subject:(neurodegeneration)

University of Rochester

1. Harder, Jeffrey M. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.

Degree: PhD, 2013, University of Rochester

► Glaucomas are a group of diseases that often lead to blindness. Glaucomas are unified by the characteristic cell death of the output neuron of the… (more)

▼ Glaucomas are a group of diseases that often lead to blindness. Glaucomas are unified by the characteristic cell death of the output neuron of the retina, the retinal ganglion cell (RGC). In glaucoma, axonal injury to RGCs is a key event that precipitates their death; however, the molecular mechanisms leading to RGC death after axonal injury remain unclear. In fact, only one molecule, BAX, has been shown to be necessary for glaucomatous RGC death. BAX is a member of the Bcl-2 family of apoptotic regulators and BAX activation is a final step in triggering apoptosis. Other Bcl-2 family members can interact with BAX and regulate its activity. Identifying the Bcl-2 family members that mediate BAX activation in RGCs is an important step toward defining the cell signaling pathways responsible for RGC death in glaucoma. This work investigates the contributions of Bcl-2 family members implicated in RGC death in vivo using mice with specific Bcl-2 family genes deleted. Based on their function, the pro-death Bcl-2 family members BIM, BBC3, and BID are the primary candidates to mediate BAX activation in RGCs. BAX activation is highly potentiated by, if not requires, direct binding between BAX and these pro-death molecules. In mice lacking these genes, RGC death following axonal injury was significantly delayed. These experiments uncovered the additive, but hierarchical nature of BIM, BBC3, and BID function in RGCs. However, these molecules were not required for RGC death after axonal injury. Although BIM potently induced RGC death after axonal injury, the loss of RGCs in a mouse model of pigmentary glaucoma was also not prevented in a Bim knockout mouse. In RGCs, alternative BAX activation may occur following inhibition of pro-survival Bcl-2 family members. BCL-X was identified as an active endogenous factor that promotes RGC survival in the adult after axonal injury. However, disrupting other pro-death Bcl-2 family members, who primarily function to antagonize BCL-X, did not alter RGC death. The results provide insight into the specific and multifaceted nature of BAX activation in RGCs and point to an important interaction between pro-survival and pro-death signaling leading to RGC death in glaucoma.

Subjects/Keywords: Neurodegeneration

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APA (6^th Edition):

Harder, J. M. (2013). The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/26812

Chicago Manual of Style (16^th Edition):

Harder, Jeffrey M. “The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.” 2013. Doctoral Dissertation, University of Rochester. Accessed March 04, 2021. http://hdl.handle.net/1802/26812.

MLA Handbook (7^th Edition):

Harder, Jeffrey M. “The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death.” 2013. Web. 04 Mar 2021.

Vancouver:

Harder JM. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1802/26812.

Council of Science Editors:

Harder JM. The Role of Bcl-2 Family Members in Retinal Ganglion Cell Death. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/26812

Cornell University

2. Brady, Owen. Investigating Mechanisms Of Ftld-Tdp Pathogenesis.

Degree: PhD, Molecular and Cell Biology, 2014, Cornell University

URL: http://hdl.handle.net/1813/36146

► Frontotemporal lobar degeneration (FTLD) is a devastating dementia disorder that causes profound changes in personality, behavior, and language abilities. Major breakthroughs in the past decade… (more)

▼ Frontotemporal lobar degeneration (FTLD) is a devastating dementia disorder that causes profound changes in personality, behavior, and language abilities. Major breakthroughs in the past decade have advanced the understanding of the molecular genetics and pathological mechanisms underlying this disease, in particular the most common subtype, FTLD-TDP. Several causative and risk modifying genes have been identified which implicate defects in protein degradation and RNA metabolism pathways. The work presented here can be split into two main projects. In the first, I examine the physical properties of TDP-43 aggregation, which is a hallmark of FTLDTDP. Specifically, I characterize the role that phosphorylation plays in mediating the aggregation propensity of TDP-43 in a mammalian cell culture system. I further show that TDP-43 aggregates are cleared by the autophagy lysosome and ubiquitin proteasome systems, with the ubiquitin binding adaptor protein, p62/SQSTM1 facilitating this process. In the second project, I sought to characterize the recently identified FTLD-TDP risk factor, TMEM106B. Using cell culture model systems, I demonstrate that TMEM106B overexpression causes specific defects in lysosome size, morphology, and degradative capacity. I also ruled out the effect of a small coding variant associated with the TMEM106B risk allele when the proteins are highly expressed at the same level, indicating that increased TMEM106B levels are the likely cause of defects seen in certain cases of FTLD-TDP. I have also identified a putative degradation pathway implicating lumenal lysosomal enzymes and a membrane bound intramembrane protease, SPPL2a, in the sequential proteolysis of TMEM106B. This pathway may represent a novel therapeutic target for controlling TMEM106B levels in vivo. Overall, my work has contributed significant findings to the field of FTLD-TDP related research and has increased the body of knowledge regarding the cellular and molecular mechanisms that contribute to this terrible disease. Advisors/Committee Members: Hu, Fenghua (chair), Lin, David M. (committee member), Brown, William J (committee member).

Subjects/Keywords: Neurodegeneration; Lysosomes; TMEM106B

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APA (6^th Edition):

Brady, O. (2014). Investigating Mechanisms Of Ftld-Tdp Pathogenesis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36146

Chicago Manual of Style (16^th Edition):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis.” 2014. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/36146.

MLA Handbook (7^th Edition):

Brady, Owen. “Investigating Mechanisms Of Ftld-Tdp Pathogenesis.” 2014. Web. 04 Mar 2021.

Vancouver:

Brady O. Investigating Mechanisms Of Ftld-Tdp Pathogenesis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/36146.

Council of Science Editors:

Brady O. Investigating Mechanisms Of Ftld-Tdp Pathogenesis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36146

University of Miami

3. Tseng, LeinWeih Andrew. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2010, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/662

► Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One… (more)

▼ Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One isoform of Npcd, neuronal pentraxin receptor (NPR), is a type-II transmembrane protein responsible for the clustering of related neuronal pentraxins 1 and 2. However, recently identified cytosolic NPCD isoforms with no known function were discovered through their interaction with the intracellular domain of a receptor protein tyrosine phosphatase PTPRO. PTPRO is a signaling molecule known to be involved in the development of the nervous system. Additionally, upregulated expression of neuronal pentraxins has been implicated in neuronal cytotoxicity and associated with neurodegenerative diseases. Here, we demonstrate that a novel cytosolic NPCD isoform interacts with the BTB-Kelch protein Mayven/KLHL2. This interaction was identified through a yeast two-hybrid screen using the C-terminal pentraxin domain region of NPCD and confirmed through mammalian cell colocalization and co-immunoprecipitation studies. Domain truncation analysis suggests that the kelch domains of Mayven/KLHL2 are responsible for this interaction with NPCD. We also show that Mayven/KLHL2 is capable of interacting with Cullin 3, an integral protein in the Cullin-RING ubiquitin ligase complex. An in-vivo ubiquitylation assay demonstrates that overexpression of Mayven/KLHL2 increases NPCD ubiquitylation, and suggests a novel E3 ubiquitin ligase function of Mayven/KLHL2 with NPCD as its substrate. Furthermore, we observed an increased propensity of overexpressed NPCD to form aggresomes with coexpression of Mayven/KLHL2. As the formation of aggresomes is often associated with protein aggregation and deposition diseases, including a multitude of neurodegenerative diseases, we tested NPCD overexpression and the effects of Mayven/KLHL2 coexpression on neuronal cytotoxicity and apoptosis. Overexpressed NPCD in hippocampal neuron cultures resulted in increased cytotoxicity and apoptosis, further exacerbated by Mayven/KLHL2 coexpression. Our findings report an interaction between NPCD and Mayven/KLHL2, demonstrate a novel role of Mayven/KLHL2 as an E3 ubiquitin ligase, and explore a possible intersection between the ubiquitin-proteasome degradation pathway, neuronal pentraxins, and neurodegenerative disease. Advisors/Committee Members: Fulvia Verde, Sandra Lemmon, Abigail Hackam, John Bixby, Nagi Ayad - Outside Committee Member.

Subjects/Keywords: Protein Aggregation; Neurodegeneration

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tseng, L. A. (2010). Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/662

Chicago Manual of Style (16^th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Doctoral Dissertation, University of Miami. Accessed March 04, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/662.

MLA Handbook (7^th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Web. 04 Mar 2021.

Vancouver:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Internet] [Doctoral dissertation]. University of Miami; 2010. [cited 2021 Mar 04]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/662.

Council of Science Editors:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Doctoral Dissertation]. University of Miami; 2010. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/662

University of Miami

4. Tseng, LeinWeih Andrew. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2010, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/928

► Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One… (more)

▼ Neuronal pentraxin with chromo domain (NPCD) belongs to a family of neuronally-expressed pentraxin proteins thought to be involved in synaptic refinement and plasticity. One isoform of Npcd, neuronal pentraxin receptor (NPR), is a type-II transmembrane protein responsible for the clustering of related neuronal pentraxins 1 and 2. However, recently identified cytosolic NPCD isoforms with no known function were discovered through their interaction with the intracellular domain of a receptor protein tyrosine phosphatase PTPRO. PTPRO is a signaling molecule known to be involved in the development of the nervous system. Additionally, upregulated expression of neuronal pentraxins has been implicated in neuronal cytotoxicity and associated with neurodegenerative diseases. Here, we demonstrate that a novel cytosolic NPCD isoform interacts with the BTB-Kelch protein Mayven/KLHL2. This interaction was identified through a yeast two-hybrid screen using the C-terminal pentraxin domain region of NPCD and confirmed through mammalian cell colocalization and co-immunoprecipitation studies. Domain truncation analysis suggests that the kelch domains of Mayven/KLHL2 are responsible for this interaction with NPCD. We also show that Mayven/KLHL2 is capable of interacting with Cullin 3, an integral protein in the Cullin-RING ubiquitin ligase complex. An in-vivo ubiquitylation assay demonstrates that overexpression of Mayven/KLHL2 increases NPCD ubiquitylation, and suggests a novel E3 ubiquitin ligase function of Mayven/KLHL2 with NPCD as its substrate. Furthermore, we observed an increased propensity of overexpressed NPCD to form aggresomes with coexpression of Mayven/KLHL2. As the formation of aggresomes is often associated with protein aggregation and deposition diseases, including a multitude of neurodegenerative diseases, we tested NPCD overexpression and the effects of Mayven/KLHL2 coexpression on neuronal cytotoxicity and apoptosis. Overexpressed NPCD in hippocampal neuron cultures resulted in increased cytotoxicity and apoptosis, further exacerbated by Mayven/KLHL2 coexpression. Our findings report an interaction between NPCD and Mayven/KLHL2, demonstrate a novel role of Mayven/KLHL2 as an E3 ubiquitin ligase, and explore a possible intersection between the ubiquitin-proteasome degradation pathway, neuronal pentraxins, and neurodegenerative disease. Advisors/Committee Members: Fulvia Verde, Sandra Lemmon, Abigail Hackam, John Bixby, Nagi Ayad.

Subjects/Keywords: Protein Aggregation; Neurodegeneration

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tseng, L. A. (2010). Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/928

Chicago Manual of Style (16^th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Doctoral Dissertation, University of Miami. Accessed March 04, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/928.

MLA Handbook (7^th Edition):

Tseng, LeinWeih Andrew. “Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity.” 2010. Web. 04 Mar 2021.

Vancouver:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Internet] [Doctoral dissertation]. University of Miami; 2010. [cited 2021 Mar 04]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/928.

Council of Science Editors:

Tseng LA. Ubiquitylation of Neuronal Pentraxin with Chromo Domain by the E3 Ubiquitin Ligase Mayven/KLHL2 and Effects on Aggresome Formation and Neuronal Cytotoxicity. [Doctoral Dissertation]. University of Miami; 2010. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/928

University of Melbourne

5. Welton, Jeremy Morris. Therapeutic implications in genetic prion disease.

Degree: 2011, University of Melbourne

URL: http://hdl.handle.net/11343/37643

► Prion diseases are fatal neurodegenerative diseases caused by the misfolding of the prion protein (PrP). Of the three subsets of prion diseases (sporadic, genetic, acquired),… (more)

▼ Prion diseases are fatal neurodegenerative diseases caused by the misfolding of the prion protein (PrP). Of the three subsets of prion diseases (sporadic, genetic, acquired), genetic prion disease is associated with a mutation of PrP, leading to an increased disposition for the mutant PrP to misfold, and adopt a disease associated conformation (PrPD ). The following project investigated how a mutation of the prion protein, the P102L mutation, affected the disease associated properties of PrP and the impact of this mutation upon therapeutic outcome. The 102L and 101L mutation were introduced into human and mouse PrP respectively and expressed in rabbit kidney epithelial (RK13) cells to further investigate the effect of this mutation on the prion protein, and the outcome of prion infection. The 102L and 101L mutant PrP produced by RK13 cells was found to increase the disease associated characteristics of human and mouse PrP. Mutant PrP was also found to enhance the binding of PrP to glycosaminoglycans, a cofactor potentially involved in conversion of PrPC to PrPD . The human and mouse PrP expressing RK13 cell with or without the 102L/101L mutation were exposed to several human and mouse strains of prions to determine the susceptibility of the cells to prion infection. Prion infection of RK13 cells expressing 102P or 102L human PrP (huPrP) was not observed. RK13 cells expressing 101L mouse PrP (moPrP) were more susceptible to infection from two strains of prions, compared with 101P moPrP expressing RK13 cells. The enhanced susceptibility of 101L moPrP expressing RK13 (moRK13) cells was determined to be due to increased uptake of protease resistant PrP (PrPres ), mediated aberrant glycosaminoglycan binding. The therapeutic efficacy of glycosaminoglycan based therapy was investigated in the 101L model of genetic prion disease to determine if the enhanced binding of 101L moPrP affected the therapeutic action. Investigation of the membrane localisation of 101P and 101L moPrP by subcellular fractionation identified a subtle difference between 101P and 101L moPrP. A reduction in the proportion of 101L moPrP was detected in the lipid raft associated fractions compared with 101P moPrP, suggesting that a population of 101L moPrP is aberrantly located in another membrane domain or intracellular compartment. The results of the study suggest that the enhanced binding of 101L moPrP to glycosaminoglycans mediates the association of 101L PrP in an aberrant membrane domain, and mediates conversion of 101L moPrP to PrPres in spite of treatment with glycosaminoglycan or lipid raft altering therapeutics. The prophylactic treatment of persons found to have pathogenic mutations associated with genetic prion disease provides the best opportunity of intervening in prion disease progression, more-so than sporadic and acquired forms of prion disease which are…

Subjects/Keywords: neurodegeneration; prion; P102L

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Welton, J. M. (2011). Therapeutic implications in genetic prion disease. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37643

Chicago Manual of Style (16^th Edition):

Welton, Jeremy Morris. “Therapeutic implications in genetic prion disease.” 2011. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/37643.

MLA Handbook (7^th Edition):

Welton, Jeremy Morris. “Therapeutic implications in genetic prion disease.” 2011. Web. 04 Mar 2021.

Vancouver:

Welton JM. Therapeutic implications in genetic prion disease. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/37643.

Council of Science Editors:

Welton JM. Therapeutic implications in genetic prion disease. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/37643

University of Arizona

6. Coyne, Alyssa N. Dysregulation of mRNA Transport and Translation in ALS .

Degree: 2016, University of Arizona

URL: http://hdl.handle.net/10150/623181

► Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease affecting upper and lower motor neurons. Although many cellular processes such as cytoskeletal maintenance and synaptic… (more)

▼ Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease affecting upper and lower motor neurons. Although many cellular processes such as cytoskeletal maintenance and synaptic function are disrupted in ALS, the molecular mechanisms by which these defects arise remain poorly understood. TDP-43, an RNA binding protein linked to the majority of ALS cases, is involved in multiple aspects of RNA metabolism. It is hypothesized that TDP-43 may sequester its mRNA targets into cytoplasmic stress granules during disease progression in turn, inhibiting their localization and/or translation. This work uses a Drosophila model of ALS based on TDP-43, to provide evidence for TDP-43’s role in translation regulation of specific mRNA targets. Using a combination of genetic, molecular, and imaging approaches this work has identified TDP-43 induced post-transcriptional alterations in futsch and hsc70-4 mRNAs. First, futsch/MAP1B is a TDP-43 mRNA target altered at the level of mRNA localization and translation. This results in microtubule instability at the NMJ as evidenced by an increased number of satellite boutons and decreased number of Futsch positive loops that are thought to indicate stable synaptic contacts. Furthermore, overexpression of Futsch mitigates defects in microtubule stability and TDP-43 dependent locomotor dysfunction and also increases lifespan. Second, this work shows that synaptic expression of Hsc70-4, a molecular chaperone critical for synaptic vesicle cycling is involved in multiple steps of the synaptic vesicle cycle, is reduced at the NMJ when TDP-43 is overexpressed in motor neurons. Using a combination of electrophysiology and FM1-43 dye uptake assays, this work shows that motor neuron expression of TDP-43 induces defects in synaptic vesicle endocytosis. Third, this work identifies Fragile X Protein (FMRP) as a neuroprotective protein partner of TDP-43. FMRP overexpression remodels RNP granules, extracts TDP-43 from insoluble complexes, and restores the translation of specific TDP-43 targets. Together, these data provides evidence for translation dysregulation underlying microtubule instability and synaptic dysfunction in ALS pathogenesis and identifies restoration of translation via remodeling RNP granules as a neuroprotective strategy to mitigate toxicity. Advisors/Committee Members: Zarnescu, Daniela C (advisor), Zarnescu, Daniela C. (committeemember), Zinsmaier, Konrad (committeemember), Buchan, John (committeemember), Madhavan, Lalitha (committeemember).

Subjects/Keywords: Drosophila; neurodegeneration; ALS

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APA (6^th Edition):

Coyne, A. N. (2016). Dysregulation of mRNA Transport and Translation in ALS . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/623181

Chicago Manual of Style (16^th Edition):

Coyne, Alyssa N. “Dysregulation of mRNA Transport and Translation in ALS .” 2016. Doctoral Dissertation, University of Arizona. Accessed March 04, 2021. http://hdl.handle.net/10150/623181.

MLA Handbook (7^th Edition):

Coyne, Alyssa N. “Dysregulation of mRNA Transport and Translation in ALS .” 2016. Web. 04 Mar 2021.

Vancouver:

Coyne AN. Dysregulation of mRNA Transport and Translation in ALS . [Internet] [Doctoral dissertation]. University of Arizona; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10150/623181.

Council of Science Editors:

Coyne AN. Dysregulation of mRNA Transport and Translation in ALS . [Doctoral Dissertation]. University of Arizona; 2016. Available from: http://hdl.handle.net/10150/623181

University of Manchester

7. Howard, Daniel. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556

► Alzheimer’s disease (AD) pathogenesis is likely to be caused by dysfunction of two neuronal proteins, amyloid-beta (Aβ) and tau. Whilst excellent in vivo assays have… (more)

Subjects/Keywords: drosophila; neurodegeneration; amyloid; tau

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APA (6^th Edition):

Howard, D. (2016). The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556

Chicago Manual of Style (16^th Edition):

Howard, Daniel. “The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.” 2016. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556.

MLA Handbook (7^th Edition):

Howard, Daniel. “The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective.” 2016. Web. 04 Mar 2021.

Vancouver:

Howard D. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Mar 04]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556.

Council of Science Editors:

Howard D. The role of the cytoskeleton in Alzheimer’s disease: a Drosophila perspective. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:300556

Vanderbilt University

8. Ward, Nicholas John. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/13386

► Neuronal responses to stress are an important component of neurodegenerative disease and may represent targets for therapeutic intervention. In normal and pathogenic physiological conditions, members… (more)

Subjects/Keywords: neurodegeneration; glaucoma; TRPV1; TRP channels

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ward, N. J. (2014). The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13386

Chicago Manual of Style (16^th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/13386.

MLA Handbook (7^th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Web. 04 Mar 2021.

Vancouver:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/13386.

Council of Science Editors:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/13386

Boston University

9. Bleiberg, Benjamin Aaron. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.

Degree: MS, Medical Sciences, 2016, Boston University

URL: http://hdl.handle.net/2144/16770

► Huntington’s disease (HD) is one of nine polyglutamine diseases and it is caused by a CAG expansion in the HTT gene. HD is an autosomal,… (more)

▼ Huntington’s disease (HD) is one of nine polyglutamine diseases and it is caused by a CAG expansion in the HTT gene. HD is an autosomal, dominantly inherited neurodegenerative disease affecting between 2 and 5 individuals per 100,000 worldwide and it is currently untreatable. HD spreads from the striatum to the rest of the brain and causes widespread motor, cognitive, and psychiatric symptoms, including Huntington’s chorea. A fruitful approach to identifying potential therapeutic targets for HD is to modify genes in a model organism in an unbiased manner and screen the effect by testing the model in a functional assay. Drosophila models of HD have emerged as key tools for these large scale genetic screens thanks to their combination of ease of maintenance, and breeding in large numbers and their ability to be tested neurobehaviorally. During the course of HD pathogenesis in mammals, the FL-HTT protein is cleaved by many proteases including caspase-6. This cleavage leads to the co-existence of N-terminal (NT) as well as full-length (FL) forms of mutant HTT in the HD neurons. Drosophila lacks caspase-6 therefore FL-HTT is not naturally cleaved at its target site, this allows us to express either the FL mutant HTT or its cleaved NT fragment independently to characterize their differential pathogenic contribution. This study aims to test the concordance of a sample of 75 NT-HTT modifiers identified through a directed screen by testing them in a FL-HTT model. In doing so, we hope to identify shared modifiers and shared functional genetic networks, which may be particularly central to HD progression and useful areas in which to discover therapeutic targets. Further, this study may help to determine what types of models are necessary for future screens to adequately understand the genetic networks that underpin HD progression. In order to assess the impact of the modifier, flies expressing both the modifier and FL-HTT were tested in a climbing assay that measures motor function taking advantage of the model’s innate negative geotactic behavior. Motor performance is measured as the percentage of flies of each genotype that climb up to a 9 cm threshold in a given time interval. Flies were tested at 6 time points on days 18, 19, 20, 21, 22, and 25 of age in order to observe their level of neurobehavioral function in comparison to a positive control of flies with FL-HTT and no modifier and a negative control of flies without mutant HTT. When NT modifiers were tested in the FL model, there was an enrichment in modifiers relative to what is seen by chance. The NT suppressor sample was significantly enriched in modifier genes that effected motor performance in the FL model. Meanwhile, NT HD enhancers were not enriched with modifiers in the FL model. Some modifiers demonstrated contradictory effects on motor performance depending on the HD model tested. This could be caused by different mechanisms of toxicity inherent to NT versus FL HD or from secondary toxicity as the FL experiment occurred over a longer time period…

Subjects/Keywords: Medicine; Drosophila; Neurodegeneration; Huntington's disease

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bleiberg, B. A. (2016). Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16770

Chicago Manual of Style (16^th Edition):

Bleiberg, Benjamin Aaron. “Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.” 2016. Masters Thesis, Boston University. Accessed March 04, 2021. http://hdl.handle.net/2144/16770.

MLA Handbook (7^th Edition):

Bleiberg, Benjamin Aaron. “Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila.” 2016. Web. 04 Mar 2021.

Vancouver:

Bleiberg BA. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. [Internet] [Masters thesis]. Boston University; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2144/16770.

Council of Science Editors:

Bleiberg BA. Evaluating the concordance of N-terminal and full length Huntington's disease modifiers and identifying potential therapeutic targets in Drosophila. [Masters Thesis]. Boston University; 2016. Available from: http://hdl.handle.net/2144/16770

University of Cambridge

10. Sohail, Anood. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/290113

► Axons possess a continuous network of smooth tubular endoplasmic reticulum (ER), extending from the nuclear envelope throughout the neuron to synapses. Mutations affecting proteins with… (more)

▼ Axons possess a continuous network of smooth tubular endoplasmic reticulum (ER), extending from the nuclear envelope throughout the neuron to synapses. Mutations affecting proteins with intramembrane hairpin domains that model tubular ER membrane can lead to the axon degenerative disease, hereditary spastic paraplegia (HSP). However, the extent and mechanisms by which HSP proteins contribute to axonal ER organization and dynamics are unclear. To understand these mechanisms, there is a need to visualize axonal ER in wild-type and mutant live axons. I have therefore aimed to develop these tools in Drosophila larvae and adults, and use them to visualize mutant phenotypes. Firstly, I developed a system to visualize fluorescently marked ER in individual axons in adult fly legs, and tested how this can be used to investigate the effects of loss of intramembrane hairpin HSP proteins on ER in adult legs. Secondly, known mutations affecting HSP hairpin proteins reduce the axonal ER network but not severely; I hypothesized that additional HSP ER membrane proteins might contribute to residual tubule formation; these include Arl6IP, also reported to promote ER tubule formation. I generated transgenic flies to overexpress a fluorescently tagged eGFP::Arl6IP1, and found that this fusion protein localizes within axonal ER. To study whether loss of Arl6IP1 function affects axonal ER, I tested the effects of knockdown on this compartment, but found no consistent effects. To achieve stronger loss of function, I also generated a mutant stock that lacked one of the transmembrane domains and showed a slight developmental delay in homozygous Drosophila larvae. Like mutations in a number of other HSP hairpin proteins, this lesion is homozygous viable, and further characterization of its phenotype will help elucidate how Arl6IP1 contributes to modeling the axonal ER network. In conclusion, my work shows the utility of GFP markers of axonal ER, it can facilitate faster screening for other genes that potentially regulate ER structure and for ageing phenotypes that are not apparent in larval stages, and suggests Arl6IP1 as another HSP protein with a role in axonal ER organization.

Subjects/Keywords: Axonal ER; neurodegeneration; drosophila

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APA (6^th Edition):

Sohail, A. (2019). Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/290113

Chicago Manual of Style (16^th Edition):

Sohail, Anood. “Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/290113.

MLA Handbook (7^th Edition):

Sohail, Anood. “Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila.” 2019. Web. 04 Mar 2021.

Vancouver:

Sohail A. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/290113.

Council of Science Editors:

Sohail A. Visualizing Roles of Spastic Paraplegia Proteins in Organizing Axonal ER in Live Drosophila. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/290113

University of Debrecen

11. Seo, Woo Sung. Role of p53 and PARP-1 in neurodegenerative diseases .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/243137

► The thesis presents a general review of major neurodegenerative diseases and also discusses the role of p53 and PARP-1 in neurodegeneration. p53 and PARP-1 are… (more)

Subjects/Keywords: Neurodegeneration; neuroscience

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APA (6^th Edition):

Seo, W. S. (n.d.). Role of p53 and PARP-1 in neurodegenerative diseases . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/243137

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 (16^th Edition):

Seo, Woo Sung. “Role of p53 and PARP-1 in neurodegenerative diseases .” Thesis, University of Debrecen. Accessed March 04, 2021. http://hdl.handle.net/2437/243137.

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 (7^th Edition):

Seo, Woo Sung. “Role of p53 and PARP-1 in neurodegenerative diseases .” Web. 04 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Seo WS. Role of p53 and PARP-1 in neurodegenerative diseases . [Internet] [Thesis]. University of Debrecen; [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2437/243137.

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:

Seo WS. Role of p53 and PARP-1 in neurodegenerative diseases . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/243137

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Manitoba

12. Acosta, Crystal May R. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).

Degree: Pharmacy, 2013, University of Manitoba

URL: http://hdl.handle.net/1993/23504

► Nerve growth factor (NGF) represents a new therapeutic strategy for multiple sclerosis (MS) because of its immunomodulatory and neuroprotective activity. To analyze changes in NGF… (more)

Subjects/Keywords: MS; NGF; Neurodegeneration; Neuroimmunology

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APA (6^th Edition):

Acosta, C. M. R. (2013). Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/23504

Chicago Manual of Style (16^th Edition):

Acosta, Crystal May R. “Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).” 2013. Masters Thesis, University of Manitoba. Accessed March 04, 2021. http://hdl.handle.net/1993/23504.

MLA Handbook (7^th Edition):

Acosta, Crystal May R. “Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).” 2013. Web. 04 Mar 2021.

Vancouver:

Acosta CMR. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). [Internet] [Masters thesis]. University of Manitoba; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1993/23504.

Council of Science Editors:

Acosta CMR. Antigenic induction of nerve growth factor (NGF) in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). [Masters Thesis]. University of Manitoba; 2013. Available from: http://hdl.handle.net/1993/23504

University of Edinburgh

13. Vincenti, James Edward. Role of activation of microglia in neurodegenerative prion disease.

Degree: PhD, 2015, University of Edinburgh

URL: http://hdl.handle.net/1842/15928

► Prion diseases are a group of fatal neurodegenerative protein-misfolding diseases. Microglia, the resident myeloid cells found within the brain, have been shown to demonstrate a… (more)

▼ Prion diseases are a group of fatal neurodegenerative protein-misfolding diseases. Microglia, the resident myeloid cells found within the brain, have been shown to demonstrate a reactive morphology during the disease process with conflicting evidence for both a neurotoxic and neuroprotective role. The studies presented here aimed to investigate the role of microglia activation using transcriptomic and morphological analysis of prion disease in mice. Initially, the host immune response to prion disease was explored using a publically available mouse prion disease dataset. Re-analysis of this dataset was performed using BioLayout Express3D; a novel software tool that supports the visualisation and clustering of correlation networks. Disease-associated genes up-regulated during the later stages of infection were present in two main clusters. The cellular origin of these genes was explored by examining their expression in a dataset comprised of pure populations of cells. This demonstrated that the primary cluster of up-regulated transcripts encompassed genes expressed mainly by microglia and to a lesser extent astrocytes and neurons. The secondary cluster comprised almost exclusively of interferon response genes. The conclusions of these analyses were different from those of the original study that suggested disease-associated genes were primarily neuronal in origin. Mouse models of prion disease were established by infecting a novel line of BALB/cJ inbred mice, expressing EGFP under control of a myeloid specific Csf1r promoter, with the 79A prion strain. Quantification of the morphological changes of EGFP expressing microglia suggested the cells accumulated in the medulla at sites of early misfolded protein deposition with minimal change in their overall appearance. An activated microglia morphology was not observed until protein deposition was extensive. Isolation of EGFP expressing microglia was performed for transcriptome analysis. The vast majority of disease associated genes demonstrated increased expression at the onset of clinical symptoms. The gene list was found to be highly enriched for genes associated with an innate immune response regulated by the NFκB signalling cascade. Also highly enriched were processes associated with protein translation, energy production and stress response. These data suggest a high metabolic load is burdened by proliferating microglia; and as part of a response which is strikingly more pro-inflammatory in nature than has previously been attributed to the microglia phenotype within prion disease. As an active contributor to normal homeostasis, microglia are more than just innate immune surveillance and are now considered an integral component in both the healthy and diseased brain. The ramifications of activation toward the microglia phenotype shown here will have direct and potentially cytotoxic influence on neighbouring microglia and other brain cell types implying microglia as major contributors to the neurotoxic environment found within the CNS during prion disease. Furthermore…

Subjects/Keywords: 612.8; microglia; neurodegeneration; neuroimmunology; prion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vincenti, J. E. (2015). Role of activation of microglia in neurodegenerative prion disease. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/15928

Chicago Manual of Style (16^th Edition):

Vincenti, James Edward. “Role of activation of microglia in neurodegenerative prion disease.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed March 04, 2021. http://hdl.handle.net/1842/15928.

MLA Handbook (7^th Edition):

Vincenti, James Edward. “Role of activation of microglia in neurodegenerative prion disease.” 2015. Web. 04 Mar 2021.

Vancouver:

Vincenti JE. Role of activation of microglia in neurodegenerative prion disease. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1842/15928.

Council of Science Editors:

Vincenti JE. Role of activation of microglia in neurodegenerative prion disease. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/15928

University of Cambridge

14. Zhu, Ye. Studies on the autophagy gene WIPI4 and its interactor UBR5.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/300658

► Autophagy is a tightly regulated process that sequesters and delivers proteins and other cellular substances for degradation in the lysosome. Dysfunction of autophagy has been… (more)

Subjects/Keywords: autophagy; proteasome; neurodegeneration disease

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APA (6^th Edition):

Zhu, Y. (2020). Studies on the autophagy gene WIPI4 and its interactor UBR5. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/300658

Chicago Manual of Style (16^th Edition):

Zhu, Ye. “Studies on the autophagy gene WIPI4 and its interactor UBR5.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/300658.

MLA Handbook (7^th Edition):

Zhu, Ye. “Studies on the autophagy gene WIPI4 and its interactor UBR5.” 2020. Web. 04 Mar 2021.

Vancouver:

Zhu Y. Studies on the autophagy gene WIPI4 and its interactor UBR5. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/300658.

Council of Science Editors:

Zhu Y. Studies on the autophagy gene WIPI4 and its interactor UBR5. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/300658

University of Florida

15. Kim, Mi-Jung. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.

Degree: PhD, Medical Sciences - Molecular Cell Biology (IDP), 2018, University of Florida

URL: https://ufdc.ufl.edu/UFE0051774

Subjects/Keywords: cochlea; neurodegeneration

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APA (6^th Edition):

Kim, M. (2018). Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0051774

Chicago Manual of Style (16^th Edition):

Kim, Mi-Jung. “Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.” 2018. Doctoral Dissertation, University of Florida. Accessed March 04, 2021. https://ufdc.ufl.edu/UFE0051774.

MLA Handbook (7^th Edition):

Kim, Mi-Jung. “Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice.” 2018. Web. 04 Mar 2021.

Vancouver:

Kim M. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. [Internet] [Doctoral dissertation]. University of Florida; 2018. [cited 2021 Mar 04]. Available from: https://ufdc.ufl.edu/UFE0051774.

Council of Science Editors:

Kim M. Roles of Mitochondrial DNA Deletions, Point Mutations and Depletion in Age-Related Cochlear Neurodegeneration and Hearing Loss in Mice. [Doctoral Dissertation]. University of Florida; 2018. Available from: https://ufdc.ufl.edu/UFE0051774

University of Missouri – Columbia

16. Pinnegar, Abbie Jolene. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.

Degree: 2012, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/35437

► [ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Unspecified swallowing impairment (dysphagia) was recently reported in dogs with degenerative myelopathy (DM), a… (more)

Subjects/Keywords: dysphagia; brainstem nuclei; neurodegeneration

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APA (6^th Edition):

Pinnegar, A. J. (2012). Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. (Thesis). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/35437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pinnegar, Abbie Jolene. “Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.” 2012. Thesis, University of Missouri – Columbia. Accessed March 04, 2021. http://hdl.handle.net/10355/35437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pinnegar, Abbie Jolene. “Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia.” 2012. Web. 04 Mar 2021.

Vancouver:

Pinnegar AJ. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. [Internet] [Thesis]. University of Missouri – Columbia; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10355/35437.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pinnegar AJ. Investigating canine degenerative myelopathy as a disease model of amyotrophic lateral sclerosis for histopathological evidence of dysphagia. [Thesis]. University of Missouri – Columbia; 2012. Available from: http://hdl.handle.net/10355/35437

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

17. Amar, Fatou. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.

Degree: PhD, Neuroscience, 2016, University of Minnesota

URL: http://hdl.handle.net/11299/178973

► Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, with asymptomatic and symptomatic phases. Hallmark lesions of AD include extracellular deposits of fibrillar amyloid-β (A β)… (more)

Subjects/Keywords: Alzheimer's disease; molecular neuroscience; neurodegeneration

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APA (6^th Edition):

Amar, F. (2016). Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/178973

Chicago Manual of Style (16^th Edition):

Amar, Fatou. “Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.” 2016. Doctoral Dissertation, University of Minnesota. Accessed March 04, 2021. http://hdl.handle.net/11299/178973.

MLA Handbook (7^th Edition):

Amar, Fatou. “Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56.” 2016. Web. 04 Mar 2021.

Vancouver:

Amar F. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. [Internet] [Doctoral dissertation]. University of Minnesota; 2016. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11299/178973.

Council of Science Editors:

Amar F. Cellular And Molecular Mechanism Of Action Of The Amyloid-Beta Oligomer Abeta Star 56. [Doctoral Dissertation]. University of Minnesota; 2016. Available from: http://hdl.handle.net/11299/178973

University of Melbourne

18. Price, Katherine Ann. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/37158

► Alzheimer’s disease (AD) and other neurodegenerative diseases such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are characterized by altered biometal homeostasis. Low intracellular… (more)

▼ Alzheimer’s disease (AD) and other neurodegenerative diseases such as Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are characterized by altered biometal homeostasis. Low intracellular copper (Cu) levels have been observed in both AD and PD affected brain regions, while abnormal Cu metabolism by superoxide dismutase (SOD) may form the basis of some cases of ALS. Despite a surge in interest, the role of abnormal biometal balance and, in particular, homeostasis of Cu in these neurodegenerative diseases remains unclear. Growing evidence suggests that these changes in Cu homeostasis are an important early step in neurodegenerative processes. Restoring normal biometal metabolism may therefore offer a unique therapeutic opportunity. Supporting this, it has previously been shown that a bis(thiosemicarbazonato)copper(II) complex (CuII(btsc)) called CuII(gtsm) was capable of increasing intracellular Cu bio-availability and inhibited the accumulation of trimeric amyloid-beta (A) and phosphorylated tau in the brains of AD model mice and restored their cognitive function. Another CuII(btsc), CuII(atsm), has also produced positive effects in preliminary studies in multiple animal and cell models of PD and ALS. These Cu-complexes were initially investigated for use in cancer therapy and as imaging agents for hypoxic (low oxygen) tissues such as tumors, and the rationale for their application in neurodegenerative disease treatment was based on their ability to deliver metals into cells. In the current project, mechanisms of uptake, intracellular distribution and efflux of two CuII(btsc) complexes in neuronal and glial-like cells were examined. The aim was to more thoroughly understand their cellular accumulation and trafficking profiles and potential use in therapy for neurodegeneration. A combination of inductively-coupled plasma mass spectrometry (ICP-MS), atomic absorption spectrometry (AAS), microscopic analyses and additional techniques were employed. This study found that no single mechanism was clearly responsible for the uptake of the CuII(btsc)s. Instead, a combination of passive diffusion and ATP-independent, facilitated uptake most likely mediated accumulation of the CuII(btsc)s in the U87MG glioblastoma and M17 neuroblastoma cell lines. Efflux of the CuII(btsc) complexes appeared to be dependent upon the ligand backbone of the complex and the data supported a rapid, ATP-dependent efflux process that was difficult to delineate temporally from uptake. To investigate the intracellular distribution of CuII(btsc) complexes, a fluorescent derivative of CuII(atsm) (termed CuIIL1) was used. Upon entry into cells, CuIIL1 localized to organelles of a lysosomal and possibly autophagic origin in the M17 cell line. This appeared to be associated with a robust down-regulation of BiP protein expression indicative of a possible role for the CuII(btsc)s in cellular ER stress. Confocal microscopic studies were also performed…

Subjects/Keywords: biometals; cell metabolism; trafficking; neurodegeneration

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APA (6^th Edition):

Price, K. A. (2012). Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37158

Chicago Manual of Style (16^th Edition):

Price, Katherine Ann. “Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.” 2012. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/37158.

MLA Handbook (7^th Edition):

Price, Katherine Ann. “Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration.” 2012. Web. 04 Mar 2021.

Vancouver:

Price KA. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/37158.

Council of Science Editors:

Price KA. Investigating the cellular uptake, efflux and trafficking of metal complexes: implications for the therapy of neurodegeneration. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37158

University of Melbourne

19. Harrington, Karra. Undetected preclinical neurodegenerative disease in models of normal cognitive aging.

Degree: 2018, University of Melbourne

URL: http://hdl.handle.net/11343/219895

► With population aging, understanding cognitive changes that occur in late life is vital to support these increasing numbers of older adults to maintain their wellbeing… (more)

Subjects/Keywords: ageing; neurodegeneration; cognition; preclinical Alzheimer

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APA (6^th Edition):

Harrington, K. (2018). Undetected preclinical neurodegenerative disease in models of normal cognitive aging. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/219895

Chicago Manual of Style (16^th Edition):

Harrington, Karra. “Undetected preclinical neurodegenerative disease in models of normal cognitive aging.” 2018. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/219895.

MLA Handbook (7^th Edition):

Harrington, Karra. “Undetected preclinical neurodegenerative disease in models of normal cognitive aging.” 2018. Web. 04 Mar 2021.

Vancouver:

Harrington K. Undetected preclinical neurodegenerative disease in models of normal cognitive aging. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/219895.

Council of Science Editors:

Harrington K. Undetected preclinical neurodegenerative disease in models of normal cognitive aging. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/219895

University of Cambridge

20. Levy, Daniel Robert Siegfried. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.

Degree: PhD, 2018, University of Cambridge

URL: https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573

► Leucine rich repeat kinase 2 (LRRK2) is a 286 kDa protein expressed in a variety of tissues and cell types, including neuronal tissue and innate… (more)

▼ Leucine rich repeat kinase 2 (LRRK2) is a 286 kDa protein expressed in a variety of tissues and cell types, including neuronal tissue and innate immune cells. Mutations in LRRK2 have been linked to inflammatory diseases, most notably Crohn’s disease and Parkinson’s disease. Further to this, LRRK2 expression is induced by innate immune stimuli, and can be phosphorylated by Myd88 directed TLR signalling. Functional experiments were performed using macrophages from WT and LRRK2 knockout mice. Many phenotypes and interactions have been described for LRRK2 in a neuronal or in vitro context; therefore experiments in macrophages were specifically designed to investigate these phenotypes and interactions in an innate immune context. LRRK2 interacts with a range of small GTPase proteins called Rabs, which coordinate and carry out vesicular trafficking, including that of innate immune receptors. Further interactions have been shown with clathrin-mediated endocytic machinery and phagocytic machinery; including cytoskeletal components actin and tubulin. Accordingly, the role of LRRK2 in the expression, membrane localisation, and ligand-induced endocytosis of the innate immune receptors such as TLR4 were assayed. TLR4 plays an important role in immune responses to alpha-synuclein, an immunogenic protein aggregate that accumulates as part of Parkinson’s disease pathology, making it a particularly interesting target for this assay. No effect was shown for LRRK2 on TLR4 expression or receptor mediated endocytosis, so attention was focused upon LRRK2 cytoskeletal interactions. An unclear role of LRRK2 has been described in phagocytosis. Application of LRRK2 KO macrophages in a series of systematic phagocytosis assays was used to demonstrate and clarify that there is no role of LRRK2 in the phagocytosis of simple beads, opsonised material, or complex bacterial targets expressing a range of immunogenic molecules such as LPS. A genome wide approach was applied to further investigate the role of LRRK2 in TLR4 mediated signalling, as well as NOD2 mediated signalling. Comparison of LPS responses between WT and LRRK2 KO genotype macrophages identified a role of LRRK2 in modulating transcription of a range of chemokines and chemokine receptors. This indicates a specific role of LRRK2 in regulating chemotaxis in LPS stimulated cells. Knockout of LRRK2 resulted in a complete reversal of the regulation of the expression of EPAC1, a cAMP inducible protein working in parallel with a previously described LRRK2 interacting protein PKA. EPAC1 acts, at least in part, via Ca2+ signalling. Modulation of signalling through pathways such as Ca2+, Wnt and cAMP appear as a theme in results described in this transcriptomic experiment. A parallel metabolomic approach allowed analysis of ceramide levels in resting and innate immune stimulated macrophages. Ceramides are lipid molecules able to activate the NLRP3 inflammasome, as well as modulate alpha-synuclein pathology via ceramide metabolomic products. In contrast to results described in neuronal tissue,…

Subjects/Keywords: 616.8; immunology; Parkinson's disease; neurodegeneration

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APA (6^th Edition):

Levy, D. R. S. (2018). Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573

Chicago Manual of Style (16^th Edition):

Levy, Daniel Robert Siegfried. “Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.” 2018. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573.

MLA Handbook (7^th Edition):

Levy, Daniel Robert Siegfried. “Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system.” 2018. Web. 04 Mar 2021.

Vancouver:

Levy DRS. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2021 Mar 04]. Available from: https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573.

Council of Science Editors:

Levy DRS. Exploring the role of Leucine Rich Repeat Kinase 2 within the innate immune system. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://doi.org/10.17863/CAM.20803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744573

University of Sydney

21. Cross, Nathan. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .

Degree: 2017, University of Sydney

URL: http://hdl.handle.net/2123/17763

► There is growing evidence that sleep disturbances share associations with neurodegeneration, and poor sleep is emerging as an independent risk factor for dementia. As a… (more)

▼ There is growing evidence that sleep disturbances share associations with neurodegeneration, and poor sleep is emerging as an independent risk factor for dementia. As a common sleep disorder, obstructive sleep apnea (OSA) has been connected to compromised cognition, brain integrity and an increased risk for dementia. However, there is a need to clarify these relationships in older adults and understand the mechanisms underpinning the link between OSA and cognitive decline. The aims of this thesis were: 1) to characterise and quantitatively analyse the relationship between OSA and cognitive function in older adults, 2) to determine whether any changes in neural oscillations during sleep or brain grey matter thickness and volume, might be associated with OSA and related to makers of cognitive decline (e.g. memory) in a sample of older adults at-risk for dementia. At-risk adults were diagnosed as health-seeking older adults (>50 years) with subjective or objective cognitive impairment. Neural oscillations were recorded using electroencephalography and brain grey matter thickness and volume were measured using magnetic resonance imaging. These findings showed that the presence of OSA in at-risk older adults is related to a marked reduction in specific neural oscillations (sleep spindles), key aspects of sleep microarchitecture that are integrally linked with memory consolidation. Furthermore, OSA-related oxygen desaturation was associated with decreased cortical thickness in both the left and right temporal lobes, while sleep disturbance was related to increased cortical thickness in in frontal, central and occipital regions of the right cortex. This work has provided evidence that OSA is related to features which may contribute to early-stage neurodegeneration and cognitive decline, which are important in identifying critical periods for intervention. Given that effective treatment exists for OSA, efforts to increase OSA screening in older adults are now warranted.

Subjects/Keywords: sleep; apnoea; ageing; neurodegeneration

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APA (6^th Edition):

Cross, N. (2017). Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17763

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cross, Nathan. “Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .” 2017. Thesis, University of Sydney. Accessed March 04, 2021. http://hdl.handle.net/2123/17763.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cross, Nathan. “Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration .” 2017. Web. 04 Mar 2021.

Vancouver:

Cross N. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2123/17763.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cross N. Obstructive sleep apnoea in older adults: Predictors of cognitive decline and neurodegeneration . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17763

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New South Wales

22. Chiu, Alexander Simon Che-Kean. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.

Degree: Biotechnology & Biomolecular Sciences, 2013, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true

► The cyanotoxin β-methylamino-L-alanine (BMAA) has long been associated with the elevated incidence of amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC). BMAA has been shown to be… (more)

▼ The cyanotoxin β-methylamino-L-alanine (BMAA) has long been associated with the elevated incidence of amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC). BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks, monkeys and zebrafish have shown that BMAA can cause neurodegenerative symptoms such as ataxia and convulsions, as well as disruption to neural development. Previous in vitro studies using mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca2+ influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. Data presented here indicate that BMAA induces increased intracellular Ca2+ influx, DNA damage, mitochondrial activity, lactate dehydrogenase (LDH) release and generation of ROS in human neurons. The amelioration of LDH release in the presence of the N methyl-D-aspartate (NMDA) receptor antagonist MK801 indicates that the neurotoxic effects of BMAA are mediated via NMDA receptor activation. Immunocytochemical stains show that BMAA induces the expression of neuronal nitric oxide synthase (nNOS) and caspase-3 indicating that it can stimulate apoptosis in human neurons, presumably via activation of NMDA receptors. Rat olfactory ensheathing cells (OECs) were also challenged with exogenous BMAA resulting in elevated cell death. Significant increases in Ca2+ influx, enhanced production of ROS, and disruption to mitochondrial activity were observed in OECs. This is the first study investigating BMAA toxicity using pure glial cells. These findings align BMAA with all proposed mechanisms of degeneration in ALS, those being non-cell autonomous death, excitotoxicity and mitochondrial dysfunction. Additionally, novel genes and proteins have been identified that were differentially expressed in BMAA treated OECs. Some of the identified genes/proteins of interest have previously been linked to Alzheimer's disease. Other genes/proteins identified have reported functions in the regulation of mitochondrial activity and cell cycle and apoptosis. Cell cycle analysis of OECs treated with BMAA resulted in cell cycle arrest at the G2/M phase. Advisors/Committee Members: Neilan, Brett, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW, Welch, Jeffrey, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: ALS/PDC; BMAA; Neurodegeneration; Cyanotoxin

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APA (6^th Edition):

Chiu, A. S. C. (2013). A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Chiu, Alexander Simon Che-Kean. “A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.” 2013. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Chiu, Alexander Simon Che-Kean. “A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity.” 2013. Web. 04 Mar 2021.

Vancouver:

Chiu ASC. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. [Internet] [Doctoral dissertation]. University of New South Wales; 2013. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true.

Council of Science Editors:

Chiu ASC. A toxicological analysis of the cyanotoxin β-methylamino-L-alanine at multiple neural levels and identification of novel modes of activity. [Doctoral Dissertation]. University of New South Wales; 2013. Available from: http://handle.unsw.edu.au/1959.4/52422 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11095/SOURCE01?view=true

Texas State University – San Marcos

23. Stavinoha, Rebecca C. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.

Degree: MS, Human Nutrition, 2015, Texas State University – San Marcos

URL: https://digital.library.txstate.edu/handle/10877/8766

No abstract prepared. Advisors/Committee Members: Vattem, Dhiraj A. (advisor), Correia, Roberta (committee member), Apostolidis, Emmanouil (committee member).

Subjects/Keywords: Cinnamon; Neurodegeneration

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APA (6^th Edition):

Stavinoha, R. C. (2015). In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. (Masters Thesis). Texas State University – San Marcos. Retrieved from https://digital.library.txstate.edu/handle/10877/8766

Chicago Manual of Style (16^th Edition):

Stavinoha, Rebecca C. “In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.” 2015. Masters Thesis, Texas State University – San Marcos. Accessed March 04, 2021. https://digital.library.txstate.edu/handle/10877/8766.

MLA Handbook (7^th Edition):

Stavinoha, Rebecca C. “In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster.” 2015. Web. 04 Mar 2021.

Vancouver:

Stavinoha RC. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. [Internet] [Masters thesis]. Texas State University – San Marcos; 2015. [cited 2021 Mar 04]. Available from: https://digital.library.txstate.edu/handle/10877/8766.

Council of Science Editors:

Stavinoha RC. In Vivo Neuroprotective Effects of Cinnamon Bioactive Compounds in C. elegans and D. melanogaster. [Masters Thesis]. Texas State University – San Marcos; 2015. Available from: https://digital.library.txstate.edu/handle/10877/8766

University of New South Wales

24. Braidy, Nady. NAD+ metabolism in neurodegeneration and aging.

Degree: Medical Sciences, 2011, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true

► Elevated levels of several kynurenine pathway (KP) metabolites, e.g. quinolinic acid (QUIN), have been implicated in the aetiology of several neurodegenerative diseases such as Alzheimer‟s… (more)

▼ Elevated levels of several kynurenine pathway (KP) metabolites, e.g. quinolinic acid (QUIN), have been implicated in the aetiology of several neurodegenerative diseases such as Alzheimer‟s disease (AD) and Multiple Sclerosis (MS). The end product of the KP is NAD+, an essential cofactor for energy metabolism. NAD+ also serves as the sole substrate for the DNA repair enzyme, poly(ADP-ribose) polymerase (PARP). More recently, NAD+ has been identified as an essential substrate for a new class of histone deacetylases known as SIRT1, which has been linked to longevity. Free radical mediated PARP activation and NAD+ depletion may contribute to brain aging and tissue damage in multiple brain disorders.Our results indicate a direct involvement of the KP in NAD+ synthesis in human brain cells, and that reduced intracellular NAD+ synthesis leads to reduced activity of NAD+ dependent histone deacetylase function. We show that the KP metabolite and NMDA receptor agonist, QUIN is a substrate of NAD+ synthesis in nanomolar concentrations in both astrocytes and neurons but is cytotoxic at higher amounts in both cell types. These results also show a clear neuroprotective effect of NMDA receptor antagonism and nitric oxide synthase inhibition against QUIN mediated neuronal and glial cytoxicity, strongly suggesting that QUIN-induced excitotoxicity in astrocytes and neurons is mediated by overactivation of the NMDA receptor. We also show that natural polyphenolic compounds can attenuate QUIN-mediated neurotoxicity by a number of mechanisms reported herein.We also provide evidence for the first time that tryptophan metabolism leading to NAD+ synthesis is unregulated in tissue obtained from aged female wistar rats. SIRT1 activity was also decreased and acetylated p53 increased in these same animals in response to an unregulated PARP-mediated NAD+ depletion. Consistent with these animal data we also found that human serum NAD+ levels are reduced in MS. Advisors/Committee Members: Grant, Ross, Medical Sciences, Faculty of Medicine, UNSW, Guillemin, Gilles, Medical Sciences, Faculty of Medicine, UNSW.

Subjects/Keywords: NAD+; metabolism; neurodegeneration; aging

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APA (6^th Edition):

Braidy, N. (2011). NAD+ metabolism in neurodegeneration and aging. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Braidy, Nady. “NAD+ metabolism in neurodegeneration and aging.” 2011. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Braidy, Nady. “NAD+ metabolism in neurodegeneration and aging.” 2011. Web. 04 Mar 2021.

Vancouver:

Braidy N. NAD+ metabolism in neurodegeneration and aging. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true.

Council of Science Editors:

Braidy N. NAD+ metabolism in neurodegeneration and aging. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51345 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10026/SOURCE02?view=true

Rhode Island College

25. DeGrange, Roy W. The Effect of Anesthesia on the Developing Brain.

Degree: MSN, 2019, Rhode Island College

URL: https://digitalcommons.ric.edu/etd/314

► Damage caused by administering general anesthetics to the developing brain in young children and pregnant mothers is of concern among practicing anesthesia providers. Studies… (more)

Subjects/Keywords:

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APA (6^th Edition):

DeGrange, R. W. (2019). The Effect of Anesthesia on the Developing Brain. (Masters Thesis). Rhode Island College. Retrieved from https://digitalcommons.ric.edu/etd/314

Chicago Manual of Style (16^th Edition):

DeGrange, Roy W. “The Effect of Anesthesia on the Developing Brain.” 2019. Masters Thesis, Rhode Island College. Accessed March 04, 2021. https://digitalcommons.ric.edu/etd/314.

MLA Handbook (7^th Edition):

DeGrange, Roy W. “The Effect of Anesthesia on the Developing Brain.” 2019. Web. 04 Mar 2021.

Vancouver:

DeGrange RW. The Effect of Anesthesia on the Developing Brain. [Internet] [Masters thesis]. Rhode Island College; 2019. [cited 2021 Mar 04]. Available from: https://digitalcommons.ric.edu/etd/314.

Council of Science Editors:

DeGrange RW. The Effect of Anesthesia on the Developing Brain. [Masters Thesis]. Rhode Island College; 2019. Available from: https://digitalcommons.ric.edu/etd/314

University of Cambridge

26. Harris, Kate. Understanding the role of dopamine in pathology and cognition in Huntington’s disease.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/315126

► Huntington’s disease is a genetic neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin gene. Dysfunction of dopamine (DA) signalling is thought to… (more)

▼ Huntington’s disease is a genetic neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin gene. Dysfunction of dopamine (DA) signalling is thought to drive several of its clinical manifestations. DA receptors in frontostriatal pathways are lost early in the disease course – a possible compensatory response to increased dopaminergic activity, which is responsible for the hyperkinetic movement disorder of HD. DA signalling in frontostriatal pathways is also critical for cognitive processes such as executive function, and disruption of normal DA signalling may therefore contribute to cognitive impairments in HD. This thesis presents a number of clinical and laboratory studies, aiming to explore the importance of dopaminergic signalling in the pathogenesis of HD, and their contribution to the observed cognitive deficits. I first sought to explore the impact of DA modulation on cognitive function in HD. Firstly, using longitudinal data from the ENROLL-HD study, I have shown that the use of DA antagonists was associated with accelerated cognitive decline in early stage HD. I then performed an interventional study, in which cognitive function was characterised after administration of sulpiride (a D2 receptor-antagonist). Whilst sulpiride resulted in impaired executive function, there were improvements in other areas of dopamine-dependent cognition, such as reward-based decision-making and facial expression recognition. Taken together, these results suggest that DA signalling contributes to cognitive manifestations of HD. This relationship is complex, with D2 antagonism demonstrating opposing effects on different aspects of cognition. I next sought to characterise the anatomical and cellular basis for such deficits, as it appeared likely that these tasks involved other regions in addition to frontostriatal pathways. The hippocampus is known to play an important role in cognition, in particular in spatial memory, novelty encoding and reward processing. Given that DA has been shown to exert a modulatory influence on hippocampal neuronal and synaptic activity, I hypothesised that HD patients may also display hippocampal-related cognitive deficits. HD mice models have shown deficits in hippocampal synaptic plasticity, but little work has been done on hippocampal function in HD in humans. I therefore administered a hippocampal-dependent spatial memory task to HD gene carriers and found that early stage patients demonstrated impairments. The question as to whether the cause of such deficits had a possible DA basis led to the subsequent studies that I undertook. Evidence shows that glial cells play important roles in the pathogenesis of neurodegenerative diseases, and astrocytes have recently been shown to be involved in DA signalling. Specifically, DA activity at astrocyte DA receptors has neurotrophic and anti-inflammatory properties, and also increases intracellular Ca2+ transients in astrocytes, leading to the release of gliotransmitters which regulate synaptic plasticity. Astrocyte dysfunction in the…

Subjects/Keywords: Neuroscience; Neurodegeneration; Huntington's disease

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APA (6^th Edition):

Harris, K. (2020). Understanding the role of dopamine in pathology and cognition in Huntington’s disease. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/315126

Chicago Manual of Style (16^th Edition):

Harris, Kate. “Understanding the role of dopamine in pathology and cognition in Huntington’s disease.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/315126.

MLA Handbook (7^th Edition):

Harris, Kate. “Understanding the role of dopamine in pathology and cognition in Huntington’s disease.” 2020. Web. 04 Mar 2021.

Vancouver:

Harris K. Understanding the role of dopamine in pathology and cognition in Huntington’s disease. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/315126.

Council of Science Editors:

Harris K. Understanding the role of dopamine in pathology and cognition in Huntington’s disease. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/315126

Kent State University

27. Kumar, Varun. Protein Kinase C Signaling in Neurodegeneration.

Degree: PhD, College of Arts and Sciences / School of Biomedical Sciences, 2016, Kent State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051

► Global cerebral ischemia occurs due to cardiac arrest, which results in delayed neurodegeneration. Pharmacological agents such as Protein Kinase C epsilon (PKC epsilon) peptide activators… (more)

▼ Global cerebral ischemia occurs due to cardiac arrest, which results in delayed neurodegeneration. Pharmacological agents such as Protein Kinase C epsilon (PKC epsilon) peptide activators when applied before ischemia are known to confer neuroprotection against ischemia-induced cell death. However, the occurrence of cardiac arrest or cerebral ischemia is unpredictable. Thus, therapeutic targets that can be applied after ischemia have to be unraveled. Moreover, the effect of PKC epsilon deletion after global cerebral ischemia has not been studied yet. Therefore, we have studied the effect of PKC epsilon deletion after global cerebral ischemia. Using mouse model of global cerebral ischemia, we found that hippocampal neurodegeneration was significantly reduced in knock-out (KO) mice compared with PKC epsilon wild-type (WT) mice three days after ischemia. To determine the mechanisms underlying the role of PKC epsilon in ischemia-induced neurodegeneration, we have investigated the role of activating transcription factor 2 (ATF2) and found that PKC epsilon regulates the subcellular localization of ATF2 via Threonine 52 (Thr52) phosphorylation and mediates apoptosis in hippocampal neurons. This study will give insight into the role of PKC epsilon-ATF2 signaling and other PKC isozymes in hippocampal neurons after global cerebral ischemia. PKC delta, another member of novel PKC family, has been implicated in stroke-reperfusion injury. To better study the role of PKC delta in normal function and disease, we have developed an ATP analog-specific PKC delta (AS-PKC delta) that is sensitive to specific kinase inhibitors and can be used to identify PKC delta substrates. To understand the mechanisms for specificity and affinity of these analogs, we have created in silico WT and AS-PKC delta homology models based on the crystal structure of Protein Kinase C iota (PKC iota). N6-(benzyl)-ATP and ATP showed similar positioning within the purine binding pocket of AS-PKC delta, while N6-(benzyl)-ATP was displaced from the pocket of WT-PKC delta and was unable to interact with the glycine-rich loop that is required for phosphoryl-transfer. The adenine ring of 1NA-PP1 and 2MB-PP1 matched the adenine ring of ATP when docked in AS-PKC delta and this interaction prevented the potential binding of ATP with Lys-378, Glu-428, and Leu-430 residues. 1NA-PP1 failed to effectively dock within WT-PKC delta. Moreover, other PP1 analogs failed effectively to interact with either AS-PKC delta or WT-PKC delta. These results provide a structural basis for the ability of AS-PKC delta to efficiently and specifically utilize N6-(benzyl)-ATP as a phosphate donor, and for its selective inhibition by 1NA-PP1 and 2MB-PP1. Such homology modeling could prove useful in designing molecules to target PKC delta and other kinases to understand their function in cell signaling and to identify unique substrates. Advisors/Committee Members: Chou, Wen-Hai (Advisor).

Subjects/Keywords: Neurobiology; PKC, Neurodegeneration, ATF2

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APA (6^th Edition):

Kumar, V. (2016). Protein Kinase C Signaling in Neurodegeneration. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051

Chicago Manual of Style (16^th Edition):

Kumar, Varun. “Protein Kinase C Signaling in Neurodegeneration.” 2016. Doctoral Dissertation, Kent State University. Accessed March 04, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051.

MLA Handbook (7^th Edition):

Kumar, Varun. “Protein Kinase C Signaling in Neurodegeneration.” 2016. Web. 04 Mar 2021.

Vancouver:

Kumar V. Protein Kinase C Signaling in Neurodegeneration. [Internet] [Doctoral dissertation]. Kent State University; 2016. [cited 2021 Mar 04]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051.

Council of Science Editors:

Kumar V. Protein Kinase C Signaling in Neurodegeneration. [Doctoral Dissertation]. Kent State University; 2016. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1455721051

University of Cambridge

28. Humoud, Ibrahim. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/310338

► Neurodegenerative diseases pose an immense challenge to the population and health care worldwide. There is a growing need for therapeutic strategies to target these diseases.… (more)

▼ Neurodegenerative diseases pose an immense challenge to the population and health care worldwide. There is a growing need for therapeutic strategies to target these diseases. Many neurodegenerative diseases are classified as protein misfolding diseases (PMDs). Despite their uniqueness, these PMDs share common pathways connected to their pathophysiology. Preclinical evidence demonstrates that these can be manipulated for new disease-modifying drug therapies. The unfolded protein response (UPR) and autophagy are two such pathways, whose dysregulation is detectable as pathological hallmarks in various neurodegenerative diseases. The modulation of both pathways individually is neuroprotective in multiple mouse models of neurodegenerative disease. Evidence from other fields of biomedical research showed the enormous potential benefit of combination therapy in various human diseases. Therefore, this project aimed at investigating the strategy of combination therapy in neurodegeneration by targeting more than one common pathway compared to targeting each one singly. Here fore, two distinct models of neurodegeneration, prion disease and the tauopathy model, rTg4510, were used. It was confirmed that both common pathways, the UPR and autophagy, are implicated in the disease progression. Furthermore, targeting of either pathway, genetically or pharmacologically, demonstrated profound neuroprotection in the hippocampus of both mouse models and extended survival of prion-diseased mice significantly. However, neither genetic nor pharmacological combination therapy showed additive benefit when given early in the disease. When starting genetic or pharmacological treatment in a later phase of disease progression, combination therapy caused an extension of lifespan in prion-diseased mice beyond the effects of monotherapy alone. These results show that the modulation of autophagy genetically and pharmacologically is neuroprotective in prion-diseased mice to a similar extent to PERK pathway modulation. The combinatorial approach did not increase lifespan over monotherapy either genetically or pharmacologically, except when used later in the disease. The reasons for this remain to be explored, but the potential of targeting several processes is an appealing potential strategy in neurodegeneration.

Subjects/Keywords: Unfolded Protein Response; Autophagy; Neurodegeneration

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APA (6^th Edition):

Humoud, I. (2019). Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/310338

Chicago Manual of Style (16^th Edition):

Humoud, Ibrahim. “Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 04, 2021. https://www.repository.cam.ac.uk/handle/1810/310338.

MLA Handbook (7^th Edition):

Humoud, Ibrahim. “Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration.” 2019. Web. 04 Mar 2021.

Vancouver:

Humoud I. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 04]. Available from: https://www.repository.cam.ac.uk/handle/1810/310338.

Council of Science Editors:

Humoud I. Investigating the potential of enhanced neuroprotection through unfolded protein response inhibition and autophagy induction in neurodegeneration. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/310338

University of Alberta

29. Mercer, Robert Corrigan Curtis. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.

Degree: PhD, Department of Medicine, 2016, University of Alberta

URL: https://era.library.ualberta.ca/files/cmp48sc82v

► Prion diseases are invariably fatal neurodegenerative diseases of humans and other mammals. While they can manifest as sporadic, infectious or genetic etiologies, the central event… (more)

Subjects/Keywords: Gerstmann-Sträussler-Schienker; Potassium Channel; Prion; Neurodegeneration

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APA (6^th Edition):

Mercer, R. C. C. (2016). The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cmp48sc82v

Chicago Manual of Style (16^th Edition):

Mercer, Robert Corrigan Curtis. “The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.” 2016. Doctoral Dissertation, University of Alberta. Accessed March 04, 2021. https://era.library.ualberta.ca/files/cmp48sc82v.

MLA Handbook (7^th Edition):

Mercer, Robert Corrigan Curtis. “The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation.” 2016. Web. 04 Mar 2021.

Vancouver:

Mercer RCC. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. [Internet] [Doctoral dissertation]. University of Alberta; 2016. [cited 2021 Mar 04]. Available from: https://era.library.ualberta.ca/files/cmp48sc82v.

Council of Science Editors:

Mercer RCC. The Prion Protein: Modulation of Potassium Channels and a Novel Mouse Model of a Disease-Causing Hydrophobic Domain Insertion Mutation. [Doctoral Dissertation]. University of Alberta; 2016. Available from: https://era.library.ualberta.ca/files/cmp48sc82v

Vanderbilt University

30. Gibson, Chelsea Lynn. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.

Degree: PhD, Neuroscience, 2018, Vanderbilt University

URL: http://hdl.handle.net/1803/11175

► Glutamate (Glu) signaling plays a critical role in regulating neural excitability, thus supporting many behaviors. Perturbed Glu homeostasis in the brain is implicated in multiple… (more)

Subjects/Keywords: C. elegans; dopamine; glia; glutamate; excitotoxicity; neurodegeneration

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APA (6^th Edition):

Gibson, C. L. (2018). Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11175

Chicago Manual of Style (16^th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11175.

MLA Handbook (7^th Edition):

Gibson, Chelsea Lynn. “Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1.” 2018. Web. 04 Mar 2021.

Vancouver:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11175.

Council of Science Editors:

Gibson CL. Neurodegeneration and Metabolomic Impact of Genetic Elimination of the Orphan Metallo Beta-Lactamase, SWIP-10/MBLAC1. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/11175

Open Access Theses and Dissertations