subject:(memantine)

1. Souza, Higo Fernando Santos. Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro).

Degree: Mestrado, Biologia da Relação Patógeno-Hospedeiro, 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42135/tde-11042015-100453/ ;

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O nosso grupo está explorando como alternativa para a identificação de novas estratégias de tratamento o reposicionamento de drogas. Nesse contexto, nosso laboratório mostrou que… (more)

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O nosso grupo está explorando como alternativa para a identificação de novas estratégias de tratamento o reposicionamento de drogas. Nesse contexto, nosso laboratório mostrou que memantina, um antagonista de receptores de glutamato NMDA, apresenta uma atividade tripanocida no ciclo de vida do T. cruzi, in vitro. Com base nessas informações, avaliamos o efeito da memantina em animais infectados com a cepa Y. O tratamento apresentou uma redução da parasitemia (40%) no 8º dpi e redução da carga parasitária no tecido cardíaco no 15º dpi. Uma vez que a cepa Y invade preferencialmente macrófagos, avaliamos o efeito de memantina em células RAW 264.7. Memantina diminuiu a produção de NO por células estimuladas com LPS, diminuiu o Ca2+i, e não houve uma redução de EROs. Memantina também interferiu no ciclo intracelular do parasita, reduzindo o número de células infectadas. Nossos resultados sugerem que o tratamento com memantina pode direcionar o sistema imune de modo a modular os receptores de tipo NMDA, através de um efeito direto ou indireto produzido pelo tratamento.

The search for new therapeutic targets has been of extreme importance for the specific treatment of Chagas disease. Our group is exploring as an alternative, a strategy for drug repurposing. In this context, our laboratory showed that memantine, an antagonistic of NMDA glutamate receptors, has a trypanocidal activity along the life cycle of T. cruzi, in vitro. Based on this information, we evaluated the effect of memantine in animals infected with Y strain. The treatment showed a reduction of parasitemia (40%) in 8th dpi and reduced parasitic load in cardiac tissues at 15th dpi. As the Y strain preferably invades macrophages, we evaluated the effect of memantine in RAW 264.7 cells. Memantine decreased NO production by cells stimulated with LPS, decreased Ca2+i, and did not cause a reduction in ROS. Memantine also interfere with the intracellular parasite cycle, reducing the number of infected cells. Our results suggest that treatment with memantine can target the immune system to modulate the NMDA receptor, through direct or indirect effect caused by the treatment.

Advisors/Committee Members: Silber, Ariel Mariano.

Subjects/Keywords: Trypanosoma cruzi; Trypanosoma cruzi; Glutamate receptor; Memantina; Memantine; Receptor de glutamato

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APA (6^th Edition):

Souza, H. F. S. (2015). Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro). (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42135/tde-11042015-100453/ ;

Chicago Manual of Style (16^th Edition):

Souza, Higo Fernando Santos. “Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro).” 2015. Masters Thesis, University of São Paulo. Accessed December 13, 2019. http://www.teses.usp.br/teses/disponiveis/42/42135/tde-11042015-100453/ ;.

MLA Handbook (7^th Edition):

Souza, Higo Fernando Santos. “Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro).” 2015. Web. 13 Dec 2019.

Vancouver:

Souza HFS. Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro). [Internet] [Masters thesis]. University of São Paulo; 2015. [cited 2019 Dec 13]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42135/tde-11042015-100453/ ;.

Council of Science Editors:

Souza HFS. Avaliação do efeito de memantina na infecção experimental pelo Trypanosoma cruzi (in vivo e in vitro). [Masters Thesis]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/42/42135/tde-11042015-100453/ ;

2. Reddy, Jambula Mukunda. Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -.

Degree: Chemistry, 2011, Jawaharlal Nehru Technological University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/4564

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Chapter-I deals with the introduction to Alzheimer?s disease, biological importance of (-)-Galanthamine, Memantine and the previous synthetic approaches cited in the literature towards the synthesis… (more)

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Chapter-I deals with the introduction to Alzheimer?s disease, biological importance of (-)-Galanthamine, Memantine and the previous synthetic approaches cited in the literature towards the synthesis of racemic.Galanthamine 1. In chapter-II, studies towards the total synthesis of (-) Galanthamine and its hydro bromide salt is described, wherein a stereo selective reduction of prochiral ketone using L-selectride followed by diastereomeric separation using di-p-toluyl-D-tartaric acid. Synthesis and characterization of Galanthamine process related chiral impurities have been described in chapter-III. A detailed study on polymorphism of Galanthamine amorphous and crystalline forms is presented in chapter-IV. An improved, cost effective and scalable process has been developed for Memantine hydrochloride. CHAPTER-I This chapter deals with the introduction to Alzheimer?s disease, biological importance of (-)-Galanthamine and the previous synthetic approaches cited in the literature towards the synthesis of racemic and (-) Galanthamine 1. CHAPTER-II This chapter describes the studies towards the total synthesis of (-) Galanthamine and its hydrobromide salt, through a stereo selective reduction of prochiral ketone using L-selectride followed by diasteromeric separation using p-diparatoluyl-D-tartaric acid. CHAPTER- III Synthesis and characterization of Galanthamine process related chiral impurities have been described in chapter-III. Impurities are in pharmaceutical industry are the unwanted chemicals that remain with the active pharmaceutical ingredients (API?s) or developed during synthesis of API or in formulation. Various regulatory authorities like ICH, USFDA, Canadian Drug and Health agency are emphasizing on the purity requirements and the identification of impurities in API?s. Formation of impurities due to incomplete chemical reactions, Impurities originating from impurities in the starting material of the synthesis.

References given chapters wise

Advisors/Committee Members: Reddy, G Mahesh, Himabindu, V.

Subjects/Keywords: Alzheimer?s Disease; Galanthamine hydrobromide; Memantine hydrochloride; Chemistry

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APA (6^th Edition):

Reddy, J. M. (2011). Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -. (Thesis). Jawaharlal Nehru Technological University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/4564

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

Chicago Manual of Style (16^th Edition):

Reddy, Jambula Mukunda. “Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -.” 2011. Thesis, Jawaharlal Nehru Technological University. Accessed December 13, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/4564.

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

MLA Handbook (7^th Edition):

Reddy, Jambula Mukunda. “Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -.” 2011. Web. 13 Dec 2019.

Vancouver:

Reddy JM. Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -. [Internet] [Thesis]. Jawaharlal Nehru Technological University; 2011. [cited 2019 Dec 13]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4564.

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

Council of Science Editors:

Reddy JM. Synthesis and characterization of (-)Galanthamine hydrobromide and memantine hydrochloride as anti Alzheimers drugs and their impurities; -. [Thesis]. Jawaharlal Nehru Technological University; 2011. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/4564

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

3. Emnett, Christine Marie. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.

Degree: PhD, Biology & Biomedical Sciences (Neurosciences), 2014, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/347

► N-methyl-D-aspartate receptors (NMDARs) are ionotropic glutamate receptors that serve crucial signaling and neurotrophic functions throughout the central nervous system. Both hyperfunction and hypofunction of… (more)

▼ N-methyl-D-aspartate receptors (NMDARs) are ionotropic glutamate receptors that serve crucial signaling and neurotrophic functions throughout the central nervous system. Both hyperfunction and hypofunction of NMDARs are associated with neurological and neuropsychiatric conditions. Thus, both positive and negative pharmacological NMDAR modulators are of clinical interest as treatments. Understanding drug mechanisms could lead to more rational drug design. Memantine and ketamine are NMDAR open channel blockers that exhibit similar pharmacodynamics at NMDARs but have different clinical uses. Memantine improves cognitive decline during Alzheimer's disease. Ketamine is an anesthetic and analgesic with psychotomimetic effects, but it is also a rapid acting and long-lived antidepressant. How these mechanistically similar blockers mediate different effects on behavior is unclear, but we hypothesized that unappreciated differences in their pharmacodynamics may contribute. This thesis investigated effects of memantine and ketamine during pathological (excitotoxic) and physiological activity in vitro, where pharmacokinetic effects could largely be ignored. We focused on non-steady state conditions that mimic synaptic transmission. I found that synaptic NMDAR activation is responsible for hypoxic excitotoxic cell death and revealed that memantine, a putative selective extrasynaptic receptor blocker, acquires its selectivity as a result of tonic agonist presentation rather than from affinity for specific populations. Further investigation into the similar synaptic pharmacodynamics of memantine and ketamine revealed a subtle difference in their response to voltage perturbations that was unmasked during physiological activity by increasing the open probability of the channel or by very strong activity. This suggests that regional differences in activity or channel open probability in vivo may control the efficacy of these blockers and partially explain their clinical differences. To further explore properties of ketamine relevant to its antidepressant action, I examined how its pharmacodynamics compares to its major metabolite, norketamine, and to chemical biology analogues of ketamine that show promise in tracking alternative targets for ketamine. In all, these studies reveal mechanistic insights into the pharmacodynamics of two NMDAR channel blockers that may partly explain their clinical effects. Advisors/Committee Members: Steven J Mennerick, James E Huettner, Daniel D Kerschensteiner, Peter D Lukasiewicz, Joseph Henry Steinbach.

Subjects/Keywords: 24-S hydroxycholesterol; anti-depressants; channel block; excitotoxicity; ketamine; memantine; Biology

10 more images…

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APA (6^th Edition):

Emnett, C. M. (2014). Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/347

Chicago Manual of Style (16^th Edition):

Emnett, Christine Marie. “Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.” 2014. Doctoral Dissertation, Washington University in St. Louis. Accessed December 13, 2019. https://openscholarship.wustl.edu/art_sci_etds/347.

MLA Handbook (7^th Edition):

Emnett, Christine Marie. “Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events.” 2014. Web. 13 Dec 2019.

Vancouver:

Emnett CM. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2014. [cited 2019 Dec 13]. Available from: https://openscholarship.wustl.edu/art_sci_etds/347.

Council of Science Editors:

Emnett CM. Modulation of NMDA Receptor Activity During Physiological and Pathophysiological Events. [Doctoral Dissertation]. Washington University in St. Louis; 2014. Available from: https://openscholarship.wustl.edu/art_sci_etds/347

Open Universiteit Nederland

4. Buyle, David M.H. Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie .

Degree: 2015, Open Universiteit Nederland

URL: http://hdl.handle.net/1820/6714

► Een derde tot de helft van de met clozapine behandelde schizofreniepatiënten behoudt matige tot ernstige restsymptomen. Aangezien ontregeling van N-methyl-d-aspartaat (NMDA)-receptoren door glutamaat betrokken lijkt… (more)

Subjects/Keywords: therapieresistente schizofrenie; positieve- en negatieve symptomen; PANSS; CANTAB,; clozapine; memantine

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

APA (6^th Edition):

Buyle, D. M. H. (2015). Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie . (Masters Thesis). Open Universiteit Nederland. Retrieved from http://hdl.handle.net/1820/6714

Chicago Manual of Style (16^th Edition):

Buyle, David M H. “Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie .” 2015. Masters Thesis, Open Universiteit Nederland. Accessed December 13, 2019. http://hdl.handle.net/1820/6714.

MLA Handbook (7^th Edition):

Buyle, David M H. “Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie .” 2015. Web. 13 Dec 2019.

Vancouver:

Buyle DMH. Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie . [Internet] [Masters thesis]. Open Universiteit Nederland; 2015. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/1820/6714.

Council of Science Editors:

Buyle DMH. Memantine-additie aan Clozapine bij Therapieresistente Schizofrenie . [Masters Thesis]. Open Universiteit Nederland; 2015. Available from: http://hdl.handle.net/1820/6714

5. Cordier, Mathilde. Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires.

Degree: Docteur es, Santé publique - sciences économiques, 2018, Paris Saclay

URL: http://www.theses.fr/2018SACLS201

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La prise en charge de la démence est un défi pour les cliniciens tant ces patients constituent une population hétérogène. Dans le cadre de cette… (more)

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La prise en charge de la démence est un défi pour les cliniciens tant ces patients constituent une population hétérogène. Dans le cadre de cette prise en charge, l’intérêt des antidémentiels (anticholinestérasiques et mémantine) est débattue : l’efficacité clinique semble discutable et les effets indésirables non négligeables. En 2010, des recommandations de bonnes pratiques ont laissé libre choix aux médecins de prescrire ou non ces médicaments. Depuis des questions restent en suspens : 1/ quelle est l’évolution des taux de prescription de ces médicaments depuis ces recommandations, en d’autres termes comment l’expertise clinique des médecins, un des piliers du tryptique de l’evidence based medicine, s’est-elle exprimée ? 2/ quels sont les facteurs qui restent associés aujourd’hui au fait de prescrire ou non ces médicaments ? et 3/ y a-t-il une sur-hospitalisation liée à leurs effets indésirables ?La question de la surmédicalisation est au cœur de notre problématique de thèse. Dans ce travail, nous avons répondu à ces 3 questions posées qui ont constitué nos 3 objectifs. Nous avons pu montrer que les médecins semblaient de moins en moins confiants vis-à-vis des antidémentiels avec une diminution de leur prescription depuis 2010 et des conséquences importantes en termes de coûts évités. Lorsqu’ils continuaient d’être prescrits, ces traitements l’étaient essentiellement chez les patients les plus jeunes ou en meilleur état de santé. Enfin, les anticholinestérasiques, essentiellement la rivastigmine, augmentaient le risque d’hospitalisation via des effets indésirables cardiaques et digestifs. Nos résultats plaident en défaveur de la prescription d’antidémentiels tant du point de vue de la morbidité que des dépenses de santé. La question du point de vue du patient reste posée.

Patients with dementia raise therapeutic challenges, as they constitute a heterogeneous population. As part of this management, the interest of antidementia drugs (cholinesterase inhibitors and memantine) is debated: the clinical efficacy seems questionable and the adverse effects appear to be significant. The 2010 recommendations gave to cliniciens the choice to prescribe or not these drugs. Since questions remain unanswered: 1 / what is the evolution of prescription rates of these drugs since these recommendations, in other words how the clinical expertise of cliniciens, one of the pillars the evidence based medicine, is expressed? 2 / what are the factors that remain today associated with prescribing these drugs or not? and 3 / Is there over-hospitalization related to their side effects?The question of medical overuse is a central point of our thesis problem. In this work, we answered these 3 questions which constituted our 3 objectives. We were able to show that cliniciens seemed less and less confident about antidementia drugs with a decrease in their prescription since 2010 and significant consequences in terms of avoided costs. When they continued to be prescribed, these treatments were mainly used in the youngest or most healthy…

Advisors/Committee Members: Pelletier-Fleury, Nathalie (thesis director).

Subjects/Keywords: Démence; Surmédicalisation; Anticholinesterasiques; Mémantine; Dementia; Medical overuse; Cholinesterase inhibitors; Memantine

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

APA (6^th Edition):

Cordier, M. (2018). Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires. (Doctoral Dissertation). Paris Saclay. Retrieved from http://www.theses.fr/2018SACLS201

Chicago Manual of Style (16^th Edition):

Cordier, Mathilde. “Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires.” 2018. Doctoral Dissertation, Paris Saclay. Accessed December 13, 2019. http://www.theses.fr/2018SACLS201.

MLA Handbook (7^th Edition):

Cordier, Mathilde. “Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires.” 2018. Web. 13 Dec 2019.

Vancouver:

Cordier M. Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires. [Internet] [Doctoral dissertation]. Paris Saclay; 2018. [cited 2019 Dec 13]. Available from: http://www.theses.fr/2018SACLS201.

Council of Science Editors:

Cordier M. Le recours aux soins dans la démence : la surmédicalisation en question. Exploitation des données de l’échantillon généraliste des bénéficiaires : Seeking Health Care in Alzheimer's Disease : Medical Overuse in Question. Exploitation of Data from the Echantillon généraliste des bénéficiaires. [Doctoral Dissertation]. Paris Saclay; 2018. Available from: http://www.theses.fr/2018SACLS201

University of Texas Southwestern Medical Center

6. Gideons, Erinn Sommer. Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/5727

► Ketamine is a N-methyl-D-aspartate receptor (NMDAR) antagonist that elicits rapid antidepressant responses in depressed patients. However, ketamine can also produce psychotomimetic effects, which limits its… (more)

▼ Ketamine is a N-methyl-D-aspartate receptor (NMDAR) antagonist that elicits rapid antidepressant responses in depressed patients. However, ketamine can also produce psychotomimetic effects, which limits its widespread use. The field has been exploring the mechanism of ketamine's antidepressant action to assist in identifying drugs that may also produce the rapid effects without the potential side effects. Memantine is a NMDAR antagonist similar to ketamine in many regards but does not produce antidepressant effects in patients. Behavioral experiments in mice recapitulated clinical findings showing that ketamine but not memantine has antidepressant-like effects in two common antidepressant efficacy tests. Ketamine and memantine effectively blocked NMDAR-mediated mEPSCs in the absence of Mg2+. However, in physiological levels of extracellular Mg2+ only ketamine was able to block the NMDAR at rest. This difference between ketamine and memantine extended to intracellular signaling coupled to NMDAR at rest, in that ketamine inhibits the phosphorylation of eukaryotic elongation factor 2 (eEF2) resulting in an augmentation of subsequent protein expression of brain-derived neurotrophic factor (BDNF), that is not triggered by memantine These results demonstrate significant differences between the efficacies of ketamine and memantine on NMDA receptor mediated neurotransmission that impacts downstream intracellular signaling which is hypothesized as the trigger for rapid antidepressant responses. In a subsequent study, the therapeutic effect of lithium, a mood stabilizer and a common treatment for Bipolar Disorder (BD) is being investigated. Lithium has antidepressant and antimanic effects in patients with BD that can be recapitulated in animal models. While lithium is effective as a mood stabilizer, the mechanisms that underlie its therapeutic effect are unclear. Lithium has previously been shown to decrease the overall phosphorylation status of eEF2, which increases BDNF protein translation at the synapse. In this study, clinically effective doses of lithium were shown to result in antidepressant and antimanic-like effects in mice. We report that neither eEF2 kinase nor BDNF are necessary for the antidepressant effects of lithium. Additionally, eEF2 kinase is not required for the antimanic effects of lithium. However, BDNF appears to be necessary for lithium's antimanic actions. To begin to understand whether this requirement of BDNF in lithium's anti-manic action was due to synaptic changes we performed electrophysiological analysis on primary hippocampal neurons treated with lithium. Chronic lithium treatment caused a significant decrease in AMPAR-mEPSC amplitude, which requires both BDNF and its high affinity receptor, TrkB. Additionally, chronic lithium treatment caused a significant decrease in surface expression of the GluA1 subunit of the AMPAR. Collectively, this data demonstrates that BDNF is required for the antimanic effects of lithium, and that lithium's effects on the regulation of AMPARs are BDNF and TrkB… Advisors/Committee Members: Rothenfluh, Adrian, Goldberg, Mark P., Kavalali, Ege T., Monteggia, Lisa.

Subjects/Keywords: Antidepressive Agents; Excitatory Amino Acid Antagonists; Ketamine; Memantine

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

APA (6^th Edition):

Gideons, E. S. (2016). Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/5727

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):

Gideons, Erinn Sommer. “Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed December 13, 2019. http://hdl.handle.net/2152.5/5727.

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

MLA Handbook (7^th Edition):

Gideons, Erinn Sommer. “Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder.” 2016. Web. 13 Dec 2019.

Vancouver:

Gideons ES. Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/2152.5/5727.

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

Council of Science Editors:

Gideons ES. Synaptic Mechanisms Underlying Treatment of Depression and Bipolar Disorder. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/5727

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

Tampere University

7. Dania, Anna. The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis .

Degree: 2014, Tampere University

URL: https://trepo.tuni.fi/handle/10024/96082

► Background: To date, clinical trials have reported inconsistent results on the efficacy of the combination therapy of Memantine plus an acetylcholinesterase inhibitor (AChEI) over a… (more)

Subjects/Keywords: Acetylcholinesterase inhibitor; Alzheimer s disease; donepezil; galantamine; memantine; rivastigmine; meta-analysis.

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

APA (6^th Edition):

Dania, A. (2014). The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis . (Masters Thesis). Tampere University. Retrieved from https://trepo.tuni.fi/handle/10024/96082

Chicago Manual of Style (16^th Edition):

Dania, Anna. “The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis .” 2014. Masters Thesis, Tampere University. Accessed December 13, 2019. https://trepo.tuni.fi/handle/10024/96082.

MLA Handbook (7^th Edition):

Dania, Anna. “The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis .” 2014. Web. 13 Dec 2019.

Vancouver:

Dania A. The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis . [Internet] [Masters thesis]. Tampere University; 2014. [cited 2019 Dec 13]. Available from: https://trepo.tuni.fi/handle/10024/96082.

Council of Science Editors:

Dania A. The efficacy of a combination therapy with memantine and an acetylcholinesterase inhibitor in alzheimer's disease: a systematic review and meta-analysis . [Masters Thesis]. Tampere University; 2014. Available from: https://trepo.tuni.fi/handle/10024/96082

Universidade do Rio Grande do Sul

8. Zimmer, Eduardo Rigon. Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica.

Degree: 2011, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/48982

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A Doença de Alzheimer (DA) é uma doença cerebral progressiva que resulta em prejuízos na memória e disfunção cognitiva global. Entre as principais características neuropatológicas… (more)

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A Doença de Alzheimer (DA) é uma doença cerebral progressiva que resulta em prejuízos na memória e disfunção cognitiva global. Entre as principais características neuropatológicas associadas a DA estão à presença de placas senis, emaranhados neurofibrilares e a hiperfosforilação da proteína Tau. A hiperativação do sistema glutamatérgico tem sido implicada na fisiopatologia da DA. O excesso de glutamato na fenda sináptica causa hiperativação do seu receptor ionótropico N-metill-D-aspartato (NMDA) o que favorece o aumento do influxo de cálcio e morte neuronal. A administração intracerebral de ácido ocadáico (AO) causa alterações morfológicas e funcionais similares à DA. O AO promove a inibição da proteína fosfatase 2A (PP2A) favorecendo as atividades cinásicas de proteínas como a cinase dependente de ciclina 5 (Cdk5). A memantina (MN) é uma das principais drogas utilizadas no tratamento da DA e o seu mecanismo de ação envolve um antagonismo não competitivo de baixa afinidade pela subunidade NR2B do receptor NMDA. Neste trabalho, foram avaliados efeitos do pré-tratamento com MN em um modelo semelhante a DA induzido pela administração intrahipocampal de AO em ratos. O pré-tratamento com MN preveniu o déficit na memória especial causado pela infusão intrahipocampal de AO. Os mecanismos envolvidos nestes efeitos neuroprotetores envolvem a prevenção do aumento de glutamato no liquido cefalorraquidiano, juntamente com a regulação da expressão de Cdk5 e em conseqüência a prevenção do aumento da fosforilação de Tau. Desta maneira, a MN pode ser um alvo terapêutico para prevenir as alterações comportamentais e neuroquímicas em um modelo similar a DA induzido pelo AO.

Alzheimer's disease (AD) is a progressive brain disease that causes memory loss and global cognitive dysfunction. The neuropathological alterations associated with AD include senile plaques, neurofibrillary tangles and Tau protein hyperphosphorylation. The glutamatergic system is implicated in the pathophysiology of AD. Indeed, the excessive glutamate levels in the synaptic cleft may cause hyperactivation of glutamate ionotropic N-metill-Daspartate (NMDA), which favors increase calcium influx and neuronal death. The intracerebral administration of okadaic acid (OA) causes morphological and functional alterations similar to AD. The OA inhibits the protein phosphatase 2A (PP2A) thus overstimulating the kinases activities. Memantine (MN) is a drug currently used in the treatment of AD, which mechanism involves a noncompetitive low affinity antagonism for NR2B subunit of NMDA receptors. In this work we evaluate the effects of pretreatment with MN in an AD-like model in rats induced by intrahippocampal administration of OA. The pretreatment with MN could prevent the spatial memory deficits caused by OA intrahipocampal administration in rats. The mechanisms underlying this neuroprotective effects involves the prevention of the increase in brain glutamate levels along with regulation of Cdk5 and, in consequence, downstream phosphorylation of Tau (ser199/202) protein.…

Advisors/Committee Members: Portela, Luis Valmor Cruz.

Subjects/Keywords: Memantina; Memantine; Ácido okadáico; Okadaic acid; Doença de Alzheimer; Neurodegenerative diseases; Glutamate; Glutamato; Cdk5; Learning; Memory

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APA (6^th Edition):

Zimmer, E. R. (2011). Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/48982

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):

Zimmer, Eduardo Rigon. “Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica.” 2011. Thesis, Universidade do Rio Grande do Sul. Accessed December 13, 2019. http://hdl.handle.net/10183/48982.

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

MLA Handbook (7^th Edition):

Zimmer, Eduardo Rigon. “Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica.” 2011. Web. 13 Dec 2019.

Vancouver:

Zimmer ER. Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2011. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10183/48982.

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

Council of Science Editors:

Zimmer ER. Efeito do pré-tratamento com memantina em um modelo de neurodegeneração induzido pela administração intrahipocampal de ácido ocadáico em ratos : uma avaliação comportamental e neuroquímica. [Thesis]. Universidade do Rio Grande do Sul; 2011. Available from: http://hdl.handle.net/10183/48982

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

IUPUI

9. Bailey, Jason A. EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES.

Degree: 2012, IUPUI

URL: http://hdl.handle.net/1805/2741

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Indiana University-Purdue University Indianapolis (IUPUI)

Alzheimer’s disease (AD) is a neurological disorder defined by the presence of plaques comprised mostly of amyloid-β (Aβ), and neurofibrillary… (more)

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Indiana University-Purdue University Indianapolis (IUPUI)

Alzheimer’s disease (AD) is a neurological disorder defined by the presence of plaques comprised mostly of amyloid-β (Aβ), and neurofibrillary tangles consisting of hyperphosphorylated microtubule associated protein tau (MAPT). AD is also characterized by widespread synapse loss and degeneration followed by death of neurons in the brain. Inflammatory processes, such as glial activation, are also implicated. In order to study mechanisms of neurodegeneration and evaluate potential therapeutic agents that could slow or reverse this process, a tissue culture system was developed based on primary embryonic cerebrocortical neurons. This culture system was observed to exhibit time-dependent neurodegeneration, glial proliferation, and synaptic marker loss consistent with AD-affected brains. The regulatory promoter regions of several genes implicated in AD, including the Aβ precursor protein (APP), β-amyloid cleaving enzyme (BACE1), and MAPT, were studied in this culture model. The MAPT gene promoter activity followed the pattern of neuronal maturation and degeneration quite closely, increasing in the initial phase of the tissue culture, then reducing markedly during neurodegeneration while APP and BACE1 gene promoters remained active. Deletion series of these promoters were tested to give an initial indication of the active regions of the gene promoter regions. Furthermore, the effects of exogenous Aβ and overexpression of p25, which are two possible pathogenic mechanisms of gene regulation in AD, were studied. Response to Aβ varied between the promoters and by length of the Aβ fragment used. Overexpression of p25 increased MAPT, but not APP or BACE1, promoter activity. This neurodegeneration model was also used to study the putative neuroprotective action of the NMDA receptor antagonist memantine. Treatment with memantine prevented loss of synaptic markers and preserved neuronal morphology, while having no apparent effect on glial activation. The protective action on synaptic markers was also observed with two other structurally distinct NMDA receptor antagonists, suggesting that the effects of memantine are produced by its action on the NMDA receptor. It is concluded that this tissue culture model will be useful for the study of gene regulation and therapeutic agents for neurodegeneration, and that the efficacy of memantine may result from preservation of synaptic connections in the brain.

Advisors/Committee Members: Lahiri, Debomoy K., Du, Yansheng, McBride, William J., 1956-, Zhou, Feng.

Subjects/Keywords: Alzheimer; synapse; neurodegeneration; primary culture; memantine; Alzheimer's disease – Research; Alzheimer's disease – Treatment – Research; Genetic regulation – Research; Nervous system – Degeneration – Research

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

APA (6^th Edition):

Bailey, J. A. (2012). EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/2741

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):

Bailey, Jason A. “EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES.” 2012. Thesis, IUPUI. Accessed December 13, 2019. http://hdl.handle.net/1805/2741.

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

MLA Handbook (7^th Edition):

Bailey, Jason A. “EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES.” 2012. Web. 13 Dec 2019.

Vancouver:

Bailey JA. EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES. [Internet] [Thesis]. IUPUI; 2012. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/1805/2741.

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

Council of Science Editors:

Bailey JA. EVALUATION OF GENE REGULATION AND THERAPEUTIC DRUGS RELATED TO ALZHEIMER’S DISEASE IN DEGENERATING PRIMARY CEREBROCORTICAL CULTURES. [Thesis]. IUPUI; 2012. Available from: http://hdl.handle.net/1805/2741

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

Cornell University

10. Coombs, Susan Elizabeth. Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease .

Degree: 2018, Cornell University

URL: http://hdl.handle.net/1813/64917

► RNA aptamers selected for two disparate targets, the nicotinic acetylcholine receptor (Ulrich et al., 1998) and beta-amyloid (Abeta) peptides (Ylera et al., 2002), share a… (more)

▼ RNA aptamers selected for two disparate targets, the nicotinic acetylcholine receptor (Ulrich et al., 1998) and beta-amyloid (Abeta) peptides (Ylera et al., 2002), share a consensus sequence (Gadalla & Hess, 2006). The RNA aptamers selected for the nicotinic acetylcholine receptors fell into two classes. Class 1 aptamers inhibited the receptor and, in the presence of an activator of the receptor, Class 2 aptamers alleviated the inhibition. The short consensus sequence of Class 1 aptamers retained this activity (Sivaprakasam et al., 2010). Gadalla and Hess (2006) recognized that the same consensus sequence occurred in the RNA aptamers selected for the Abeta(1-40) peptide by Ylera et al. (2002). Some organic compounds that bind to the acetylcholine receptor, and affect its function, were assigned to either Class 1 or Class 2 (Hess et al., 2000). (+) MK-801 (dizocilpine) is a Class 1 compound. In the work reported here, the effects of (+) MK-801 and of memantine on the aggregation pathway of Abeta(1-40) and Abeta(1-42) peptides have been examined using the Thioflavin T fluorescence assay, nuclear magnetic resonance spectroscopy, and electron microscopy. Memantine is FDA-approved for the treatment of mild-moderate Alzheimer’s Disease. Both compounds accelerated the initial formation of beta-sheets by the Abeta peptides, (+) MK-801 more rapidly than memantine. But in the presence of either compound a decrease in the fluorescence signal followed the initial rise, a decrease that was not observed when they were absent. The decrease may represent an abruptly formed, insoluble aggregated state, rather than a return to the initial non-beta-sheet state. In the absence of either compound, the fluorescence signal indicating beta-sheet formation reaches a plateau. NMR spectra of the soluble peptides in the presence and absence of (+) MK-801 were compared to the fluorescence measurements and showed a similar difference for the initial phase. However, no return to the monomeric form was observed, possibly suggesting that the decrease in fluorescence in the Thioflavin T assay represented the formation of insoluble aggregates. Consistent with this interpretation, electron microscopy of the insoluble peptides formed over time showed a more rapid rate of formation of clumped fibrils in the presence of (+) MK-801 than in its absence. Thus, as observed by three different techniques, (+) MK-801 and memantine increase the rate of Abeta peptide aggregation as compared to the aggregation that occurs in their absence. This raises a question: What is the effect on patients of long-term treatment with memantine? Is there an explanation for the observation that led to this study, the shared consensus sequence between aptamers selected for two different targets? This cannot yet be answered. In this study, it was recognized that the consensus sequences of the two classes of RNA aptamers targeting the acetylcholine receptor are complementary in the 5’-3’ and 3’-5’ directions. Is this of biological significance? The selection of… Advisors/Committee Members: Nicholson, Linda K. (committeeMember), Feigenson, Gerald W. (committeeMember), Weiland, Gregory Arthur (committeeMember).

Subjects/Keywords: memantine; MK-801; nicotinic acetylcholine receptor; Molecular biology; Pharmacology; RNA aptamers; Neurosciences; Alzeheimer's Disease; Beta-amyloid

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APA (6^th Edition):

Coombs, S. E. (2018). Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/64917

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):

Coombs, Susan Elizabeth. “Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease .” 2018. Thesis, Cornell University. Accessed December 13, 2019. http://hdl.handle.net/1813/64917.

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

MLA Handbook (7^th Edition):

Coombs, Susan Elizabeth. “Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease .” 2018. Web. 13 Dec 2019.

Vancouver:

Coombs SE. Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease . [Internet] [Thesis]. Cornell University; 2018. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/1813/64917.

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

Council of Science Editors:

Coombs SE. Effects of (+) MK-801 (dizocilpine) and non-coding RNA on aggregation of beta-amyloid peptides linked to Alzheimer's Disease . [Thesis]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64917

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

Freie Universität Berlin

11. Repantis, Dimitrios. Psychopharmaceutical interventions for neuroenhancement in healthy individuals.

Degree: 2011, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-9505

► The term neuroenhancement refers to improvement in the cognitive, emotional and motivational functions of healthy individuals through, inter alia, the use of drugs. Of known… (more)

Subjects/Keywords: Neuroenhancement; Enhancement; Cognitive enhancement; Antidepressants; Memantine; Modafinil; Methylphenidate; Systematic Review; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6^th Edition):

Repantis, D. (2011). Psychopharmaceutical interventions for neuroenhancement in healthy individuals. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-9505

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):

Repantis, Dimitrios. “Psychopharmaceutical interventions for neuroenhancement in healthy individuals.” 2011. Thesis, Freie Universität Berlin. Accessed December 13, 2019. http://dx.doi.org/10.17169/refubium-9505.

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

MLA Handbook (7^th Edition):

Repantis, Dimitrios. “Psychopharmaceutical interventions for neuroenhancement in healthy individuals.” 2011. Web. 13 Dec 2019.

Vancouver:

Repantis D. Psychopharmaceutical interventions for neuroenhancement in healthy individuals. [Internet] [Thesis]. Freie Universität Berlin; 2011. [cited 2019 Dec 13]. Available from: http://dx.doi.org/10.17169/refubium-9505.

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

Council of Science Editors:

Repantis D. Psychopharmaceutical interventions for neuroenhancement in healthy individuals. [Thesis]. Freie Universität Berlin; 2011. Available from: http://dx.doi.org/10.17169/refubium-9505

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

Universitat de Girona

12. Blanco Silvente, Lídia. La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer.

Degree: Departament de Ciències Mèdiques, 2019, Universitat de Girona

URL: http://hdl.handle.net/10803/667938

► Les evidències disponibles en la literatura mèdica són concloents que la relació benefici-risc dels medicaments actualment indicats per la malaltia d'Alzheimer no és favorable. Aquesta… (more)

Subjects/Keywords: Malaltia d'Alzheimer; Alzheimer's disease; Enfermedad de Alzheimer; Demència; Dementia; Demencia; Colinesterasa; Menantina; Cholinesterase; Memantine; Tractaments farmacològics; Pharmacological treatments; Tratamientos farmacológicos; 616.8

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APA (6^th Edition):

Blanco Silvente, L. (2019). La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer. (Thesis). Universitat de Girona. Retrieved from http://hdl.handle.net/10803/667938

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):

Blanco Silvente, Lídia. “La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer.” 2019. Thesis, Universitat de Girona. Accessed December 13, 2019. http://hdl.handle.net/10803/667938.

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

MLA Handbook (7^th Edition):

Blanco Silvente, Lídia. “La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer.” 2019. Web. 13 Dec 2019.

Vancouver:

Blanco Silvente L. La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer. [Internet] [Thesis]. Universitat de Girona; 2019. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10803/667938.

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

Council of Science Editors:

Blanco Silvente L. La relación beneficio-riesgo del tratamiento farmacológico para la enfermedad de Alzheimer. [Thesis]. Universitat de Girona; 2019. Available from: http://hdl.handle.net/10803/667938

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

University of Oulu

13. Rimpiläinen, J. (Jussi). Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest.

Degree: 2001, University of Oulu

URL: http://urn.fi/urn:isbn:951425886X

► Abstract Ischaemic cerebral injury follows a well attested sequence of events including three phases, i.e. depolarization, biochemical cascade and reperfusion injury. Glutamate excitotoxicity plays an… (more)

▼ Abstract Ischaemic cerebral injury follows a well attested sequence of events including three phases, i.e. depolarization, biochemical cascade and reperfusion injury. Glutamate excitotoxicity plays an important role in the development of ischaemic brain injury following prolonged hypothermic circulatory arrest (HCA), and leukocyte infiltration and a cytokine-mediated inflammatory reaction are known to play a pivotal role in the reperfusion phase. The aim of this series of experimental studies was to develop biochemical and reperfusion-related strategies to improve brain protection. We tested the hypotheses that the Na+ channel blocker lamotrigine (I) or the N-Methyl-D-Aspartate-receptor antagonist memantine (III) could improve the cerebral outcome after HCA and studied whether a leukocyte-depletion filter (L-DF; LeukoGuard LG6®, Pall Biomedical, Portsmouth, U.K) could mitigate brain injury (II). The aim of the fourth study was to find out whether lamotrigine combined with the leukocyte-depleting filter can potentiate cerebral protection (IV). A chronic porcine model was used, in which haemodynamic, electrophysiological, metabolic and temperature monitoring were performed for four hours after the instigation of rewarming and S-100β measured up to 20 hours. Cytokines were measured, microdialysis was performed, and daily behavioural assessments were made until death or elective sacrifice on the seventh postoperative day, upon which a histopathological analysis of the brain was carried out. The rate of EEG burst recovery was higher in the lamotrigine-treated animals, the median being 40% of the baseline compared with 17% in the placebo group at 4 hours after the start of rewarming (p = 0.02) and 80% compared with 20% at 4 hours (p = 0.01). Complete behavioural recovery was seen in 5/8 of cases (63%) after lamotrigine administration, compared with 1/8 (13%) in the placebo group (p = 0.02). The median behavioural score among the animals that survived for 7 days was higher in the lamotrigine group (8) than in the controls (7) (p = 0.02). Mortality was 2/10 in the L-DF group and 5/10 in the controls, the median behavioural score on day 7 being higher in the L-DF group (8.5 vs. 3.5 p = 0.04). The median of the total histopathological score was 6.5 in the L-DF group and 15.5 in the control group (p = 0.005). In the memantine group 5/10 animals survived seven days, as compared with 9/10 in the placebo group, and the median behavioural score on day 7 was 3.5 compared with 7.5 in the placebo group (p = 0.39). The median of the total histopathological score was 16 in the memantine group and 14 in the placebo group (p = 0.25). In the LD-F + lamotrigine group 7/8 animals survived for seven days, as compared with 4/8 in the lamotrigine only group and 3/8 among the controls. EEG burst recovery 7 hours after the start of rewarming was highest in the LDF + lamotrigine group, the median being 94% (p = 0.024 vs. controls), compared with 81% in the lamotrigine group and 64% in the control group. The median behavioural score on day 7…

Subjects/Keywords: brain protection; hypothermic circulatory arrest; lamotrigine; leukocyte-depletion; memantine; reperfusion injury

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

APA (6^th Edition):

Rimpiläinen, J. (. (2001). Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:951425886X

Chicago Manual of Style (16^th Edition):

Rimpiläinen, J (Jussi). “Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest.” 2001. Doctoral Dissertation, University of Oulu. Accessed December 13, 2019. http://urn.fi/urn:isbn:951425886X.

MLA Handbook (7^th Edition):

Rimpiläinen, J (Jussi). “Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest.” 2001. Web. 13 Dec 2019.

Vancouver:

Rimpiläinen J(. Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest. [Internet] [Doctoral dissertation]. University of Oulu; 2001. [cited 2019 Dec 13]. Available from: http://urn.fi/urn:isbn:951425886X.

Council of Science Editors:

Rimpiläinen J(. Biochemical and reperfusion targeting strategies to improve brain protection during prolonged hypothermic circulatory arrest. [Doctoral Dissertation]. University of Oulu; 2001. Available from: http://urn.fi/urn:isbn:951425886X

14. Κανή, Χαρίκλεια. Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση.

Degree: 2009, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/19819

► To examine whether Cholinesterase Inhibitors (ChEIs) and memantine are superior to placebo in the treatment a) of Alzheimer’s disease (AD) for at least 6 months… (more)

▼ To examine whether Cholinesterase Inhibitors (ChEIs) and memantine are superior to placebo in the treatment a) of Alzheimer’s disease (AD) for at least 6 months b) of Vascular Dementia (VaD). Methods: Extensive literature search in three electronic databases (PubMed, Cochrane Database, EMBASE) and four registers (Cochrane Collaboration Trial Register, Clinical Trial.gov, EU-Psi PsiTri, International Federation of Pharmaceutical Manufacturers & Associations Clinical Trial Portal) was done to retrieve all relevant records up to November 2007 for AD and up to June 2008 for VaD. A standarized data extraction form, developed especially for this review, was used. Due to variation expected, due to the wide variations found in AD and in VaD and in their response to treatment, a random effects model was used to calculate combined estimates of all treatment effects. The reporting quality was assessed by Jadad, Chalmers modified scales and CONSORT 22-items, Delphi checklists. Results: 22 trials met the inclusion criteria for AD (10 trials for donepezil, 3 for galantamine, 4 for rivastigmine and 5 for memantine). Data suggest rather modest benefit for ChEIs and memantine in cognition (Weighted Mean Difference-WMD for ADAS-cog -2.56, 95% CI -3.12, -2.01). Benefits have been observed in global function (Number-Needed-to-Treat-ΝΝΤ=10 for patients stabilized or improved in CIBIC-Plus & WMD for GDS 0.14, 95% CI 0.05-0.24). Available data suggest that memantine may also have a positive effect on behaviour (WMD for NPI -2.90, 95% CI -4.57, -1.22). Dropouts and total adverse events were higher in the treatment group for the ChEIs (Number-Needed-to-Harm-NNH 13 & 11, respectively) and not statistically significant for memantine. A subgroup analysis for severe dementia defined as MMSE?12) revealed modest benefits of donepezil and memantine in cognition, global function, activities of daily living and behavior , but as the number of trials is small the results can not be conclusive. Height trials met the inclusion criteria for VaD (2 on donepezil, 2 on galantamine, 2 on rivastigmine and 2 on memantine). Data on ADAS-cog suggest a rather small benefit of ChEIs and memantine in cognition deficits in VaD (WMD=-1.70; 95% CI -2.20, -1.20 for ChEIs & WMD=-1.85; 95% CI -2.83, -0.88 for memantine), while the NNT for global responders was not statistically significant. Results for activities on daily living were available only for the donepezil trials. Dropouts due to any cause were higher in treatment arms with a NNH 12(10-17) for ChEIs and 15(9-100) for memantine, respectively. Conclusions: The use of ChEIs and memantine were associated with modest benefits in cognition and global function in patients with AD, while dropouts and total adverse events were higher in the treatment group of ChEIs. Generalization of the results should be done with caution, as the included population in the trials does not fully represent the general AD population. However, it should be taken into account that even small benefits matter a great deal to patients and…

Subjects/Keywords: Δονεπεζίλη; Γκαλανταμίνη; Ριβαστιγμίνη; Μεμαντίνη; Νόσος Alzheimer; Άνοια, Αγγειακή; Συστηματική ανασκόπηση; Μετά - ανάλυση; Donepezil; Galantamine; Rivastigmine; Memantine; Alzheimer's disease; Vascular dementia; Systematic review; Meta - analysis

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

APA (6^th Edition):

Κανή, . �. (2009). Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/19819

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):

Κανή, Χαρίκλεια. “Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση.” 2009. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed December 13, 2019. http://hdl.handle.net/10442/hedi/19819.

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

MLA Handbook (7^th Edition):

Κανή, Χαρίκλεια. “Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση.” 2009. Web. 13 Dec 2019.

Vancouver:

Κανή �. Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10442/hedi/19819.

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

Council of Science Editors:

Κανή �. Εκτίμηση ασφάλειας και αποτελεσματικότητας των φαρμάκων που χρησιμοποιούνται στην αντιμετώπιση της άνοιας: μετα-ανάλυση. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. Available from: http://hdl.handle.net/10442/hedi/19819

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

Universidade do Rio Grande do Sul

15. Kalinine, Eduardo. Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.

Degree: 2014, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/112063

►

Nos últimos anos, houve um aumento significativo no uso abusivo dos Esteróides Anabólicos Andrógenos (EAAs). Um dos efeitos comportamentais mais marcantes da administração crônica de… (more)

▼

Nos últimos anos, houve um aumento significativo no uso abusivo dos Esteróides Anabólicos Andrógenos (EAAs). Um dos efeitos comportamentais mais marcantes da administração crônica de EAAs como o Decanoato de Nandrolona (DN) é a indução do comportamento agressivo exacerbado. Atualmente o sistema glutamatérgico tem sido associado ao comportamento agressivo induzido pelos EAAs, principalmente no que se refere à modulação dos receptores N-Methyl-D-Aspartato NMDA (NMDAr). Nós investigamos os efeitos centrais e periféricos da administração do DN ao longo do tempo (4, 11 e 19 dias consecutivos de administração), e a participação de mecanismos glutamatérgicos. Para isso, camundongos CF-1 tratados com DN foram avaliados em relação ao comportamento agressivo pelo teste do intruso. Além disso, investigamos a captação de glutamato, o imunoconteúdo de GLT-1, os níveis de glutamato no líquido extracelular, e a participação dos NMDAr na manifestação do comportamento agressivo. O fenótipo agressivo foi evidenciado somente no longo tempo de exposição à DN (19 dias). Na mesma janela temporal que os animais apresentaram o fenótipo agressivo houve redução significativa de captação de glutamato em fatias cerebrais de córtex e hipocampo, como também a redução do imunoconteúdo do transportador astrocitário GLT-1 nas mesmas estruturas cerebrais. A administração de antagonistas de NMDAr como MK-801 e memantina antes do teste do intruso diminuiu o comportamento agressivo dos animais tratados cronicamente com DN a níveis iguais aos do grupo controle. Ainda, o comportamento agressivo induzido pela administração crônica de DN diminuiu a remoção do glutamato da fenda sináptica, culminando com o aumento do glutamato extracelular no SNC, o que resultou na hiperexcitabilidade dos NMDAr. Este trabalho enfatiza o papel da comunicação entre astrócitos e neurônios e a relevância da hiperstimulação de NMDAr na manifestação do comportamento agressivo.

Nandrolone decanoate (ND), an anabolic androgenic steroid (AAS), induces an aggressive phenotype by mechanisms involving glutamate-induced N-methyl-d-aspartate receptor (NMDAr) hyperexcitability. The astrocytic glutamate transporters remove excessive glutamate surrounding the synapse. However, the impact of supraphysiological doses of ND on glutamate transporters activity remains elusive. We investigated whether ND-induced aggressive behavior is correlated with GLT-1 activity, glutamate levels and abnormal NMDAr responses. Two-month-old untreated male mice (CF1, n=20) were tested for baseline aggressive behavior in the resident-intruder test. Another group of mice (n=188) was injected with ND (15mg/kg) or vehicle for 4, 11 and 19 days (short-, mid- and long-term endpoints, respectively) and was evaluated in the resident-intruder test. Each endpoint was assessed for GLT-1 expression and glutamate uptake activity in the frontoparietal cortex and hippocampal tissues. Only the long-term ND endpoint significantly decreased the latency to first attack and increased the number of attacks, which was associated…

Advisors/Committee Members: Portela, Luis Valmor Cruz.

Subjects/Keywords: Decanoatos; Aggressive behavior; Nandrolona; Nandrolone decanoate; Agressividade; Glutamate transporter 1 (GLT-1); N-methyl-D-aspartate receptor (NMDAr); Receptores de N-metil-D-aspartato; Memantine; Ácido glutâmico; Memantina; MK-801

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

APA (6^th Edition):

Kalinine, E. (2014). Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/112063

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):

Kalinine, Eduardo. “Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.” 2014. Thesis, Universidade do Rio Grande do Sul. Accessed December 13, 2019. http://hdl.handle.net/10183/112063.

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

MLA Handbook (7^th Edition):

Kalinine, Eduardo. “Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.” 2014. Web. 13 Dec 2019.

Vancouver:

Kalinine E. Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2014. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10183/112063.

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

Council of Science Editors:

Kalinine E. Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. [Thesis]. Universidade do Rio Grande do Sul; 2014. Available from: http://hdl.handle.net/10183/112063

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

North-West University

16. Retief, Renché. The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief .

Degree: 2004, North-West University

URL: http://hdl.handle.net/10394/731

► Depressive disorders are among the most frequent psychiatric diseases in the Western world with prevalence between 9% and 18%. Poor compliance and inappropriate antidepressant discontinuation… (more)

▼ Depressive disorders are among the most frequent psychiatric diseases in the Western world with prevalence between 9% and 18%. Poor compliance and inappropriate antidepressant discontinuation invokes long-term morbidity, and appear linked to hippocampal shrinkage. Despite major advances in pharmacological treatment of the illness over the past 3040 years, currently available agents have distinct shortfalls both in clinical efficacy and in maintenance of response. This implies a greater long-term morbidity with significant impact on the patient, the patient's family as well as economic implications to health care managers and providers. The major reason for this state of affairs is our poor understanding of the neurobiology of depression and hence, of antidepressant (AD) action. AD drugs are thus not addressing the crucial neurobiological target underlying the illness, and new strategies and treatments are urgently needed. In recent years, depression has been associated with disturbances in excitotoxic glutamatergic activity, yet this has not been systematically evaluated. While the role of neurotransmitters such as serotonin, noradrenaline and dopamine has been extensively studied, new evidence suggests a role for the unique neurotransmitter nitric oxide (NO). Nitric oxide (NO), is activated by glutamatergic systems in various limbic and other regions of the brain, and has recently also been implicated in anxiety and affective disorders. Of special interest is the putative role of NO in cellular memory, synaptic plasticity and cell survival, all-important processes in the neuropathology and neurodevelopment of depression. Recent clinical studies have provided evidence of the role of the NO-pathway in depression, while preclinical studies have demonstrated the anxiolytic and antidepressant actions of nitric oxide synthase (NOS)-inhibitors. Moreover, NO interacts with other classical transmitters that have a regulatory role on mood, particularly the monoamines, as well as glutamate and gammaaminobutyric acid (GABA). In the current study the role of the NO-cGMP pathway in AD action was investigated, after chronic imipramine (IMI) and after IMI withdrawal, using a learned helplessness paradigm. Behavioural changes, hippocampal NOS activity and cGMP accumulation was determined together with pharmacological manipulation of the NO-cGMP pathway. Chronic IMI, 15 mg/kg/day intraperitoneal (ip) administration induced a pronounced reduction in swim immobility time in the forced swim test (FST), with no effect on horizontal or vertical locomotor activity. These behavioural changes were accompanied by a significant reduction in NOS enzyme activity and cGMP accumulation. In order to confirm the involvement of the NO-cGMP pathway in the AD action of IMI, chronic (3 weeks) IMI treatment was followed by an acute withdrawal of 7 days. Acute withdrawal, after chronic IMI treatment, resulted in a significant increase in swim immobility time and an increase in NOS enzyme activity and cGMP levels. In fact,…

Subjects/Keywords: Depression; Antidepressant; Withdrawal; Imipramine; NO-cGMP pathway; Methylene blue; Memantine; Ritanserin

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

APA (6^th Edition):

Retief, R. (2004). The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief . (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/731

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):

Retief, Renché. “The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief .” 2004. Thesis, North-West University. Accessed December 13, 2019. http://hdl.handle.net/10394/731.

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

MLA Handbook (7^th Edition):

Retief, Renché. “The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief .” 2004. Web. 13 Dec 2019.

Vancouver:

Retief R. The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief . [Internet] [Thesis]. North-West University; 2004. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10394/731.

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

Council of Science Editors:

Retief R. The role of the NO-cGMP pathway as a putative target in antidepressant action / Renché Retief . [Thesis]. North-West University; 2004. Available from: http://hdl.handle.net/10394/731

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

University of Lund

17. Stubendorff, Kajsa. Markers of Prognosis in Neurodegenerative Dementia.

Degree: 2014, University of Lund

URL: http://lup.lub.lu.se/record/4393393 ; http://portal.research.lu.se/ws/files/3718338/4393400.pdf

► Background: A prognostic marker should provide information about course and outcome of disease, e.g. predict time to a given endpoint or rate of progression due… (more)

Subjects/Keywords: Klinisk medicin; Neurologi; Lewy body disease; Alzheimer's disease; dementia with Lewy bodies; prognosis; survival; longitudinal studies; biomarkers; cerebrospinal fluid; dysautonomic orthostatic hypotension; memantine

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

APA (6^th Edition):

Stubendorff, K. (2014). Markers of Prognosis in Neurodegenerative Dementia. (Doctoral Dissertation). University of Lund. Retrieved from http://lup.lub.lu.se/record/4393393 ; http://portal.research.lu.se/ws/files/3718338/4393400.pdf

Chicago Manual of Style (16^th Edition):

Stubendorff, Kajsa. “Markers of Prognosis in Neurodegenerative Dementia.” 2014. Doctoral Dissertation, University of Lund. Accessed December 13, 2019. http://lup.lub.lu.se/record/4393393 ; http://portal.research.lu.se/ws/files/3718338/4393400.pdf.

MLA Handbook (7^th Edition):

Stubendorff, Kajsa. “Markers of Prognosis in Neurodegenerative Dementia.” 2014. Web. 13 Dec 2019.

Vancouver:

Stubendorff K. Markers of Prognosis in Neurodegenerative Dementia. [Internet] [Doctoral dissertation]. University of Lund; 2014. [cited 2019 Dec 13]. Available from: http://lup.lub.lu.se/record/4393393 ; http://portal.research.lu.se/ws/files/3718338/4393400.pdf.

Council of Science Editors:

Stubendorff K. Markers of Prognosis in Neurodegenerative Dementia. [Doctoral Dissertation]. University of Lund; 2014. Available from: http://lup.lub.lu.se/record/4393393 ; http://portal.research.lu.se/ws/files/3718338/4393400.pdf

18. Martin, Elodie. Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.

Degree: Docteur es, Sciences de la vie et de la sante, 2017, Clermont Auvergne

URL: http://www.theses.fr/2017CLFAS012

► Les antagonistes du récepteur N-méthyl-D-aspartate (NMDA) comme la kétamine, le dextrométhorphane et la mémantine sont utilisés pour la prise en charge de la douleur neuropathique.… (more)

▼ Les antagonistes du récepteur N-méthyl-D-aspartate (NMDA) comme la kétamine, le dextrométhorphane et la mémantine sont utilisés pour la prise en charge de la douleur neuropathique. La kétamine est très efficace contre les douleurs neuropathiques réfractaires aux traitements conventionnels. Cependant, son utilisation est limitée du fait de nombreux effets indésirables. Un relais antalgique est alors proposé. Ce travail de thèse s’insère dans un programme de recherche dédié aux antagonistes du récepteur NMDA dans la prise en charge de la douleur neuropathique. Le premier objectif était d’évaluer dans une étude clinique randomisée, en simple insu, en groupes parallèles, contrôlée versus placebo, les effets antalgiques du dextrométhorphane et de la mémantine, administrés en relais de la kétamine chez 60 patients souffrant de douleurs neuropathiques d’origine périphérique. L’impact de ces traitements sur le statut cognitivo-émotionnel des patients et leur qualité de vie a également été examiné, ainsi que la modulation des effets de ces médicaments par le polymorphisme génétique impliqué dans le métabolisme (CYP2D6, CYP3A4,5), la biodisponibilité et l’élimination (NR1I2) de ces deux molécules. En parallèle une étude mécanistique centrée sur le dextrométhorphane a été réalisée chez vingt volontaires sains (étude randomisée, en double aveugle, en groupes croisés). L’objectif était d’étudier dans un modèle d’hyperalgie induite par le froid « Freeze injury » les caractéristiques pharmacologiques et mécanistiques déterminant les effets anti-nociceptifs, centraux et cognitifs du dextrométhorphane ainsi que le polymorphisme génétique impliqué dans leur modulation. Chez les patients, les effets antalgiques immédiats de la kétamine ont été confirmés et s’accompagnaient de l’amélioration des scores d’anxiété et de dépression, des aspects cognitifs et affectifs et du sommeil. Toutefois, par rapport au placebo, la mémantine et le dextrométhorphane n’ont pas permis de renforcer significativement l’antalgie induite par la kétamine. Chez les volontaires sains, le dextrométhorphane a révélé des effets anti-hyperalgiques suite à une sensibilisation périphérique et centrale. Cependant, aucun effet analgésique sur la douleur thermique aiguë n’a été observé. Ces deux approches clinique et mécanistique concernant l’effet curatif des antagonistes du récepteur NMDA ont permis d’une part de montrer : 1 - chez le patient, l’effet curatif prolongé de la kétamine et l’intérêt du dextrométhorphane et de la mémantine dans la prise en charge du retentissement négatif de la douleur neuropathique sur le statut cognitivo-émotionnel et la qualité de vie des patients; 2 - chez le volontaire sain, l’efficacité anti-hyperalgique du dextrométhorphane sur les phénomènes de sensibilisation périphérique et centrale ainsi que ses répercussions sédatives et cognitives. En complément de ces deux études et dans le but de confirmer en clinique les effets curatifs du dextrométhorphane sur le triptyque douleur-cognition-émotion, une étude clinique randomisée, en double… Advisors/Committee Members: Pickering, Gisèle (thesis director).

Subjects/Keywords: Kétamine; Mémantine; Récepteur N-méthyl-D-aspartate; Dextrométhorphane; Qualité de vie liée à la santé; Dextromethorphan; Ketamine; Memantine; N-methyl-D-aspartate receptor; Health Related Quality of Life; 612.82

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

APA (6^th Edition):

Martin, E. (2017). Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. (Doctoral Dissertation). Clermont Auvergne. Retrieved from http://www.theses.fr/2017CLFAS012

Chicago Manual of Style (16^th Edition):

Martin, Elodie. “Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.” 2017. Doctoral Dissertation, Clermont Auvergne. Accessed December 13, 2019. http://www.theses.fr/2017CLFAS012.

MLA Handbook (7^th Edition):

Martin, Elodie. “Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.” 2017. Web. 13 Dec 2019.

Vancouver:

Martin E. Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. [Internet] [Doctoral dissertation]. Clermont Auvergne; 2017. [cited 2019 Dec 13]. Available from: http://www.theses.fr/2017CLFAS012.

Council of Science Editors:

Martin E. Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. [Doctoral Dissertation]. Clermont Auvergne; 2017. Available from: http://www.theses.fr/2017CLFAS012

19. Sarwary, Mariam. Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine.

Degree: Pharmacology, 2017, Umeå University

URL: http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-136250

Subjects/Keywords: Alzheimer´s disease; Donepezil; Rivastigmine; Galantamine; Memantine and randomized controlled trails; Pharmaceutical Sciences; Farmaceutiska vetenskaper

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

APA (6^th Edition):

Sarwary, M. (2017). Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine. (Thesis). Umeå University. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-136250

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):

Sarwary, Mariam. “Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine.” 2017. Thesis, Umeå University. Accessed December 13, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-136250.

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

MLA Handbook (7^th Edition):

Sarwary, Mariam. “Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine.” 2017. Web. 13 Dec 2019.

Vancouver:

Sarwary M. Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine. [Internet] [Thesis]. Umeå University; 2017. [cited 2019 Dec 13]. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-136250.

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

Council of Science Editors:

Sarwary M. Comparison of cognitive decline medications of Alzheimer´s disease : Efficacy and safety of Donepezil, Galantamine, Rivastigmine and Memantine. [Thesis]. Umeå University; 2017. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-136250

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

University of Debrecen

20. Choi, Hyun Duck. Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/242811

► To date, there are only symptomatic treatments approved by the FDA and in wide clinical usage: Rivastigmine, Galantamine, Donepezil, and Memantine. However, their actual clinical… (more)

Subjects/Keywords: Alzheimer; Dementia; Efficacy; Safety; Tolerability; Comparison; AchEI; NMDA antagonist; Acetylcholinesterase inhibitor; Pharmacological; Clinical; treatment; Review; Memantine; Donepezil; Rivastigmine; Galantamine

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

APA (6^th Edition):

Choi, H. D. (n.d.). Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/242811

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):

Choi, Hyun Duck. “Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia .” Thesis, University of Debrecen. Accessed December 13, 2019. http://hdl.handle.net/2437/242811.

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):

Choi, Hyun Duck. “Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia .” Web. 13 Dec 2019.

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

Vancouver:

Choi HD. Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia . [Internet] [Thesis]. University of Debrecen; [cited 2019 Dec 13]. Available from: http://hdl.handle.net/2437/242811.

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:

Choi HD. Pharmacological and Clinical Review of AchEI against NMDA antagonist in treatment of Alzheimer Dementia . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/242811

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

North-West University

21. Bothma, Tanya. Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma .

Degree: 2004, North-West University

URL: http://hdl.handle.net/10394/477

► Posttraumatic stress disorder (PTSD) is a severe anxiety disorder characterised by hypothalamic-pituitary-adrenal (HPA)-axis abnormalities, hyperarousal, anxiety, flashbacks of trauma memories and avoidance. Increasing evidence is… (more)

▼ Posttraumatic stress disorder (PTSD) is a severe anxiety disorder characterised by hypothalamic-pituitary-adrenal (HPA)-axis abnormalities, hyperarousal, anxiety, flashbacks of trauma memories and avoidance. Increasing evidence is now accumulating that the disorder is also associated with shrinkage of the hippocampus and cognitive dysfunction that may have its origin in stress-induced excitotoxicity. Animal studies have indeed highlighted a potential role of the excitotoxic glutamatenitric oxide (NO) pathway in the stress response. Since PTSD appears to be an illness that progresses and worsens over time after an initial severe traumatic event, this study has used an animal model that emphasises repeated trauma to investigate the effect of stress on hippocampal NO synthase (NOS) activity, the release of the nitrogen oxide metabolites of NO (NOx), and also the evoked release of cGMP. Furthermore, the modulation and dependency of these responses on glutamate, NO and cGMP activity using drugs selective for these targets, will also be investigated. Rats (n=10/group) were exposed to repeated stress together with saline or drug administration immediately after the stress procedure and continuing for one week post-stress. The animals were then sacrificed for assay of hippocampal NOS activity, NO, and cGMP accumulation. Animals received either the glutamate-NMDA receptor antagonist, memantine (MEM;5mg/kg ip/d), the neuronal NOS selective inhibitor, 7- nitroindazole monosodium salt (7-NINA;20mg/kg ip/d), the cGMP-specific PDE inhibitor, sildenafil (SIL;10mg/kg ip/d) or the NFkb antagonist, pyrollidine dithiocarbamate (PDTC;70mg/kg ip/d). The latter inhibits the nuclear transcription factor, NFkb, responsible for inducing the expression of iNOS, while it also appears to mediate the glutamatergic actions on NOS expression, Stress significantly increased hippocampal NOS activity, as well as significantly increased hippocampal cGMP and NO, levels. These increases were blocked by pretreatment with either PDTC or 7-NINA, while memantine was without effect. Sildenafil significantly augmented stress induced NO, accumulation, as well as cGMP. although the latter failed to reach significance. 7-NINA and memantine significantly blocked the increase in cGMP evoked by time-dependent sensitisation (TDS)-stress, with PDTC attenuating this response, but not significantly. Additionally, administration of each drug separately for seven days without exposure to stress, did not evoke significant changes in NOx levels, compared to the control group. However, significant increases in cGMP levels, compared to the control group, were found with all four drugs. Repeated trauma therefore activates the NO-cGMP pathway, possibly involving actions on both nNOS and iNOS. The NMDA receptor appears less involved after chronic repeated stress, and may have limited therapeutic implications. Sub-cellular NO-modulation, however, may represent an important therapeutic strategy in preventing the effects of severe stress and…

Subjects/Keywords: PTSD; Nitric oxide; Time-dependent sensitisation; Stress; 7-Nitroindazole monosodium salt (7-NINA); Memantine; PDTC; Sildenafil; Glutamate; Cyclic GMP (cGMP)

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

APA (6^th Edition):

Bothma, T. (2004). Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma . (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/477

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):

Bothma, Tanya. “Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma .” 2004. Thesis, North-West University. Accessed December 13, 2019. http://hdl.handle.net/10394/477.

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

MLA Handbook (7^th Edition):

Bothma, Tanya. “Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma .” 2004. Web. 13 Dec 2019.

Vancouver:

Bothma T. Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma . [Internet] [Thesis]. North-West University; 2004. [cited 2019 Dec 13]. Available from: http://hdl.handle.net/10394/477.

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

Council of Science Editors:

Bothma T. Investigating the role of the NO-cGMP pathway in an animal model of posttraumatic stress disorder (PTSD) / Tanya Bothma . [Thesis]. North-West University; 2004. Available from: http://hdl.handle.net/10394/477

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

Freie Universität Berlin

22. Baumann, Lisa Katharina. The importance of biomarkers for the progression of the Alzheimer’s disease.

Degree: 2019, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-4207

► Background: Mild cognitive impairment (MCI) clinically precedes Alzheimer’s dementia (AD). For AD a symptomatic treatment with acetylcholinesterase-inhibitors (AChE-I) and the N-Methyl-D-Aspartat Receptor antagonist memantin is… (more)

Subjects/Keywords: Acetylcholinesterase inhibitor; amyloid β1-42; Cerebrospinal fluid; Combination treatment; Dementia; Florbetaben; Galantamine; hippocampal atrophy; Memantine; PET-tracer; total-Tau; Mild Cognitive Impairment; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit

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

APA (6^th Edition):

Baumann, L. K. (2019). The importance of biomarkers for the progression of the Alzheimer’s disease. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-4207

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):

Baumann, Lisa Katharina. “The importance of biomarkers for the progression of the Alzheimer’s disease.” 2019. Thesis, Freie Universität Berlin. Accessed December 13, 2019. http://dx.doi.org/10.17169/refubium-4207.

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

MLA Handbook (7^th Edition):

Baumann, Lisa Katharina. “The importance of biomarkers for the progression of the Alzheimer’s disease.” 2019. Web. 13 Dec 2019.

Vancouver:

Baumann LK. The importance of biomarkers for the progression of the Alzheimer’s disease. [Internet] [Thesis]. Freie Universität Berlin; 2019. [cited 2019 Dec 13]. Available from: http://dx.doi.org/10.17169/refubium-4207.

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

Council of Science Editors:

Baumann LK. The importance of biomarkers for the progression of the Alzheimer’s disease. [Thesis]. Freie Universität Berlin; 2019. Available from: http://dx.doi.org/10.17169/refubium-4207

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

University of Lund

23. Larsson, Victoria. Living with Lewy body dementia. Treatment, survival & quality of life.

Degree: 2018, University of Lund

URL: http://lup.lub.lu.se/record/e91ccf95-7dcb-44d0-a2ae-b3855676cd36 ; https://portal.research.lu.se/ws/files/49806490/Thesis.pdf

► Background: Patients with Lewy body dementias (LBD) have a complex clinical picture. With no prevention or cure, management focuses around symptomatic relief, however pharmacological and… (more)

▼ Background: Patients with Lewy body dementias (LBD) have a complex clinical picture. With no prevention or cure, management focuses around symptomatic relief, however pharmacological and non-pharmacological options have been inadequately investigated. Moreover, the understanding of survival, prognostic factors and impact of the diagnosis in an already ageing and comorbid population is limited. Even though well-being is the ultimate goal in current management, the constituents of well-being in LBD, as well as the preferences of patients, have not been extensively explored. Aim: To understand the impact of living with Lewy body dementias, with a focus on pharmacological and non-pharmacological treatments, survival and quality of life. Study populations: The studies comprise of LBD patients included in an RCT of memantine (Study I-II) and from the Memory Clinic, Malmö, Sweden (Study III-V).Results: I) Physical activity during sleep decreased in LBD patients treated with memantine compared to placebo over 24 weeks. II) Quality of life in LBD is constructed of physical and socio-environmental domains. Treatment with memantine suggest a possible benefit over placebo for measures of caregiver-rated quality of life over 24 weeks. III) Swallowing dysfunction is common and sometimes asymptomatic in LBD patients. Carbonated thin liquid improves swallowing function compared to thin and thickened liquid. IV) Mortality is over three-times higher in patients with LBD compared to an age- and sex-matched general population. Excess mortality is found primarily in younger patients, females, those with lower MMSE and APOE ε4 carriers. V) It is feasible to conduct in-depth interviews with persons with DLB. Three themes characterise the experience of living with DLB; disease impact, self-perception and coping, and importance of others. Conclusions: This thesis emphasises the importance of pharmacological and non-pharmacological management in LBD, particularly in view of the poor prognosis compared to the general population. This includes management of non-cognitive symptoms such as swallowing dysfunction, for which carbonated thin liquid might be a therapeutic option. Ultimately, improving well-being is of utmost importance, and for this to be achieved involvement of patients with LBD in research is crucial. A multifaceted approach is recommended, addressing physical, social and psychological needs.

Subjects/Keywords: Medical and Health Sciences; Lewy bodies; Lewy body dementia; Lewy body disease; QUALITATIVE; Lewy Body Disease: drug therapy; Lewy Body Disease: mortality; Lewy Body Disease: therapy; DEMENTIA; dementia with Lewy bodies; Parkinson's disease dementia; Parkinson disease; memantine; Prognosis and survival; Prognosis; Survival; mortality; Dysphagia; Carbonated beverages; Swallowing disorders; Therapeutics; Video recording; video analysing technique; QUALITY OF LIFE

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

APA (6^th Edition):

Larsson, V. (2018). Living with Lewy body dementia. Treatment, survival & quality of life. (Doctoral Dissertation). University of Lund. Retrieved from http://lup.lub.lu.se/record/e91ccf95-7dcb-44d0-a2ae-b3855676cd36 ; https://portal.research.lu.se/ws/files/49806490/Thesis.pdf

Chicago Manual of Style (16^th Edition):

Larsson, Victoria. “Living with Lewy body dementia. Treatment, survival & quality of life.” 2018. Doctoral Dissertation, University of Lund. Accessed December 13, 2019. http://lup.lub.lu.se/record/e91ccf95-7dcb-44d0-a2ae-b3855676cd36 ; https://portal.research.lu.se/ws/files/49806490/Thesis.pdf.

MLA Handbook (7^th Edition):

Larsson, Victoria. “Living with Lewy body dementia. Treatment, survival & quality of life.” 2018. Web. 13 Dec 2019.

Vancouver:

Larsson V. Living with Lewy body dementia. Treatment, survival & quality of life. [Internet] [Doctoral dissertation]. University of Lund; 2018. [cited 2019 Dec 13]. Available from: http://lup.lub.lu.se/record/e91ccf95-7dcb-44d0-a2ae-b3855676cd36 ; https://portal.research.lu.se/ws/files/49806490/Thesis.pdf.

Council of Science Editors:

Larsson V. Living with Lewy body dementia. Treatment, survival & quality of life. [Doctoral Dissertation]. University of Lund; 2018. Available from: http://lup.lub.lu.se/record/e91ccf95-7dcb-44d0-a2ae-b3855676cd36 ; https://portal.research.lu.se/ws/files/49806490/Thesis.pdf

24. Welch, Emily L. Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder.

Degree: 2016, University of Florida

URL: http://ufdc.ufl.edu/AA00047939

BACKGROUND

Subjects/Keywords: Alcoholic beverages; Alcoholism; Alcohols; Craving; Medications; N methyl D aspartate receptors; Relapse; Side effects; Symptomatology; Urine; alcohol; alcohol use disorder; detoxification; feasibility; memantine

…FEASIBILITY OF INVESTIGATION OF MEMANTINE 8 administration because hepatotoxicity… …OF MEMANTINE 9 effective at reducing relapse rates or number of drinking days… …cognitive deficits. Memantine as a Novel Treatment The limited success of acamprosate, which has… …x29;. Memantine is an NMDA receptor inhibitor that is currently FDA-approved to boost… …memantine to treat alcohol-related dementia patients have shown significant ability to improve…

13 more images…

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

APA (6^th Edition):

Welch, E. L. (2016). Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder. (Thesis). University of Florida. Retrieved from http://ufdc.ufl.edu/AA00047939

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):

Welch, Emily L. “Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder.” 2016. Thesis, University of Florida. Accessed December 13, 2019. http://ufdc.ufl.edu/AA00047939.

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

MLA Handbook (7^th Edition):

Welch, Emily L. “Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder.” 2016. Web. 13 Dec 2019.

Vancouver:

Welch EL. Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder. [Internet] [Thesis]. University of Florida; 2016. [cited 2019 Dec 13]. Available from: http://ufdc.ufl.edu/AA00047939.

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

Council of Science Editors:

Welch EL. Feasibility of Clinical Investigation of Memantine in Individuals Diagnosed with Alcohol Use Disorder. [Thesis]. University of Florida; 2016. Available from: http://ufdc.ufl.edu/AA00047939

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

25. Muriithi, Paul Mutuanyingi. A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory.

Degree: PhD, 2014, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/a-case-for-memory-enhancement-ethical-social-legal-and-policy-implications-for-enhancing-the-memory(bf11d09d-6326-49d2-8ef3-a40340471acf).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603223

► The desire to enhance and make ourselves better is not a new one and it has continued to intrigue throughout the ages. Individuals have continued… (more)

▼ The desire to enhance and make ourselves better is not a new one and it has continued to intrigue throughout the ages. Individuals have continued to seek ways to improve and enhance their well-being for example through nutrition, physical exercise, education and so on. Crucial to this improvement of their well-being is improving their ability to remember. Hence, people interested in improving their well-being, are often interested in memory as well. The rationale being that memory is crucial to our well-being. The desire to improve one’s memory then is almost certainly as old as the desire to improve one’s well-being. Traditionally, people have used different means in an attempt to enhance their memories: for example in learning through storytelling, studying, and apprenticeship. In remembering through practices like mnemonics, repetition, singing, and drumming. In retaining, storing and consolidating memories through nutrition and stimulants like coffee to help keep awake; and by external aids like notepads and computers. In forgetting through rituals and rites. Recent scientific advances in biotechnology, nanotechnology, molecular biology, neuroscience, and information technologies, present a wide variety of technologies to enhance many different aspects of human functioning. Thus, some commentators have identified human enhancement as central and one of the most fascinating subject in bioethics in the last two decades. Within, this period, most of the commentators have addressed the Ethical, Social, Legal and Policy (ESLP) issues in human enhancements as a whole as opposed to specific enhancements. However, this is problematic and recently various commentators have found this to be deficient and called for a contextualized case-by-case analysis to human enhancements for example genetic enhancement, moral enhancement, and in my case memory enhancement (ME). The rationale being that the reasons for accepting/rejecting a particular enhancement vary depending on the enhancement itself. Given this enormous variation, moral and legal generalizations about all enhancement processes and technologies are unwise and they should instead be evaluated individually. Taking this as a point of departure, this research will focus specifically on making a case for ME and in doing so assessing the ESLP implications arising from ME. My analysis will draw on the already existing literature for and against enhancement, especially in part two of this thesis; but it will be novel in providing a much more in-depth analysis of ME. From this perspective, I will contribute to the ME debate through two reviews that address the question how we enhance the memory, and through four original papers discussed in part three of this thesis, where I examine and evaluate critically specific ESLP issues that arise with the use of ME. In the conclusion, I will amalgamate all my contribution to the ME debate and suggest the future direction for the ME debate.

Subjects/Keywords: 174; adderall; ampakines; amphetamine; appeal to empathy; aricept; Aristotle; Baddeley; benzodiazepines; bioethics; Bostrom; brain stimulation; brain-computer interface; brain-machine interface; Brunet; Buchanan; caffeine; Cahil; Caplan; case; coercion; computers; confidentiality; consent; consequentialist; consistency; consolidation; conventional; criminal; damages; d-amphetamine; declarative memory; deep brain stimulation; Degrazia; deontological; diazepam; discrimination; donepezil; Douglas; drug mongering; duty; duty to remember; Dworkin; electroconvulsive therapy; Elliott; emotional distress; emotions; encoding; enhancement; enhancing technologies; epistemic knowledge; equality; ethical; evidence; exelon; explicit memory; eyewitness; eyewitness evidence; eyewitness testimony; Facebook; Farah; forget; Fukuyama; galantamine; gatekeepers; Ghetti; ginkgo biloba; Glover; glucocorticoids; glucose; greater good; Habermas; Harris; health; human dignity; human diversity; human enhancement; human nature; human rights; Hunter; identity; implicit memory; inauthentic; individual autonomy; inevitable; informed consent; internet; Jackson; justice; Kamm; Kass; Kolber; laissez faire; learning; legal; legal approach; lifelogging; living authentically; Loftus; long-term memory; Lynch; malleability of memory; mastery; McKibben; medicalization; meditation; Mehlman; Meilaender; memantine; Memory; memory dampening; memory enhancement; memory manipulation; memory processes; memory retention; memory retrieval; memory storage; methylphenidate; midazalom; misidentification of witnesses; mistaken identifications; mitigation; mnemonics; modafinil; moratorium; music; negative emotions; negligence; nondeclarative memory; non-pharmacological memory enhancement; nutrition; obligation; obstruction of justice; omega-3; optimum memory; Parens; person identity; personality; perverting justice; pharmacological means; philosophical approach; photographic; physical exercise; Pitman; policy; poly unsaturated fatty acids; precautionary approach; precautionary principle; preserving memories; President’s Council; primary memory; privacy; procedural memory; propofol; propranolol; provigil; razadyne; recall; recording audio; reference memory; regulation; regulatory authorities; regulatory bodies; relational memory; remembering; remembering fitly; remembering truly; risks; ritalin; rites; rituals; rivastigmine; safety; Sahakian; Sandberg; Sandel; Savulescu; Schacter; secondary memory; short-term memory; sleep; slippery slope; social; societies' interests; species-typical; society interests; species-typical functioning; Squire; Stanton; Strange; technological means; testimony; therapeutic; therapy; therapy-enhancement distinction; traditional; transcrannial direct current stimulation; transcrannial magnetic stimulation; traumatic memories; Tulving; ultimate prize; unnatural; unnatural means; Vaiva; video devices; virtual social networking; virtue ethics; Wagenaar; well-being; Wells; working memory; wrongful; wrongful acquittals; wrongful convictions; yoga; Kahane; Giordano; Bennett; Holm; Mental Capacity Act

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

APA (6^th Edition):

Muriithi, P. M. (2014). A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/a-case-for-memory-enhancement-ethical-social-legal-and-policy-implications-for-enhancing-the-memory(bf11d09d-6326-49d2-8ef3-a40340471acf).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603223

Chicago Manual of Style (16^th Edition):

Muriithi, Paul Mutuanyingi. “A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory.” 2014. Doctoral Dissertation, University of Manchester. Accessed December 13, 2019. https://www.research.manchester.ac.uk/portal/en/theses/a-case-for-memory-enhancement-ethical-social-legal-and-policy-implications-for-enhancing-the-memory(bf11d09d-6326-49d2-8ef3-a40340471acf).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603223.

MLA Handbook (7^th Edition):

Muriithi, Paul Mutuanyingi. “A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory.” 2014. Web. 13 Dec 2019.

Vancouver:

Muriithi PM. A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory. [Internet] [Doctoral dissertation]. University of Manchester; 2014. [cited 2019 Dec 13]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/a-case-for-memory-enhancement-ethical-social-legal-and-policy-implications-for-enhancing-the-memory(bf11d09d-6326-49d2-8ef3-a40340471acf).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603223.

Council of Science Editors:

Muriithi PM. A case for memory enhancement : ethical, social, legal, and policy implications for enhancing the memory. [Doctoral Dissertation]. University of Manchester; 2014. Available from: https://www.research.manchester.ac.uk/portal/en/theses/a-case-for-memory-enhancement-ethical-social-legal-and-policy-implications-for-enhancing-the-memory(bf11d09d-6326-49d2-8ef3-a40340471acf).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603223

26. Muriithi, Paul Mutuanyingi. A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory.

Degree: 2014, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:220498

► The desire to enhance and make ourselves better is not a new one and it has continued to intrigue throughout the ages. Individuals have continued… (more)

▼ The desire to enhance and make ourselves better is not a new one and it has continued to intrigue throughout the ages. Individuals have continued to seek ways to improve and enhance their well-being for example through nutrition, physical exercise, education and so on. Crucial to this improvement of their well-being is improving their ability to remember. Hence, people interested in improving their well-being, are often interested in memory as well. The rationale being that memory is crucial to our well-being. The desire to improve one’s memory then is almost certainly as old as the desire to improve one’s well-being. Traditionally, people have used different means in an attempt to enhance their memories: for example in learning through storytelling, studying, and apprenticeship. In remembering through practices like mnemonics, repetition, singing, and drumming. In retaining, storing and consolidating memories through nutrition and stimulants like coffee to help keep awake; and by external aids like notepads and computers. In forgetting through rituals and rites.Recent scientific advances in biotechnology, nanotechnology, molecular biology, neuroscience, and information technologies, present a wide variety of technologies to enhance many different aspects of human functioning. Thus, some commentators have identified human enhancement as central and one of the most fascinating subject in bioethics in the last two decades. Within, this period, most of the commentators have addressed the Ethical, Social, Legal and Policy (ESLP) issues in human enhancements as a whole as opposed to specific enhancements. However, this is problematic and recently various commentators have found this to be deficient and called for a contextualized case-by-case analysis to human enhancements for example genetic enhancement, moral enhancement, and in my case memory enhancement (ME). The rationale being that the reasons for accepting/rejecting a particular enhancement vary depending on the enhancement itself. Given this enormous variation, moral and legal generalizations about all enhancement processes and technologies are unwise and they should instead be evaluated individually.Taking this as a point of departure, this research will focus specifically on making a case for ME and in doing so assessing the ESLP implications arising from ME. My analysis will draw on the already existing literature for and against enhancement, especially in part two of this thesis; but it will be novel in providing a much more in-depth analysis of ME. From this perspective, I will contribute to the ME debate through two reviews that address the question how we enhance the memory, and through four original papers discussed in part three of this thesis, where I examine and evaluate critically specific ESLP issues that arise with the use of ME. In the conclusion, I will amalgamate all my contribution to the ME debate and suggest the future direction for the ME debate. Advisors/Committee Members: HARRIS, JOHN JM, Harris, John, Stanton, Catherine.

Subjects/Keywords: adderall; ampakines; amphetamine; appeal to empathy; aricept; Aristotle; Baddeley; benzodiazepines; bioethics; Bostrom; brain stimulation; brain-computer interface; brain-machine interface; Brunet; Buchanan; caffeine; Cahil; Caplan; case; coercion; computers; confidentiality; consent; consequentialist; consistency; consolidation; conventional; criminal; damages; d-amphetamine; declarative memory; deep brain stimulation; Degrazia; deontological; diazepam; discrimination; donepezil; Douglas; drug mongering; duty; duty to remember; Dworkin; electroconvulsive therapy; Elliott; emotional distress; emotions; encoding; enhancement; enhancing technologies; epistemic knowledge; equality; ethical; evidence; exelon; explicit memory; eyewitness; eyewitness evidence; eyewitness testimony; Facebook; Farah; forget; Fukuyama; galantamine; gatekeepers; Ghetti; ginkgo biloba; Glover; glucocorticoids; glucose; greater good; Habermas; Harris; health; human dignity; human diversity; human enhancement; human nature; human rights; Hunter; identity; implicit memory; inauthentic; individual autonomy; inevitable; informed consent; internet; Jackson; justice; Kamm; Kass; Kolber; laissez faire; learning; legal; legal approach; lifelogging; living authentically; Loftus; long-term memory; Lynch; malleability of memory; mastery; McKibben; medicalization; meditation; Mehlman; Meilaender; memantine; Memory; memory dampening; memory enhancement; memory manipulation; memory processes; memory retention; memory retrieval; memory storage; methylphenidate; midazalom; misidentification of witnesses; mistaken identifications; mitigation; mnemonics; modafinil; moratorium; music; negative emotions; negligence; nondeclarative memory; non-pharmacological memory enhancement; nutrition; obligation; obstruction of justice; omega-3; optimum memory; Parens; person identity; personality; perverting justice; pharmacological means; philosophical approach; photographic; physical exercise; Pitman; policy; poly unsaturated fatty acids; precautionary approach; precautionary principle; preserving memories; President’s Council; primary memory; privacy; procedural memory; propofol; propranolol; provigil; razadyne; recall; recording audio; reference memory; regulation; regulatory authorities; regulatory bodies; relational memory; remembering; remembering fitly; remembering truly; risks; ritalin; rites; rituals; rivastigmine; safety; Sahakian; Sandberg; Sandel; Savulescu; Schacter; secondary memory; short-term memory; sleep; slippery slope; social; societies' interests; species-typical; society interests; species-typical functioning; Squire; Stanton; Strange; technological means; testimony; therapeutic; therapy; therapy-enhancement distinction; traditional; transcrannial direct current stimulation; transcrannial magnetic stimulation; traumatic memories; Tulving; ultimate prize; unnatural; unnatural means; Vaiva; video devices; virtual social networking; virtue ethics; Wagenaar; well-being; Wells; working memory; wrongful; wrongful acquittals; wrongful convictions; yoga; Kahane; Giordano; Bennett; Holm; Mental Capacity Act

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Muriithi, P. M. (2014). A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:220498

Chicago Manual of Style (16^th Edition):

Muriithi, Paul Mutuanyingi. “A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory.” 2014. Doctoral Dissertation, University of Manchester. Accessed December 13, 2019. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:220498.

MLA Handbook (7^th Edition):

Muriithi, Paul Mutuanyingi. “A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory.” 2014. Web. 13 Dec 2019.

Vancouver:

Muriithi PM. A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory. [Internet] [Doctoral dissertation]. University of Manchester; 2014. [cited 2019 Dec 13]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:220498.

Council of Science Editors:

Muriithi PM. A Case for Memory Enhancement: Ethical, Social, Legal, and Policy Implications for Enhancing the Memory. [Doctoral Dissertation]. University of Manchester; 2014. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:220498

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Open Access Theses and Dissertations