011. Masters Thesis, Penn State University. Accessed November 20, 2019.
https://etda.libraries.psu.edu/catalog/11947.
MLA Handbook (7th Edition):
Srinivasan, Mahadevan. “A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA.” 2011. Web. 20 Nov 2019.
Vancouver:
Srinivasan M. A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA. [Internet] [Masters thesis]. Penn State University; 2011. [cited 2019 Nov 20].
Available from: https://etda.libraries.psu.edu/catalog/11947.
Council of Science Editors:
Srinivasan M. A NEURAL NETWORK BASED APPROACH FOR PREDICTING A PATIENT'S
CONVERSION TO ALZHEIMER'S DISEASE BASED ON BRAIN SCAN DATA. [Masters Thesis]. Penn State University; 2011. Available from: https://etda.libraries.psu.edu/catalog/11947
University of Southern California
12.
Brommelhoff, Jessica Anne.
Underlying neural mechanisms of depression and
dementia.
Degree: PhD, Psychology, 2010, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/409934/rec/7659
► Studies have shown that white matter changes and other neuropathology frequently found in individuals with dementia, also may be related to late-life depression, or "vascular…
(more)
▼ Studies have shown that white matter changes and other
neuropathology frequently found in individuals with dementia, also
may be related to late-life depression, or "vascular dementia." As
these two conditions frequently coexist, the question of whether
there is a relationship between these neuropathological changes and
depression among individuals with manifest dementia has not been
established. The aim of the present study was to examine whether
there were neuroanatomical differences evident on the CT scans of
individuals with dementia based upon depression onset (no
depression versus early-onset versus late-onset) and history of
late-life depression (any episode of depression after age 60). We
hypothesized that individuals with dementia and late-onset
depression and/or late-life depression would be more likely than
non-depressed individuals with dementia to exhibit frontal lobe
deep white matter, subcortical white matter, and subcortical gray
matter hypodensities. We found that compared to individuals with
Alzheimer'
s disease and no depression, individuals with
Alzheimer'
s
disease and late-onset depression had a greater number of striatal
hypodensities (gray matter hypodensities in the caudate nucleus and
lentiform nucleus, which includes the putamen and globis pallidus).
In addition, we found that although there were no differences
between the non-depressed and late-onset and late-life depression
groups with respect to white matter hypodensities, the late-onset
depression and late-life depression groups in comparison to the
non-depressed group displayed a significantly higher degree of
global functional impairment, as well as impairment within the
domains of memory, orientation, and in the context of their home
activities and hobbies. These findings suggest that late-onset
depression may be a process that is distinct from the
neurodegenerative changes caused by
Alzheimer'
s
disease.
Advisors/Committee Members: Gatz, Margaret (Committee Chair), Mack, Wendy J. (Committee Member), Pedersen, Nancy L. (Committee Member), Prescott, Carol A. (Committee Member), Spann, Bryan M. (Committee Member).
Subjects/Keywords: late-life depression; dementia; Alzheimer'; s disease; computed tomography
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Brommelhoff, J. A. (2010). Underlying neural mechanisms of depression and
dementia. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/409934/rec/7659
Chicago Manual of Style (16th Edition):
Brommelhoff, Jessica Anne. “Underlying neural mechanisms of depression and
dementia.” 2010. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/409934/rec/7659.
MLA Handbook (7th Edition):
Brommelhoff, Jessica Anne. “Underlying neural mechanisms of depression and
dementia.” 2010. Web. 20 Nov 2019.
Vancouver:
Brommelhoff JA. Underlying neural mechanisms of depression and
dementia. [Internet] [Doctoral dissertation]. University of Southern California; 2010. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/409934/rec/7659.
Council of Science Editors:
Brommelhoff JA. Underlying neural mechanisms of depression and
dementia. [Doctoral Dissertation]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/409934/rec/7659
University of Southern California
13.
Hsieh, Chia-Ling.
Protein phosphatase 2A and annexin A5: modulators of
cellular functions.
Degree: PhD, Genetic, Molecular and Cellular Biology, 2015, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/248384/rec/5295
► In the past several years, I focused on two different projects for my PhD studies. The first project is to achieve a better understanding of…
(more)
▼ In the past several years, I focused on two different
projects for my PhD studies. The first project is to achieve a
better understanding of the mechanism of rhodopsin
dephosphorylation. Protein phosphatase 2A (PP2A) has been
recognized as the phosphatase responsible for rhodopsin
dephosphorylation for years. However, due to the absence of in vivo
evidence, the role of PP2A in regulating rhodopsin regeneration is
still questionable. This work not only clarifies the position of
PP2A in modulating rhodopsin function under physiological
condition, but also presents novel findings in the detail
mechanism. Previous isoelectric focusing results revealed that
arrestin-1 may play a positive role in modulating rhodopsin
dephosphorylaiton. Taking advantage of arrestin-1 knockout mice, we
isolated rod outer segments to compare how arrestin-1 influences
the distribution of PP2A subunits after light stimulation. Western
blot results revealed that the movement of PP2A scaffolding subunit
is regulated by arrestin-1 protein. In addition to inactivating
rhodopsin, arrestin-1 may mediate rhodopsin dephosphorylation by
modulating the cellular localization of PP2A in rod photoreceptors.
❧ Identifying the role of annexin A5 in amyloidogenesis is the goal
of my second project. Annexin A5 is an abundant protein without
clear physiological function. Earlier studies suggested a
protection effect of annexin A5 in against amyloid toxicity. We
generated APP-PS1/ANXA5KO mice by breeding APP-PS1dE9, a widely
used mouse model for Alzheimer’
s disease, under annexin A5 knockout
background. No overt difference in the number of brain Aβ plaques
were seen between the APP-PS1dE9 and the APP-PS1/ANXA5KO mice.
Interesting, sudden death was noticed in APP-PS1/ANXA5KO mice at
early age. Morphology shown in trichrome staining and
ultrastructural examination revealed severe damages in
cardiomyocytes from ANXA5KO and APP-PS1/ANXA5KO mice. These two
strain of mice also exhibited lower heart rates and higher QT
interval in electrocardiogram analysis. Furthermore, the level of
αB-crystallin, a chaperon molecule, is significantly increased in
the membrane fraction of cardiac extraction, and a specific
perinuclear distribution of αB-crystallin is also observed by
immunocytochemistry in ANXA5KO and APP-PS1/ANXA5KO mice. Therefore,
annexin A5 may play an important role in regulating cardiac
function in Alzheimer’
s disease model mice.
Advisors/Committee Members: Chen, Jeannie (Committee Chair), Hinton, David R. (Committee Member), Langen, Ralf (Committee Member).
Subjects/Keywords: protein phosphatase 2A; annexin A5; rhodopsin; Alzheimer'; s disease
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hsieh, C. (2015). Protein phosphatase 2A and annexin A5: modulators of
cellular functions. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/248384/rec/5295
Chicago Manual of Style (16th Edition):
Hsieh, Chia-Ling. “Protein phosphatase 2A and annexin A5: modulators of
cellular functions.” 2015. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/248384/rec/5295.
MLA Handbook (7th Edition):
Hsieh, Chia-Ling. “Protein phosphatase 2A and annexin A5: modulators of
cellular functions.” 2015. Web. 20 Nov 2019.
Vancouver:
Hsieh C. Protein phosphatase 2A and annexin A5: modulators of
cellular functions. [Internet] [Doctoral dissertation]. University of Southern California; 2015. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/248384/rec/5295.
Council of Science Editors:
Hsieh C. Protein phosphatase 2A and annexin A5: modulators of
cellular functions. [Doctoral Dissertation]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/248384/rec/5295
University of Southern California
14.
Rettberg, Jamaica Rhae.
Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype.
Degree: PhD, Neuroscience, 2015, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/436359/rec/1929
► Alzheimer’s disease is a progressive, fatal neurodegenerative disorder for which there is no preventative treatment or cure. Over 5 million Americans are currently living with…
(more)
▼ Alzheimer’
s disease is a progressive, fatal
neurodegenerative disorder for which there is no preventative
treatment or cure. Over 5 million Americans are currently living
with sporadic late‐onset Alzheimer’
s disease; of those diagnosed,
65% are women. Metabolic changes in the brain are among the
earliest features of the Alzheimer’
s pathological cascade. Estrogen
positively regulates the bioenergetic system of the brain from
glucose uptake to aerobic glycolysis, mitochondrial function and
ATP generation. Estrogen also regulates the peripheral metabolic
profile, and peripheral changes in metabolic homeostasis are
coincident with metabolic changes occurring in the brain. Loss of
ovarian hormones at menopause could initiate a bioenergetic and
metabolic crisis, resulting in a metabolic phenotype consistent
with increased risk for AD. ❧ To address this hypothesis, we
conducted an unbiased principal components analysis followed by
k‐means clustering of clinical data and bioenergetic indicators
derived from plasma from women in the Early vs. Late Intervention
Trial with Estradiol (ELITE). Nine metabolic biomarkers were
assessed. Metabolic clusters were compared by early‐ vs.
late‐menopause, and correlated with cognitive performance.
Metabolic clusters were also compared longitudinally between women
randomized to hormone therapy (HT) vs. placebo, to investigate the
effects of HT usage on metabolic biomarkers as well as cognitive
function. ❧ Metabolic variables measured at baseline generated
three distinct clusters. Women in one cluster had a healthy
metabolic profile; women in the second cluster were characterized
by high blood pressure; and women in the third cluster had an
overall unhealthy metabolic profile. Metabolic biomarkers within
all profiles were very stable and differed significantly among
clusters over the five years of the trial. At baseline, women in
the unhealthy metabolic cluster showed a trend towards worse
performance on tests of verbal memory than women in the healthy
cluster. Women in all clusters showed an improvement in cognitive
testing over five years, although women with the unhealthy
metabolic phenotype had the greatest improvement, and women with
high blood pressure had the least improvement. Longitudinal changes
in cognitive function differed significantly between women in early
and late menopause on select neuropsychological tests. Hormone
therapy had little overall effect on longitudinal cognitive
trajectories within the three clusters; however, women with the
high blood pressure phenotype showed the greatest metabolic and
cognitive benefit from hormone therapy. ❧ Alzheimer’s‐related
changes in the brain are known to begin years before clinically
detectable dementia; thus, identification of biomarkers indicating
the earliest preclinical changes is increasingly important.
Overall, this systems‐level approach demonstrates that metabolic
biomarkers, even within a healthy population, can be used to
identify phenotypes consistent with Alzheimer’
s risk. This
plasma‐based biomarker panel represents an…
Advisors/Committee Members: Brinton, Roberta D. (Committee Chair), Cadenas, Enrique (Committee Member), Mack, Wendy Jean (Committee Member), Hodis, Howard N. (Committee Member).
Subjects/Keywords: aging; female; metabolism; biomarker; phenotype; Alzheimer'; s disease
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rettberg, J. R. (2015). Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/436359/rec/1929
Chicago Manual of Style (16th Edition):
Rettberg, Jamaica Rhae. “Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype.” 2015. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/436359/rec/1929.
MLA Handbook (7th Edition):
Rettberg, Jamaica Rhae. “Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype.” 2015. Web. 20 Nov 2019.
Vancouver:
Rettberg JR. Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype. [Internet] [Doctoral dissertation]. University of Southern California; 2015. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/436359/rec/1929.
Council of Science Editors:
Rettberg JR. Development of biomarker profiles for early detection of
women with an at-risk for Alzheimer's disease phenotype. [Doctoral Dissertation]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/436359/rec/1929
University of Southern California
15.
Liu, Lifei.
Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases.
Degree: PhD, Neuroscience, 2009, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/279040/rec/3077
► Discovery of adult neurogenesis shed light on the exciting possibility that stimulation of this process can be applied as a novel regenerative strategy for CNS…
(more)
▼ Discovery of adult neurogenesis shed light on the
exciting possibility that stimulation of this process can be
applied as a novel regenerative strategy for CNS
disease
intervention. When compared to stem cell transplantation, this
regenerative strategy possesses several potential advantages:
first, the endogenous source of stem cells avoids immunological
reactions which are not uncommon in tissue transplantation. Second,
pharmacotherapy targeting the endogenous stem cell provides a
potentially more costeffective therapeutic intervention than stem
cell transplant. Lastly, little ethical or political concerns would
apply to this strategy. While the list of intrinsic and extrinsic
factors regulating adult neurogenesis is rapidly growing
(Kempermann and Gage 2000; Ming and Song 2005; Pozniak and Pleasure
2006), an increasing body of literature has shed light on the
involvement of gonadal hormones in this process (Gould, McEwen et
al. 1997; McEwen 2002; Brinton, Thompson et al. 2008; Brinton
2009). When compared to other regulators of neurogenesis such as
growth factors, gonadal hormones possess unique advantages
including small molecular weight and steady penetration of blood
brain barrier (Brinton 2009), making them competitive candidates as
neuroregenerative therapeutics. Among the gonadal hormones,
estrogens have been extensively studied for their regulatory roles
in neurogenesis, and multiple laborotaries have reported its
functions in promoting both neural progenitor cell proliferation
and survival (Gould, McEwen et al. 1997; McEwen 2002; Brinton,
Thompson et al. 2008; Brinton 2009). The effects of progesterone on
neurogenesis, however, were largely undetermined. As such, I
undertook a series of studies using cellular, morphological,
biochemical, genomic and behavioral approaches to characterize the
impact of progesterone on neurogenesis and its underlying
mechanism.; In the first part of my thesis, I described the effect
of progesterone in regulating neurogenesis and underlying
mechanism. My experiments showed that PRA mRNA was not detected in
rNPCs, whereas membrane associated PRs, Progesterone Receptor
Membrane Components (PGRMC) 1 and 2 mRNA were expressed.
Progesterone induced a significant increase in BrdU incorporation
that was confirmed by FACS analysis, which indicated that
progesterone promoted rNPC exit of G0/G1 phase at 5 hours, followed
by an increase in
S-phase at 6 hours and M-phase at 8 hours,
respectively. Microarray analysis of cell-cycle genes and RT-PCR
and Western blot validation revealed that progesterone increased
expression of genes that promote mitosis while decreasing
expression of genes that repress cell proliferation.
Progesterone-induced proliferation was not dependent upon
conversion to metabolites and was antagonized by the ERK1/2
inhibitor UO126. Progesterone-induced proliferation was isomer and
steroid specific. Computational structural analysis of progesterone
and its isomers indicated that the proliferative effect of
progesterone is likely to be mediated by PGRMC1/2. These data…
Advisors/Committee Members: Brinton, Roberta Diaz (Committee Chair), Alkana, Ronald (Committee Member), Neamati, Nouri (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; neurogenesis; regenerative medicine; gonadal hormone; progesterone; allopregnanolone
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APA (6th Edition):
Liu, L. (2009). Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/279040/rec/3077
Chicago Manual of Style (16th Edition):
Liu, Lifei. “Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases.” 2009. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/279040/rec/3077.
MLA Handbook (7th Edition):
Liu, Lifei. “Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases.” 2009. Web. 20 Nov 2019.
Vancouver:
Liu L. Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/279040/rec/3077.
Council of Science Editors:
Liu L. Gonadal hormone regulation of neurogenesis and therapeutic
implications for neurodegenerative diseases. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/279040/rec/3077
University of Southern California
16.
Carroll, Jenna C.
Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease.
Degree: PhD, Neuroscience, 2009, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/177259/rec/2507
► This dissertation seeks to investigate the broad issue of the effects of sex steroid hormones on neuroprotective measures related to aging and the prevention of…
(more)
▼ This dissertation seeks to investigate the broad issue
of the effects of sex steroid hormones on neuroprotective measures
related to aging and the prevention of the progression of
Alzheimer’
s disease (AD). In particular, this dissertation will
focus on the effects of female sex steroid hormones, estrogen and
progesterone both alone and in combination on AD in women. Abundant
evidence implicates sex steroid depletion in postmenopausal women
as a risk factor for the development of AD. However, there appears
to be a disconnect between experimental data clearly establishing
multiple estrogen protective functions, and clinical findings
showing that estrogen-based hormone therapy fails to prevent and
slow progression of cognitive decline and AD. Furthermore, while
estrogen’
s many beneficial effects in the brain have been well
established, the effects of progesterone, both alone and in
combination with estrogen, are currently unclear and
under-investigated. The Women’
s Health Initiative Memory Study
(WHIMS) raised several questions regarding the actions of
progestins in the brain and the efficacy of hormone therapy in
lowering the risk of AD in post-menopausal women. These questions
are the basis behind the experiments described in this
dissertation; a) the effects of estrogen and progesterone, both
alone and in combination on AD-like neuropathology, b) the
difference between various, clinically-relevant progestin exposures
in combination with estrogen, c) the “critical window hypothesis”
of aging brain responsiveness, d) the effects of
clinically-relevant selective estrogen receptor modulators (SERMs)
and e) the effects of activational vs. organizational sex steroid
hormone exposure.; The data demonstrate that aged rodents have
altered neuroprotective responsiveness to the hormone treatment,
that continuous progesterone treatment attenuates estrogen
neuroprotection against kainate lesion and Aβ accumulation, cyclic
progesterone has more beneficial effects than continuous
progesterone treatment, synthetic estrogen-like compounds can mimic
estrogen action, and that gender differences in AD pathogenesis can
be regulated by perinatal hormone action. Overall, these results
demonstrate that estrogen and progesterone therapies remain
important and potentially powerful preventive and intervention
strategies against AD and other age-related neurodegenerative
disorders. Understanding the effects of both estrogen and
progesterone in the brain is essential for future optimization of
estrogen-based hormone therapy for the potential prevention and
treatment of AD in post-menopausal women.
Advisors/Committee Members: Pike, Christian J. (Committee Chair), Finch, Caleb E. (Committee Member), Thompson, Richard (Committee Member), Miller, Carol (Committee Member), Mack, Wendy J. (Committee Member).
Subjects/Keywords: estrogen; progesterone; Alzheimer'; s disease; beta amyloid; tau; transgenic
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MLA ·
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Manager
APA (6th Edition):
Carroll, J. C. (2009). Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/177259/rec/2507
Chicago Manual of Style (16th Edition):
Carroll, Jenna C. “Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease.” 2009. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/177259/rec/2507.
MLA Handbook (7th Edition):
Carroll, Jenna C. “Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease.” 2009. Web. 20 Nov 2019.
Vancouver:
Carroll JC. Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/177259/rec/2507.
Council of Science Editors:
Carroll JC. Estrogen and progesterone-based hormone therapy and the
development of Alzheimer's disease. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/177259/rec/2507
University of Southern California
17.
George, Patricia Ann.
Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve.
Degree: PhD, Psychology, 2012, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/206250/rec/5291
► Cognitive reserve refers to the fact that some people are better able to compensate for compromised brain structures than others (Stern, 2009). This ability to…
(more)
▼ Cognitive reserve refers to the fact that some people
are better able to compensate for compromised brain structures than
others (Stern, 2009). This ability to respond differentially to
brain damage can be measured using different proxies, such as
education, occupation and leisure activities. The aim of this study
is to investigate if cognitive reserve moderates the relationship
between dementia severity, dementia duration, and age of onset with
the amount of atrophy in the brain. This study involved 193
individuals (123 females; 70 males) from the Swedish Twin Registry.
CT scans were rated using linear measurements to measure atrophy in
various parts of the brain. The results found that cognitive
reserve does moderate the relationship between dementia severity,
dementia duration and age of onset with the amount of atrophy in
the brain. Those who have higher cognitive reserve have more brain
damage at a given level of dementia severity and at a given level
of dementia duration. Individuals who have higher cognitive reserve
have a later age of onset than those who have less reserve.
Specific parts of the brain, like the temporal ventricle area,
frontal lobe and third ventricle are especially affected by this
relationship.
Advisors/Committee Members: Gatz, Margaret (Committee Chair), Mintz, Toben H. (Committee Member), Mack, Wendy Jean (Committee Member), Spann, Bryan (Committee Member).
Subjects/Keywords: protective factors; Alzheimer'; s disease; cognitive reserve; CT
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MLA ·
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CSE |
Export
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Manager
APA (6th Edition):
George, P. A. (2012). Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/206250/rec/5291
Chicago Manual of Style (16th Edition):
George, Patricia Ann. “Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve.” 2012. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/206250/rec/5291.
MLA Handbook (7th Edition):
George, Patricia Ann. “Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve.” 2012. Web. 20 Nov 2019.
Vancouver:
George PA. Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/206250/rec/5291.
Council of Science Editors:
George PA. Protective factors against the clinical onset of Alzheimer's
disease: a case for cognitive reserve. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/206250/rec/5291
University of Southern California
18.
Rosario, Emily R.
Age-related androgen depletion and the development of
Alzheimer's disease.
Degree: PhD, Neuroscience, 2007, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/330176/rec/581
► Advancing age is the most significant risk factor for the development of Alzheimer's disease (AD), however, which age-related changes underlie this effect remains unclear. In…
(more)
▼ Advancing age is the most significant risk factor for
the development of
Alzheimer'
s disease (AD), however, which
age-related changes underlie this effect remains unclear. In men,
one normal consequence of aging is a robust decline in the
circulating levels of the sex steroid hormone testosterone.
Testosterone depletion leads to functional impairments in
androgen-responsive tissues that are often manifested as the
clinical syndrome 'androgen deficiency in aging males'. Although
the brain is an androgen-responsive tissue unknown is (1) whether
brain levels of T decline during aging, and if so, (2) whether low
brain T levels place the aging brain at increased risk for AD, and
if so (3) what do androgens regulate that may modulate the
increased risk for AD. My thesis work investigated these questions
and others examining the relationships between sex steroid
hormones, advancing age, and development of AD. In Chapters Two and
Three we observed that brain levels of androgens but not estrogens
are significantly lower in men with moderate to severe AD in
comparison to normal men. To examine how low testosterone levels
may contribute to AD development we examined androgen regulation of
A[beta], a causal factor in the development of AD. In Chapters,
Three through Six we investigated the effects of androgens on
regulation and development of A[beta] pathology. We found that low
levels of testosterone, both in humans and a rodent model of male
reproductive aging, correlated with increased levels of soluble
A[beta]. Using a transgenic mouse model of AD we found that
depletion of endogenous androgens resulted in increased
accumulation of A[beta] pathology and behavioral impairments.
Replacement of androgens in these mice was able to prevent this
increased accumulation. These findings suggest the use of androgen
replacement therapy in men with low levels of
androgens.
Advisors/Committee Members: Pike, Christian J. (Committee Chair), Brinton, Roberta Diaz (Committee Member), Swanson, Larry W. (Committee Member), Thompson, Richard (Committee Member), Gatz, Margaret (Committee Member).
Subjects/Keywords: androgen; Alzheimer'; s disease
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rosario, E. R. (2007). Age-related androgen depletion and the development of
Alzheimer's disease. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/330176/rec/581
Chicago Manual of Style (16th Edition):
Rosario, Emily R. “Age-related androgen depletion and the development of
Alzheimer's disease.” 2007. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/330176/rec/581.
MLA Handbook (7th Edition):
Rosario, Emily R. “Age-related androgen depletion and the development of
Alzheimer's disease.” 2007. Web. 20 Nov 2019.
Vancouver:
Rosario ER. Age-related androgen depletion and the development of
Alzheimer's disease. [Internet] [Doctoral dissertation]. University of Southern California; 2007. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/330176/rec/581.
Council of Science Editors:
Rosario ER. Age-related androgen depletion and the development of
Alzheimer's disease. [Doctoral Dissertation]. University of Southern California; 2007. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/330176/rec/581
University of Southern California
19.
Singh, Chanpreet.
Memory abnormalities in Alzheimer's disease and anxiety
models.
Degree: PhD, Neuroscience, 2010, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/341763/rec/4035
► This dissertation seeks to investigate the memory abnormalities that result from Alzheimer's disease and anxiety disorders. In particular, this dissertation will focus on investigating if…
(more)
▼ This dissertation seeks to investigate the memory
abnormalities that result from
Alzheimer'
s disease and anxiety
disorders. In particular, this dissertation will focus on
investigating if neurogenic deficits in the hippocampus contribute
to the etiology of
Alzheimer'
s disease by studying a
hippocampal-dependent associative behavior test. Additionally, we
will study the potential of allopregnanolone (APα), a metabolite of
progesterone, to increase neurogenesis in the hippocampus of mice
and to determine the functional significance of these new neurons.
Our data has demonstrated that APα reverses the neurogenic and
cognitive deficits of
Alzheimer'
s disease mice to levels of
age-matched normal mice. This study suggests that APα could serve
as a regenerative therapeutic to prevent or delay neurogenic and
cognitive deficits associated with mild cognitive impairment and
Alzheimer'
s disease. As a second part of this thesis, we have
investigated memory abnormalities in a mouse model of anxiety. This
mouse model does not have any monoamine oxidase A and B and hence,
has significantly elevated levels of monoaminergic
neurotransmitters. Previous study has shown that MAO A/B KO mice
have anxiety-like behavior. As a further characterization of these
mice, we have found that there is a significant enhancement of
emotional memories in these mutants and point to these mice as an
interesting animal model to study the role of monoamines in
fear-related behaviors and post-traumatic stress disorder.
Furthermore, MAO A/B KO mice have shown enhanced level of learning
in cerebellar-dependent delay eyeblink conditioning, further
shedding light on the possible role of monoaminergic afferents in
the modulation of motor learning in the cerebellum.
Advisors/Committee Members: Thompson, Richard F. (Committee Chair), Brinton, Roberta Diaz. (Committee Member), Baudry, Michel (Committee Member), Swanson, Larry W. (Committee Member), Madigan, Stephen A. (Committee Member).
Subjects/Keywords: allopregnanolone; Alzheimer'; s disease; anxiety; eyeblink conditioning; learning and memory; neurogenesis
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APA ·
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MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Singh, C. (2010). Memory abnormalities in Alzheimer's disease and anxiety
models. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/341763/rec/4035
Chicago Manual of Style (16th Edition):
Singh, Chanpreet. “Memory abnormalities in Alzheimer's disease and anxiety
models.” 2010. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/341763/rec/4035.
MLA Handbook (7th Edition):
Singh, Chanpreet. “Memory abnormalities in Alzheimer's disease and anxiety
models.” 2010. Web. 20 Nov 2019.
Vancouver:
Singh C. Memory abnormalities in Alzheimer's disease and anxiety
models. [Internet] [Doctoral dissertation]. University of Southern California; 2010. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/341763/rec/4035.
Council of Science Editors:
Singh C. Memory abnormalities in Alzheimer's disease and anxiety
models. [Doctoral Dissertation]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/341763/rec/4035
University of Southern California
20.
Dave, Jennifer B.
Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status.
Degree: PhD, Psychology, 2009, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/407218/rec/485
► The purpose of this study was to determine whether subjective complaints about change in memory, attention, and language accurately reflect past decline or predict future…
(more)
▼ The purpose of this study was to determine whether
subjective complaints about change in memory, attention, and
language accurately reflect past decline or predict future
cognitive decline on neuropsychological tests in older adults with
normal cognition or with Alzheimer’
s disease. Further, the effect
of dementia status and depressive symptoms on these relationships
was assessed. Using the USC Alzheimer’
s Disease Research Center
longitudinal dataset, subjective cognitive complaints, cognitive
performance, and depressive symptoms were assessed in 132
participants. Overall, neither diagnostic group’
s complaints
accurately reflected past decline for any cognitive domain. Rather,
depressive symptoms predicted endorsement of complaints for all
domains. In addition, dementia status moderated the effect of
depression on future memory decline. Finally, language complaints
predicted future language decline in the entire sample, but similar
relationships were not present for attention and memory.
Implications of these findings are discussed.
Advisors/Committee Members: Knight, Bob G. (Committee Chair), Prescott, Carol A. (Committee Member), McCleary, Carol (Committee Member), Walsh, David (Committee Member), Walsh, John P. (Committee Member).
Subjects/Keywords: dementia; Alzheimer'; s disease; subjective complaints; aging; depression
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Dave, J. B. (2009). Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/407218/rec/485
Chicago Manual of Style (16th Edition):
Dave, Jennifer B. “Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status.” 2009. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/407218/rec/485.
MLA Handbook (7th Edition):
Dave, Jennifer B. “Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status.” 2009. Web. 20 Nov 2019.
Vancouver:
Dave JB. Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status. [Internet] [Doctoral dissertation]. University of Southern California; 2009. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/407218/rec/485.
Council of Science Editors:
Dave JB. Accuray of subjective cognitive complaints in a longitudinal
context: the effect of depression and dementia status. [Doctoral Dissertation]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/407218/rec/485
University of Southern California
21.
Jones, Randi Schnur.
Communication and home-based interventions in Alzheimer’s
disease – a review.
Degree: MA, Psychology, 2009, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/250876/rec/1467
► Communication is a basic human need, and communication problems are endemic among individuals with Alzheimer's disease (AD), with specific problems common at each stage of…
(more)
▼ Communication is a basic human need, and communication
problems are endemic among individuals with
Alzheimer'
s disease
(AD), with specific problems common at each stage of the
disease.
Because the majority of individuals with AD reside with family
caregivers in the community, evidence-based interventions to
improve communications between the members of these dyads, whose
needs differ from those of individuals living in long-term care
facilities with professional caregivers, are essential. This paper
discusses typical communication changes and difficulties that arise
during the course of AD and their psychosocial ramifications for
both caregivers and care recipients. It also reviews nine studies
of evidence-based interventions involving community-residing dyads
and finds that key attributes required for success are caregiver
education, individualization, and practicality.
Advisors/Committee Members: Gatz, MargaretAndersen, Elaine S. (Committee Chair), Knight, Bob G. (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; caregiver; communication; dementia; intervention; language
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jones, R. S. (2009). Communication and home-based interventions in Alzheimer’s
disease – a review. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/250876/rec/1467
Chicago Manual of Style (16th Edition):
Jones, Randi Schnur. “Communication and home-based interventions in Alzheimer’s
disease – a review.” 2009. Masters Thesis, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/250876/rec/1467.
MLA Handbook (7th Edition):
Jones, Randi Schnur. “Communication and home-based interventions in Alzheimer’s
disease – a review.” 2009. Web. 20 Nov 2019.
Vancouver:
Jones RS. Communication and home-based interventions in Alzheimer’s
disease – a review. [Internet] [Masters thesis]. University of Southern California; 2009. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/250876/rec/1467.
Council of Science Editors:
Jones RS. Communication and home-based interventions in Alzheimer’s
disease – a review. [Masters Thesis]. University of Southern California; 2009. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/250876/rec/1467
University of Southern California
22.
Neuse, James Leroy.
Aging, Azheimer’s disease and the visual sensory memory
system.
Degree: PhD, Psychology, 2010, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/311634/rec/589
► Prior research had indicated an unusually rapid decay of iconic memory for a subject who later developed indications of Alzheimer’s disease. Using the partial report…
(more)
▼ Prior research had indicated an unusually rapid decay
of iconic memory for a
subject who later developed indications of
Alzheimer’
s disease. Using the partial report paradigm (Sperling,
1960) three groups of subjects were tested. Subjects included older
subjects with a mild cognitive impairment (MCI), college-aged
students, and older control subjects. Long exposure times were used
for each of the groups of subjects to assure the researcher that
older subjects could visually process the stimuli. A battery of
neuropsychological tests was administered to each of the older
groups. It was found that those subjects with MCI had a much more
rapid decay of iconic memory than the older control group, although
visual acuity and short term memory were not significantly
different.
Advisors/Committee Members: Madigan, Stephen (Committee Chair), Lu, Zhong-Lin (Committee Member), Walsh, David A. (Committee Member), Hellige, Joseph (Committee Member), Murdock, Gail (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; sensory memory; iconic memory; aging
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APA (6th Edition):
Neuse, J. L. (2010). Aging, Azheimer’s disease and the visual sensory memory
system. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/311634/rec/589
Chicago Manual of Style (16th Edition):
Neuse, James Leroy. “Aging, Azheimer’s disease and the visual sensory memory
system.” 2010. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/311634/rec/589.
MLA Handbook (7th Edition):
Neuse, James Leroy. “Aging, Azheimer’s disease and the visual sensory memory
system.” 2010. Web. 20 Nov 2019.
Vancouver:
Neuse JL. Aging, Azheimer’s disease and the visual sensory memory
system. [Internet] [Doctoral dissertation]. University of Southern California; 2010. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/311634/rec/589.
Council of Science Editors:
Neuse JL. Aging, Azheimer’s disease and the visual sensory memory
system. [Doctoral Dissertation]. University of Southern California; 2010. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/311634/rec/589
University of Southern California
23.
Xu, Xiaobo.
Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration.
Degree: PhD, Neuroscience, 2013, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/335637/rec/6155
► Alzheimer’s disease is characterized by progressive memory loss and cognitive deficits, accumulation of ß-amyloid plaques and intracellular neurofibrillary tangles within the brain, and neuronal death.…
(more)
▼ Alzheimer’
s disease is characterized by progressive
memory loss and cognitive deficits, accumulation of ß-amyloid
plaques and intracellular neurofibrillary tangles within the brain,
and neuronal death. In addition to ß-amyloid and tau pathology,
mitochondrial dysfunction and free radical damage are also
hallmarks of AD brain, suggesting that oxidative stress might be
important in AD pathology. In the companion study we set out to
define the role oxidative stress plays in AD pathogenesis by
chronically treating mice that model human AD with the superoxide
dismutase (SOD)/catalase mimetic, EUK-207, starting before the
onset of pathology and cognitive deficits, and continuing until 9
months of age, when the AD phenotype is established. In the present
study, we initiated the treatment after the onset of pathology at 9
months of age. After 3 months of treatment, cognitive performance,
brain ß-amyloid and tau pathology as well as oxidative stress were
analyzed. At 12 months of age, 3xTg-AD mice exhibited a decline in
performance in both contextual and cued fear memory tasks as
compared to wild-type mice; EUK-207-treated 3xTg-AD mice did not
display any deficit in fear conditioning performance, as compared
to wild-type controls. Chronic treatment with EUK-207 protected
against increased levels of oxidized nucleic acids and lipid
peroxidation in brain and reduced ß-amyloid, tau and
hyperphosphorylated tau accumulation in amygdala and hippocampus of
3xTg-AD mice. Our results thus confirm a critical role for
oxidative stress in AD progression and strongly suggest the
potential usefulness for salen-manganese complexes as a treatment
for AD. ❧ Systemic injection of kainate produces repetitive seizure
activity in both adult and juvenile rats. However, while
kainate-induced seizure results in neurodegeneration in the limbic
system of adult rats, juvenile rats have been repeatedly shown to
be immune to the neurotoxic effects of kainate. The mechanisms
underlying this differential effect of seizure activity in adult
and juvenile rat brain are not clear. We previously reported that
kainate-induced seizure activity differentially affected calpain
activation in neonatal and adult rat brain. We recently discovered
that calpain could truncate the phosphatase PTEN, resulting in mTOR
activation and stimulation of protein synthesis, including Arc
synthesis. In the present study, we evaluated the effects of
kainate-induced seizure activity on levels of calpain, PTEN, mTOR,
and Arc in hippocampus from adult and postnatal rats. In adult
rats, seizure activity rapidly stimulated calpain-2, as evidenced
by decreased in drebrin and PTEN levels throughout the hippocampus.
It was also associated with increased mTOR and Arc levels in fields
CA1 and CA3 4 h after seizure initiation. PTEN truncation was
blocked by systemic injection of the calpain inhibitor calpepetin
before KA injection, but mTOR and Arc levels were not affected.
Interestingly, in p12-14 rats, seizure activity was not associated
with a rapid calpain activation and PTEN loss in any…
Advisors/Committee Members: Walsh, John P. (Committee Chair), Baudry, Michel (Committee Member), Watts, Alan G. (Committee Member), Dane, Joseph A. (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; oxidative stress; kainic acid; seizures
Record Details
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Xu, X. (2013). Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/335637/rec/6155
Chicago Manual of Style (16th Edition):
Xu, Xiaobo. “Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration.” 2013. Doctoral Dissertation, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/335637/rec/6155.
MLA Handbook (7th Edition):
Xu, Xiaobo. “Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration.” 2013. Web. 20 Nov 2019.
Vancouver:
Xu X. Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/335637/rec/6155.
Council of Science Editors:
Xu X. Studies of intracellular cascades mediating neuronal damage
in two animal models of neurodegeneration. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/335637/rec/6155
University of Southern California
24.
Rege, Sanket Vilas.
A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain.
Degree: MS, Physiology and Biophysics, 2015, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/583266/rec/436
► The receptor for advanced glycation end‐products (RAGE) binds to a repertoire of ligands resulting in sustained periods of cellular activation and perturbation as observed in…
(more)
▼ The receptor for advanced glycation end‐products
(RAGE) binds to a repertoire of ligands resulting in sustained
periods of cellular activation and perturbation as observed in
chronic inflammatory responses associated with diabetes,
Alzheimer’
s disease (AD), and amyloidoses. Studies have shown that
RAGE in the endothelium is a mediator for cerebral blood flow (CBF)
changes, inflammatory cytokines upregulation, as well as disruption
of tight junction proteins resulting from RAGE‐ligand interaction,
thus signifying a pivotal role in vascular dysfunction. In this
study we have generated Tie2-hRAGE+/0 mice, a transgenic mouse
model, in order to determine the effects of overexpressing human
RAGE (hRAGE) in endothelial cells. The expression was confirmed by
qRT-PCR, mass spectrometry, Western blotting, and
immunofluorescence staining. We observed an increased influx of Aβ
into the brain after systemic administration of fluorescent‐labeled
Aβ with these mice; while the levels of transporters responsible
for clearing Aβ from the brain, such as low density lipoprotein
receptor‐related protein 1 (LRP1) and p-glycoprotein 1 (Pgp1),
remained unaltered. The expression of tight junction proteins in
brain microvessels was also unchanged in these mice. Thus, we have
established a mouse model retaining an intact blood‐brain-barrier
in the resting state with hRAGE overexpressed in the endothelium.
This mouse model provides a valuable tool for studying the
contribution of vascular RAGE upregulation to chronic diseases like
AD, diabetes, and inflammatory disorders, along with the ability to
target RAGE with inhibitors to assess the potential to rescue the
phenotype seen with
disease models alone.
Advisors/Committee Members: Zlokovic, Berislav V. (Committee Chair), Kaslow, Harvey R. (Committee Member), Farley, Robert A. (Committee Member).
Subjects/Keywords: Alzheimer'; s disease; amyloid‐beta; RAGE; blood‐brain barrier
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rege, S. V. (2015). A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/583266/rec/436
Chicago Manual of Style (16th Edition):
Rege, Sanket Vilas. “A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain.” 2015. Masters Thesis, University of Southern California. Accessed November 20, 2019.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/583266/rec/436.
MLA Handbook (7th Edition):
Rege, Sanket Vilas. “A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain.” 2015. Web. 20 Nov 2019.
Vancouver:
Rege SV. A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain. [Internet] [Masters thesis]. University of Southern California; 2015. [cited 2019 Nov 20].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/583266/rec/436.
Council of Science Editors:
Rege SV. A transgenic mouse model with overexpression of human RAGE
in endothelial cells presents enhanced amyloid-beta transport into
the brain. [Masters Thesis]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/583266/rec/436
Tampere University
25.
Dania, Anna.
The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
.
Degree: 2014, Tampere University
URL: https://trepo.tuni.fi/handle/10024/96082
► Background: To date, clinical trials have reported inconsistent results on the efficacy of the combination therapy of Memantine plus an acetylcholinesterase inhibitor (AChEI) over a…
(more)
▼ Background: To date, clinical trials have reported inconsistent results on the efficacy of the combination therapy of Memantine plus an acetylcholinesterase inhibitor (AChEI) over a single-drug therapy in the treatment of Alzheimer s disease. This meta-analysis aim is to assess the efficacy of the combination therapy of Memantine plus an AChEI in the treatment of Alzheimer s disease compared with a single-drug therapy using an AChEI.
Methods: PubMed, Embase, and Cochrane library databases were searched through December 2013. Seven randomized controlled trials were included in the meta-analysis. A random-effects meta-analysis was used. Heterogeneity and publication bias were assessed.
Results: A combination therapy of an AChEI with memantine was associated with modestly better effects in terms of cognition and global function compared to a monotherapy with an AChEI. The effects of the combination therapy were no better than a monotherapy for daily living activity. However, the combination therapy showed benefits over a monotherapy for the behavioral outcome and the effect was independent of the stage of the disease. Moreover, the rate of adverse effects did not differ between a combination therapy and a single therapy.
Conclusions: The findings of this meta-analysis suggest that the combination therapy is more appropriate and should be administered for patients in more advanced stages. However, not all patients may benefit from the combination treatment. Identification of subgroups of patients with Alzheimer s disease who will benefit more from the combination treatment is needed.
Subjects/Keywords: Acetylcholinesterase inhibitor;
Alzheimer s disease;
donepezil;
galantamine;
memantine;
rivastigmine;
meta-analysis.
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Dania, A. (2014). The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
. (Masters Thesis). Tampere University. Retrieved from https://trepo.tuni.fi/handle/10024/96082
Chicago Manual of Style (16th Edition):
Dania, Anna. “The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
.” 2014. Masters Thesis, Tampere University. Accessed November 20, 2019.
https://trepo.tuni.fi/handle/10024/96082.
MLA Handbook (7th Edition):
Dania, Anna. “The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
.” 2014. Web. 20 Nov 2019.
Vancouver:
Dania A. The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
. [Internet] [Masters thesis]. Tampere University; 2014. [cited 2019 Nov 20].
Available from: https://trepo.tuni.fi/handle/10024/96082.
Council of Science Editors:
Dania A. The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis
. [Masters Thesis]. Tampere University; 2014. Available from: https://trepo.tuni.fi/handle/10024/96082
Freie Universität Berlin
26.
Burgert, Tilman.
Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer.
Degree: 2013, Freie Universität Berlin
URL: https://refubium.fu-berlin.de/handle/fub188/10594
► „Sortilin-related receptor with low-density lipoprotein receptor class A repeats“ (SORLA) ist ein 250 kDa Typ-I Transmembranprotein, das in Neuronen hauptsächlich im trans-Golgi Netzwerk (TGN) lokalisiert,…
(more)
▼ „Sortilin-related receptor with low-density lipoprotein receptor class A
repeats“ (SORLA) ist ein 250 kDa Typ-I Transmembranprotein, das in Neuronen
hauptsächlich im trans-Golgi Netzwerk (TGN) lokalisiert, wo es das „amyloid
precursor protein“ (APP) bindet. Diese Interaktion verhindert den Transport
von APP in endosomale Kompartimente der Zelle, in denen die Spaltung des
Proteins in das Peptid Aß, welches das molekulare Merkmal der
Alzheimer
Krankheit darstellt, stattfindet. Der zytoplasmatische Bestandteil von SORLA
enthält Bindestellen für zytosolische Adapterproteine, die den intrazellulären
Aufenthaltsort des SORLA/APP Komplexes in kultivierten Zellen beeinflussen.
Allerdings ist die Bedeutung der Adapter für den intrazellulären Transport von
SORLA und die Prozessierung von APP in vivo nicht bekannt. Ziel meiner
Dissertation war es, die Bedeutung zytosolischer Adapter sowohl für den
Transport von SORLA als auch für amyloidogene Vorgänge aufzuklären. Dabei habe
ich mich auf die Interaktion von SORLA mit zwei Adaptern fokussiert, die im
retrograden Proteintransport von Endosomen zurück in das TGN involviert sind.
Dazu habe ich neue, transgene Mausmodelle generiert, die einen mutierten SORLA
Rezeptor exprimieren, dem entweder die Bindestelle für den „retromer” Komplex
oder für das „phosphofurin acidic cluster sorting protein” (PACS) 1 fehlt. Wie
erwartet führen diese Mutationen in primären Neuronen zu einem veränderten
Transport von SORLA und APP sowie im Gehirn von Mäusen zu einer erhöhten APP
Spaltung. Damit weisen diese Ergebnisse zum ersten Mal auf die Bedeutung von
Adapter-vermitteltem retrograden Transport von SORLA für die Prozessierung von
APP in vivo hin. Die Bindestelle für PACS1, die in dem von mir generierten
Mausmodell mutiert wurde, überlappt mit der Bindestelle für den Adapter AP2.
Aus diesem Grund habe ich näher untersucht, welche Funktion speziell PACS1 im
Verlauf der
Alzheimer Krankheit übernimmt. Der „knockdown” von PACS1 in Zellen
der neuronalen Linie SH-SY5Y führt zu einer verringerten Proteinexpression des
Adapters und, wie in dem PACS1-bindedefizienten Mausmodell, zu einem
veränderten intrazellulären Transport der SORLA/APP Komplexe sowie zu einer
erhöhten Spaltung von APP. Überraschenderweise bewirkt der „knockdown“ von
PACS1 - SORLA-unabhängig - eine Erhöhung der Menge an Aß42. PACS1 ist in den
intrazellulären Transport des „cation-independent mannose-6-phosphate
receptors“ (CI-MPR) involviert, der für die Reifung der Aß-abbauenden Protease
Cathepsin B verantwortlich ist. Eine verringerte Proteinexpression von PACS1
führt darum zu einem fehlerhaften Transport des CI-MPR, was eine geringere
Cathepsin B Aktivität und, daraus resultierend, eine Erhöhung der Menge an
Aß42 zur Folge hat. Meine Ergebnisse konnten damit sowohl eine SORLA-abhängige
als auch eine SORLAunabhängige Funktion von PACS1 in amyloiden Prozessen
aufdecken.
Advisors/Committee Members: [email protected] (contact), m (gender), Prof. Dr. Rathjen (firstReferee), Prof. Dr. Willnow (furtherReferee).
Subjects/Keywords: Alzheimer´s disease; intracellular trafficking; receptor; APP; 500 Naturwissenschaften und Mathematik
Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Burgert, T. (2013). Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/10594
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Burgert, Tilman. “Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer.” 2013. Thesis, Freie Universität Berlin. Accessed November 20, 2019.
https://refubium.fu-berlin.de/handle/fub188/10594.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Burgert, Tilman. “Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer.” 2013. Web. 20 Nov 2019.
Vancouver:
Burgert T. Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer. [Internet] [Thesis]. Freie Universität Berlin; 2013. [cited 2019 Nov 20].
Available from: https://refubium.fu-berlin.de/handle/fub188/10594.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Burgert T. Relevanz der Interaktion zwischen SORLA und den Adaptorproteinen PACS1 und
VPS35 für molekulare Prozesse bei Morbus Alzheimer. [Thesis]. Freie Universität Berlin; 2013. Available from: https://refubium.fu-berlin.de/handle/fub188/10594
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Hong Kong University of Science and Technology
27.
Shen, Xuting LIFS.
Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia.
Degree: 2016, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-99719
;
https://doi.org/10.14711/thesis-b1626984
;
http://repository.ust.hk/ir/bitstream/1783.1-99719/1/th_redirect.html
► Alzheimer's disease (AD) is a largely sporadic neurodegenerative disorder that rarely strikes before the 7th decade with primary neuronal losses in hippocampus, frontal cortex and…
(more)
▼ Alzheimer's disease (AD) is a largely sporadic neurodegenerative disorder that rarely strikes before the 7th decade with primary neuronal losses in hippocampus, frontal cortex and certain subcortical nuclei. Ataxia telangiectasia (A-T), by contrast, is a multisystemic disease caused by mutations in the ATM (A-T mutated) gene. It strikes before age 5 and is characterized by dysfunctions in many tissues including the CNS where it leads to neurodegeneration, primarily in cerebellum. Despite these differences, AD and A-T share several characteristics including neurodegeneration associated with ectopic neuronal cell cycle event (CCE). This led me to explore the hypothesis that ATM reduction plays a role in AD pathogenesis. Partial ATM deficiency is able to drive epigenetic phenotypes and neuronal CCE, which can serve as markers for ATM reduction. I found that in AD mouse models, neurons under stress show evidence for a loss of ATM. In human AD, reduced ATM immunostaining is found in the same groups of neurons that are positive for the ATM loss-of-function markers in multiple brain regions where degeneration is prevalent. Though these ATM-deficient neurons represent only a fraction of the total cells in each affected region, their numbers significantly correlate with disease stage. This suggests that failure of ATM function is involved in AD pathology and may be an important contributor to the death of neurons. To understand its mechanism, we generated mice that were double heterozygotes for ATM mutations and AD-causing human transgenes. I found that the addition of the AD transgene to the heterozygous, Atm+/-, mice led to an exaggerated reduction in ATM protein level of frontal cortex. Compared to AD mice, the double heterozygotes have a shorter lifespan, reduced motor ability but no obvious aggravation of cognitive impairment. At the molecular level, ATM reduction suppresses the PI3/Akt pathway, leading to GSK3β activation and tau hyperphosphorylation. Another classic AD pathology, amyloid deposition, is increased even more dramatically by adding ATM deficiency to the AD mouse model. At a cellular level, double heterozygosity exacerbates cell death related processes including CCE, DNA damage response, and changes in the epigenetic landscape. By contrast, double heterozygotes have no significant changes in their inflammatory response. Significantly, only by combining aging with APP (PS/APP) genes does ATM reduction reveal its ability to accelerate AD progression. This is consistent with the case in human AD, which requires multiple factors rather than a single one to begin. I found that while many markers of degeneration are enhanced, the cells also try to protect themselves. Thus I document an increase of the NFkB subunit p50, which is neuroprotective. Hence neuronal fates are determined by the balance between protection and exacerbation. Taken together, ATM reduction is involved in AD pathogenesis via multiple pathologies including tau, amyloid deposits and neuronal death. Given my…
Subjects/Keywords: Alzheimer'; s disease
; Pathogenesis
; Ataxia telangiectasia
; Nervous system
; Degeneration
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Shen, X. L. (2016). Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-99719 ; https://doi.org/10.14711/thesis-b1626984 ; http://repository.ust.hk/ir/bitstream/1783.1-99719/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Shen, Xuting LIFS. “Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed November 20, 2019.
http://repository.ust.hk/ir/Record/1783.1-99719 ; https://doi.org/10.14711/thesis-b1626984 ; http://repository.ust.hk/ir/bitstream/1783.1-99719/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Shen, Xuting LIFS. “Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia.” 2016. Web. 20 Nov 2019.
Vancouver:
Shen XL. Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2019 Nov 20].
Available from: http://repository.ust.hk/ir/Record/1783.1-99719 ; https://doi.org/10.14711/thesis-b1626984 ; http://repository.ust.hk/ir/bitstream/1783.1-99719/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Shen XL. Translational research on Alzheimer's disease : the role of ATM in neurodegeneration and non-pharmacologic approaches to people with dementia. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: http://repository.ust.hk/ir/Record/1783.1-99719 ; https://doi.org/10.14711/thesis-b1626984 ; http://repository.ust.hk/ir/bitstream/1783.1-99719/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Hong Kong University of Science and Technology
28.
Yuen, Wai Hin LIFS.
Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease.
Degree: 2016, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-100407
;
https://doi.org/10.14711/thesis-b1731888
;
http://repository.ust.hk/ir/bitstream/1783.1-100407/1/th_redirect.html
► Alzheimer’s disease (AD) is a prevalent neurodegenerative disease characterized by progressive memory loss and synaptic dysfunctions. Converging lines of evidence suggest that soluble oligomeric amyloid-beta…
(more)
▼ Alzheimer’s disease (AD) is a prevalent neurodegenerative disease characterized by progressive memory loss and synaptic dysfunctions. Converging lines of evidence suggest that soluble oligomeric amyloid-beta (Aβ) contributes substantially to the synaptic loss in AD. Our group previously demonstrated that Eph receptor A4 (EphA4) mediates neurotoxicity of Aβ and that its activation impairs synaptic transmission and long-term potentiation. Importantly, oral administration of rhynchophylline (Rhy), a novel EphA4 inhibitor found in a Chinese medicinal herb (Uncaria rhynchophylla), improves synaptic impairment in APP/PS1 mice, an AD transgenic mouse model. To understand the mechanism by which Rhy exerts its beneficial effect, we conducted DNA microarray technology to analyze the transcriptome in the brains of APP/PS1 mice after Rhy treatment. A panel of candidate genes was identified to be upregulated in APP/PS1 mouse brains when compared to the wild-type controls. Accordingly, Rhy treatment restored the transcription levels of these genes to the wild-type control level. Gene ontology analysis revealed that these genes participate in innate and adaptive immunity. Among these candidates, Spp1 was one of the most differentially expressed genes in both comparisons and thus was selected for further characterization. The gene and protein regulation of Spp1 in APP/PS1 mouse brains after the Rhy treatment was verified by quantitative real-time PCR and ELISA respectively. Moreover, its protein expression increased significantly in APP/PS1 mice from 11 to 13 months of age, suggesting a correlation between Spp1 expression and AD progression. In addition, Aβ induced Spp1 production and secretion in cortical neuronal culture. This may explain the source of its elevated level in APP/PS1 mice. Together, these findings highlighted that Spp1 may be modulated by Rhy and it may contribute to the pathogenesis of AD.
Subjects/Keywords: Herbs
; Therapeutic use
; Alzheimer'; s disease
; Messenger RNA
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Manager
APA (6th Edition):
Yuen, W. H. L. (2016). Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-100407 ; https://doi.org/10.14711/thesis-b1731888 ; http://repository.ust.hk/ir/bitstream/1783.1-100407/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yuen, Wai Hin LIFS. “Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed November 20, 2019.
http://repository.ust.hk/ir/Record/1783.1-100407 ; https://doi.org/10.14711/thesis-b1731888 ; http://repository.ust.hk/ir/bitstream/1783.1-100407/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yuen, Wai Hin LIFS. “Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease.” 2016. Web. 20 Nov 2019.
Vancouver:
Yuen WHL. Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2019 Nov 20].
Available from: http://repository.ust.hk/ir/Record/1783.1-100407 ; https://doi.org/10.14711/thesis-b1731888 ; http://repository.ust.hk/ir/bitstream/1783.1-100407/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yuen WHL. Effect of rhynchophylline on the transcriptome in a mouse model of Alzheimer's disease. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: http://repository.ust.hk/ir/Record/1783.1-100407 ; https://doi.org/10.14711/thesis-b1731888 ; http://repository.ust.hk/ir/bitstream/1783.1-100407/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Debrecen
29.
Albertsson, Kristján Flygenring.
History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
.
Degree: DE – Általános Orvostudományi Kar, University of Debrecen
URL: http://hdl.handle.net/2437/233604
► In this thesis the history, ethiopathology and therapeutical possibilities of the disease will be described using informations gathered from scientific articles that where collected from…
(more)
▼ In this thesis the history, ethiopathology and therapeutical possibilities of the
disease will be described using informations gathered from scientific articles that where collected from the MEDLINE database by the use of the PupMed search engine and official books, see references.
With greater knowledge of pathoetiology, genetics and advanced imaging and diagnostic tools the diagnosis and early intervening of the
disease is possible. Furthermore with understanding of the pathoetiology of the
disease on the molecular level the researchers have now shifted their focus more on how we can slow down the progress of the
disease or even prevent it.
Advisors/Committee Members: Égerházi, Anikó (advisor), Department Of Psychiatry (advisor).
Subjects/Keywords: Alzheimer´s disease;
Therapy of alzheimer´s
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Record Details
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Albertsson, K. F. (n.d.). History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
. (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/233604
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Albertsson, Kristján Flygenring. “History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
.” Thesis, University of Debrecen. Accessed November 20, 2019.
http://hdl.handle.net/2437/233604.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Albertsson, Kristján Flygenring. “History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
.” Web. 20 Nov 2019.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
Albertsson KF. History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
. [Internet] [Thesis]. University of Debrecen; [cited 2019 Nov 20].
Available from: http://hdl.handle.net/2437/233604.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
Albertsson KF. History, ethiopathology and therapeutical possibilities of the Alzheimer’s disease
. [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/233604
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
30.
Panigrahi, Priya Pradayani.
Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;.
Degree: 2015, Jaypee University of Information Technology, Solan
URL: http://shodhganga.inflibnet.ac.in/handle/10603/48869
► Current progresses in whole genome sequencing have altered the way biologists tackle problems in diverse areas such as; biomedical research, bioinformatics, biotechnology, molecular biology, environmental…
(more)
▼ Current progresses in whole genome sequencing have
altered the way biologists tackle problems in diverse areas such
as; biomedical research, bioinformatics, biotechnology, molecular
biology, environmental biology etc Biology has currently become a
big data science principally supported by the advances in high
throughput experimental technologies Data intensive science
consists of three basic activities capture, curation, and analysis
All three of these phases of managing huge data elevate many new
research challenges to pursue in systems biology Scientists of the
21st century are rising up to the challenge of deciphering the
workings of multifaceted processes that involve the interaction of
numerous biomolecules such as genes, proteins etc The success of
future investigators in this area will depend in huge part on
broad, yet rigorous, training that accentuates the intertwine
nature of biological systems, whether it is the amino acids and
polypeptides in a protein complex, the gene products that make up a
developmental pathway or signaling pathway The purpose of systems
biology is the system level understanding of a cell, organism, or
disease, which can be recapitulated in the context of molecular
networks as an understanding of the structure of all the components
of a cell or organism up to molecular level, the capability to
predict the future condition of the cell or organism or disease
under a normal environment, the capacity to predict the output
responses for a given input stimulus, and the aptitude to estimate
the changes in system behavior upon perturbation of the components
or the environment newlineThe most familiar category of dementia
amongst older people is Alzheimer s disease AD, which primarily
involves the parts of the brain that control thought, memory and
language It was first described by German psychiatrist and
neuropathologist Dr Aloi Alzheimer in 1906 and was named after him
AD continues to be one of the most complicated human diseases to
treat
Advisors/Committee Members: Tiratha Raj Singh.
Subjects/Keywords: Alzheimer s Disease; Biomolecules; Enrichment Analysis; Genetic Association Study; System s Biology
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Panigrahi, P. P. (2015). Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;. (Thesis). Jaypee University of Information Technology, Solan. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/48869
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Panigrahi, Priya Pradayani. “Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;.” 2015. Thesis, Jaypee University of Information Technology, Solan. Accessed November 20, 2019.
http://shodhganga.inflibnet.ac.in/handle/10603/48869.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Panigrahi, Priya Pradayani. “Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;.” 2015. Web. 20 Nov 2019.
Vancouver:
Panigrahi PP. Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;. [Internet] [Thesis]. Jaypee University of Information Technology, Solan; 2015. [cited 2019 Nov 20].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/48869.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Panigrahi PP. Analysis of Bio Molecules for System Level Understanding
of Alzheimer s Disease;. [Thesis]. Jaypee University of Information Technology, Solan; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/48869
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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Open Access Theses and Dissertations