Academic literature on the topic 'APOE2'
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Journal articles on the topic "APOE2"
Hudák, Anett, Katalin Jósvay, Ildikó Domonkos, Annamária Letoha, László Szilák, and Tamás Letoha. "The Interplay of Apoes with Syndecans in Influencing Key Cellular Events of Amyloid Pathology." International Journal of Molecular Sciences 22, no. 13 (June 30, 2021): 7070. http://dx.doi.org/10.3390/ijms22137070.
Full textYamauchi, Kazuyoshi, and Yasushi Kawakami. "The redox status of cysteine thiol residues of apolipoprotein E impacts on its lipid interactions." Biological Chemistry 401, no. 5 (April 28, 2020): 617–27. http://dx.doi.org/10.1515/hsz-2019-0414.
Full textHOFFMANN, MICHAEL M., HUBERT SCHARNAGL, ELEFTHERIA PANAGIOTOU, WERNER T. BANGHARD, HEINRICH WIELAND, and WINFRIED MÄRZ. "Diminished LDL Receptor and High Heparin Binding of Apolipoprotein E2 Sendai Associated with Lipoprotein Glomerulopathy." Journal of the American Society of Nephrology 12, no. 3 (March 2001): 524–30. http://dx.doi.org/10.1681/asn.v123524.
Full textLi, Meng-Yu, Man-Ki Kwok, and Catherine Mary Schooling. "Investigating Effects of Plasma Apolipoprotein E on Ischemic Heart Disease Using Mendelian Randomization Study." Nutrients 13, no. 7 (June 28, 2021): 2215. http://dx.doi.org/10.3390/nu13072215.
Full textVilleneuve, Sylvia, Diane Brisson, and Daniel Gaudet. "Influence of Abdominal Obesity on the Lipid-Lipoprotein Profile in Apoprotein E2/4 Carriers: The Effect of an Apparent Duality." Journal of Lipids 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/742408.
Full textIannucci, Jaclyn, Abhik Sen, and Paula Grammas. "Isoform-Specific Effects of Apolipoprotein E on Markers of Inflammation and Toxicity in Brain Glia and Neuronal Cells In Vitro." Current Issues in Molecular Biology 43, no. 1 (May 27, 2021): 215–25. http://dx.doi.org/10.3390/cimb43010018.
Full textSantos-Ferreira, Cátia, Rui Baptista, Manuel Oliveira-Santos, Regina Costa, José Pereira Moura, and Lino Gonçalves. "Apolipoprotein E2 Genotype Is Associated with a 2-Fold Increase in the Incidence of Type 2 Diabetes Mellitus: Results from a Long-Term Observational Study." Journal of Lipids 2019 (August 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/1698610.
Full textAlata, Wael, Yue Ye, Isabelle St-Amour, Milène Vandal, and Frédéric Calon. "Human Apolipoprotein E ε4 Expression Impairs Cerebral Vascularization and Blood—Brain Barrier Function in Mice." Journal of Cerebral Blood Flow & Metabolism 35, no. 1 (October 22, 2014): 86–94. http://dx.doi.org/10.1038/jcbfm.2014.172.
Full textPohlkamp, Theresa. "Apolipoprotein E: Cholesterol metabolism and Alzheimer’s pathology." Neuroforum 26, no. 1 (February 25, 2020): 25–30. http://dx.doi.org/10.1515/nf-2019-0030.
Full textMarin, Guilherme B., Marli H. Tavella, João F. Guerreiro, Sidney E. B. Santos, and Marco A. Zago. "Absence of the E2 allele of apolipoprotein in Amerindians." Brazilian Journal of Genetics 20, no. 4 (December 1997): 741–43. http://dx.doi.org/10.1590/s0100-84551997000400029.
Full textDissertations / Theses on the topic "APOE2"
Reverté, Soler Ingrid. "Neurobehavioural effects associated with postnatal exposure to decabromodiphenyl ether in apoe2, apoe3 and apoe4 transgenic mice." Doctoral thesis, Universitat Rovira i Virgili, 2012. http://hdl.handle.net/10803/76782.
Full textDecabromodiphenyl Ether (BDE-209) is a flame retardant widely used and source of concern because ofthe toxicity showed by other Polibrominateddiphenyl ethers (PBDEs). The presenceof PBDEs in human’s breast milkmakes worrying its exposure during development. We hypothesised that an early exposure to BDE-209 can induce long-term impairments and interact with genetic factors, such as ApolipoproteinE genotype. Mice carrying the different Human ApoE isoforms treated with an acute oral dose of 0, 10 or 30 mg/kg of BDE-209 on postnatal day 10 were assessed for neurobehaviourduring development, in young adulthood and old age. BDE-209 exposure inducesadelay in physic and neuromotordevelopment and in myelin compaction in ApoE2 mice, decreases the levels of free thyroxin in adult femalesand decreases activity in ApoE4 mice. The most consistent effects across the lifespan are observed in ApoE3 mice and consist of impaired learning at 4 months, and impaired learning and memory and increased anxiety at 12 months.
Cieslak, Stephen Gerard. "The Effects of L-Cysteine on Alzheimer's Disease Pathology in APOE2, APOE3, and APOE4 Homozygous Mice." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6585.
Full textDonovan, Alexandra. "Comparative Biophysical Analysis of APOE3 and APOE4| A Mechanistic Investigation." Thesis, California State University, Long Beach, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10606132.
Full textApolipoprotein E is an exchangeable apolipoprotein whose isoforms are associated with various disease risk profiles. Individuals bearing the APOE ϵ4 allele are at increased risk for developing Alzheimer’s disease compared to those bearing the APOE ϵ3 allele. The two isoforms differ in amino acid at position 112: apoE3 bears a Cys while apoE4 bears an Arg. It is hypothesized that the Cys to Arg substitution in apoE4 causes a decrease in stability in comparison to apoE3, which is exaggerated at endosomal pH <6.0. In our study, changes in secondary structure were monitored using circular dichroism at pH 7.4 and pH 3.5. Chemical denaturation indicated that both apoE3 and apoE4 retained their helical secondary structure at the lower pH, with a biphasic and monophasic guanidine HCl denaturation profile, respectively. Tertiary structure was monitored at both pH’s through fluorescence spectral characteristics and mobility of a fluorescent probe attached to each of the 7 major amphipathic α-helices of apoE3 and apoE4. The data showed decreases in fluorescence emission (FE), changes in fluorescence polarization (FP), and fluctuations in probe mobility, which were interpreted as likely formation of a molten globule. Formation of a molten globule appeared to occur during denaturation primarily for apoE4, and thermodynamic parameters of apoE4 showed a lower stability than apoE3, with a larger effect of pH. Taken together, our results suggest that the acidic pH in the endosomal compartments could interact with the native structure of apoE4 to generate a molten globule state that is able to bind endosomal membranes, other proteins, or itself. This study offers mechanistic insight into the impact of the single residue difference between apoE3 and apoE4 with regard to folding/unfolding behavior, and with regard to its physiological and pathological implications.
Farsian, Farnas [Verfasser], and Jörg Heeren [Akademischer Betreuer]. "ApoE Regulates Corticospinal Neuronal Survival Through ApoER2 / Farnas Farsian. Betreuer: Jörg Heeren." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2013. http://d-nb.info/1045024538/34.
Full textBour, Alexandra. "Implication d'un dérivé sécrété du précurseur de la protéine β-amyloi͏̈de (sAPP695) et de différentes isoformes de l'apolipoprotéine E humaine (apoE3 et apoE4 ) dans les processus mnésiques chez la Souris." Université Louis Pasteur (Strasbourg) (1971-2008), 2004. https://publication-theses.unistra.fr/public/theses_doctorat/2004/BOUR_Alexandra_2004.pdf.
Full textAn alteration of the beta-amyloid precursor protein (APP) metabolism is associated with Alzheimer's disease (AD) as well as age-related memory impairments. This alteration seems to affect cerebral level of sAPP, a promnestic and soluble form of APP. On the other hand, the epsilon 4 allele, but not the epsilon 3 allele, of apolipoprotéine E (apoE) gene is a genetic risk factor for AD and for age-related memory impairments. Moreover, APP metabolism seems to be influenced by apoE. First, the effects of exogenous sAPP administration in mice were evaluated in object recognition, spatial recognition and bar-press learning tasks. According to the results, sAPP seems to promote early memory processes. The post-training blockade of endogenous sAPPs with specific antibodies induced memory deficits suggesting a central role of sAPPs in memory consolidation mechanisms. Besides this study, we showed the deleterious effect of the new ventilation system of some animal housing rooms on mice memory performance. Then, the memory performance of "aged" (14-15 months) apoE3 and apoE4 transgenic mice (homozygous carriers of the human apoE allele epsilon 3 and epsilon 4, respectively) were evaluated in spatial memory tasks (spatial recognition and Morris water maze) and active and passive avoidance memory tasks. Compared to apoE3 mice, apoE4 mice, especially females, showed more severe memory deficits. Thus, apoE4 female mice appear as a good model for the study of age-related memory deficits. In a last experiment using the Morris water maze task, the administration of sAPP restored a good level of spatial memory performance in "aged" female apoE4 mice. Altogether, our results suggest that the modulation of cerebral sAPP levels must be considered as a potential therapeutic approach in the treatment of age-related memory deficits in general, or those associated with AD in peculiar
Cambon, Karine. "Influence of ApoE polymorphism on synaptic morphometry during aging in the dentate gyrus of ApoE knockout and human ApoE transgenic mice." Thesis, [n.p.], 2000. http://oro.open.ac.uk/19118/.
Full textEvans, Vanessa. "Intramuscular gene transfer of apolipoprotein E (ApoE) to reverse hyperlipidaemia and atherosclerosis in ApoE-deficient mice." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444704/.
Full textRantsi, P. (Petra). "Apoe 4-alleelien rooli saamelaisväestön muistisairauksissa." University of Oulu, 2017. http://urn.fi/URN:NBN:fi:oulu-201711083079.
Full textCarvalho, Liliana Patrícia Rodrigues de. "Genetic profiling of ApoE in dementia." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/10720.
Full textA demência é uma das principais causas de incapacidade entre os idosos, afetando mais de 36 milhões de pessoas em todo o mundo. É caracterizada pela deterioração progressiva das funções cognitivas, resultando em dificuldades no desempenho das atividades diárias do indivíduo. A idade de aparecimento dos sintomas, bem como a sua taxa de progressão, são variáveis entre a maior parte das demências, sendo estas geralmente caracterizadas por uma natureza progressiva, aumentando de gravidade ao longo do tempo. Entre os tipos mais frequentes de demência encontram-se a Doença de Alzheimer (DA), Demência Vascular, Demência de Corpos de Lewy e Demência Frontotemporal. O diagnóstico diferencial das demências é realizado tipicamente por testes neuro-psicológicos (para a exclusão de outras demências) e por exames imagiológicos. Contudo, muitos dos sintomas clínicos característicos podem sobrepor-se entre os diversos tipos de demência, o que pode constituir um problema devido a falta de especificidade e erros de diagnóstico. A compreensão dos fatores de risco ambientais e genéticos que podem modular o aparecimento e/ou progressão de doenças abre novas perspetivas relativamente à gestão destas neuropatologias. O gene da apolipoproteína E (ApoE) é reconhecido como o maior fator de risco na demência, desempenhando um papel central em particular no desenvolvimento da DA, sendo que os portadores do alelo ε4 são mais suscetíveis para a doença. Além disso, possíveis associações foram também propostas entre este gene e outras doenças neurológicas, sendo no entanto estes dados ainda controversos. Assim, o objetivo principal deste trabalho consistiu em determinar as frequências alélicas e genotípicas do gene ApoE num grupo de estudo piloto de pacientes com demência na região de Aveiro. Este grupo foi subdividido com base no diagnóstico neuroquímico, no qual foram avaliados os níveis de Aβ1-42, Tau-total e fosfo-Tau 181 no líquido cefalorraquidiano dos pacientes. Como resultado, observou-se que o alelo ε3 foi o mais frequente no grupo total, independentemente do tipo de patologia, e que o alelo ε2 foi o menos comum. O alelo ε4 foi de facto mais frequente em pacientes com DA do que em pacientes com outras neuropatologias, o que está de acordo com a relação proposta por outros autores. Adicionalmente, foi possível verificar que a frequência deste alelo nos pacientes com patologia amilóide é semelhante à observada no grupo DA, sugerindo um papel relevante para o ApoE no metabolismo e acumulação cerebral do Aβ. Consequentemente, estes indivíduos podem ter uma maior suscetibilidade para o desenvolvimento de DA no futuro. Deste modo, os nossos dados corroboram a ideia de que o alelo ε4 é um forte fator de risco para a DA e que deve ser considerado como um teste genético relevante que pode contribuir para o diagnóstico clínico da demência.
Dementia is one of the leading causes of disability among the elderly, affecting over 36 million people worldwide. It is characterized by progressive deterioration in cognitive functions that impair the successful performance of daily living activities. Most forms of dementia are progressive in nature, increasing in severity over time, with the rate of symptoms progression and the age at onset differing among the major dementing disorders. The most frequent types of dementia include Alzheimer´s Disease (AD), Vascular Dementia, Dementia of Lewy bodies and Frontotemporal Dementia. Differential diagnosis of dementia is typically done by neuropsychological testing (for exclusion of other dementias) and neuroimaging investigations. However, many of the clinical symptoms typical of dementia may overlap across dementia subtypes, which may constitute a diagnosis problem leading to lack of specificity and misdiagnosis. Understanding the environmental and genetic factors that modulate risks and outcomes of diseases can open new perspectives on the management of these neurological disorders. Apolipoprotein E gene (ApoE) is recognized as the major genetic risk factor in dementia, in particular playing a central role in AD development, being that ApoE allele ε4 carriers are more susceptible to disease. Furthermore, putative associations have also been proposed between this gene and other neurological disorders, nonetheless controversial data have been reported regarding these aspect. Hence, the aim of this work was to determine ApoE genotypic and allelic frequencies in a pilot study group of dementing patients from the catchment area of the “Hospital de São Sebastião” in “Santa Maria da Feira”. This group was subdivided according to their neurochemical-based diagnosis of dementia, in which Aβ1-42, phospho-Tau 181 and total-Tau levels in patients’ cerebrospinal fluid were evaluated. In this study, we could observe that allele ε3 was the most frequent in the total study group, independent of the type of pathology, and that allele ε2 was the less frequent. Allele ε4 was in fact more frequent in AD patients than in other neurological disease patients, in agreement with the proposed link established by other authors. Additionally, we also find that allele ε4 frequency in patients suffering from amyloid pathology is similar to that observed in AD group, suggesting a role for ApoE in Aβ metabolism and brain accumulation. Potentially, these patients have a higher susceptibility to develop AD pathology in the future. Thus, our data supports the idea that ApoE allele ε4 is a strong risk factor for AD development and that it may be considered as a relevant genetic test that may assist in the clinical diagnosis of dementia.
Lundbäck, Daniel. "Alkoholkonsumtion och episodiskt minne.Kan APOE genen vid olika konsumtionsnivåer ha betydelse?" Thesis, Stockholms universitet, Psykologiska institutionen, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-88448.
Full textBetula
Books on the topic "APOE2"
Hartigan, Anne Le Marquand. Now is a moveable feast: Apoem and drawings. Galway: Salmon, 1991.
Find full textDonaghy, Michael. Machines: Apoem by Michael Donaghy with Artwork by Barbara Tetenbaum. Guildford: Circle Press, 1986.
Find full textThe Apoe gene diet: A breakthrough in lowering cholesterol, weight, and the risk of cardiovascular and Alzheimer's disease through knowledge of your body's genes. Santa Rosa, CA: Elite Books, 2007.
Find full textApolipoprotein E (ApoE) allelic variants: Involvement in type 2 dibetes. Ottawa: National Library of Canada, 2003.
Find full textBrahm, Amanda J., and Robert A. Hegele. Monogenic Chylomicronemia: Deficiency of Lipoprotein Lipase and Related Factors. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0033.
Full textAllen, Shelley J. Pathophysiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0002.
Full textHarold, Denise, and Julie Williams. Molecular genetics and biology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0008.
Full textBook chapters on the topic "APOE2"
Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "APOE." In Encyclopedia of Psychopharmacology, 131. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4065.
Full textScharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "APOC2 Deficiency." In Encyclopedia of Molecular Mechanisms of Disease, 133. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6527.
Full textYamamoto, Tokuo. "Receptors for Apoe-Containing Lipoproteins." In Drugs Affecting Lipid Metabolism, 281–83. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_34.
Full textPradier, L., C. Czech, L. Mercken, S. Moussaoui, M. Reibaud, P. Delaère, and G. Tremp. "App, Apoe, and Presenilin Transgenics." In Advances in Behavioral Biology, 25–30. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_5.
Full textCorzo, L., L. Fernández-Novoa, R. Zas, K. Beyer, J. I. Lao, X. A. Alvarez, and R. Cacabelos. "Influence of the Apoe Genoptype on Serum Apoe Levels in Alzheimer’s Disease Patients." In Advances in Behavioral Biology, 765–71. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_109.
Full textSullivan, Patrick M. "APOE-Based Models of “Pre-Dementia”." In Neuromethods, 439–47. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-898-0_22.
Full textAbrams, David B., J. Rick Turner, Linda C. Baumann, Alyssa Karel, Susan E. Collins, Katie Witkiewitz, Terry Fulmer, et al. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 122. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1245.
Full textWhang, William. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 1. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6439-6_1245-2.
Full textWhang, William. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 142–43. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1245.
Full textYin, Yuemiao, and Zhao Wang. "ApoE and Neurodegenerative Diseases in Aging." In Advances in Experimental Medicine and Biology, 77–92. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1117-8_5.
Full textConference papers on the topic "APOE2"
Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.
Full text"APOE Gene Expression in Patients with Alzheimer’s Disease." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916409.
Full textLi, Ziying. "New APOE-related therapeutic options for Alzheimer’s disease." In INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2018). Author(s), 2019. http://dx.doi.org/10.1063/1.5085515.
Full textWang, Ying, John A. Johnson, Abigail Fulp, Michael A. Sutton, and Susan M. Lessner. "Adhesive Strength of Atherosclerotic Plaques Depends on Collagen Content." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80433.
Full textTsao, Sinchai, Niharika Gajawelli, Darryl H. Hwang, Stephen Kriger, Meng Law, Helena Chui, Michael Weiner, and Natasha Lepore. "Mapping of ApoE4 related white matter damage using diffusion MRI." In SPIE Medical Imaging, edited by Maria Y. Law and Tessa S. Cook. SPIE, 2014. http://dx.doi.org/10.1117/12.2043925.
Full text"Methylation and expression profiles in Apoe vicinity point to specific neighboring interaction of Apoe and TOMM40 genes: implication for the Alzheimer disease." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-127.
Full textMengesha, Birga Anteneh, and Huang Jian. "Genome-wide Association of APOE and FOXO3A for human longevity." In ICBBS 2019: 2019 8th International Conference on Bioinformatics and Biomedical Science. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3369166.3369169.
Full textGoryawala, Mohammed, Qi Zhou, Ranjan Duara, David Loewenstein, Mercedes Cabrerizo, Warren Barker, and Malek Adjouadi. "Altered small-world anatomical networks in Apolipoprotein-E4 (ApoE4) carriers using MRI." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944122.
Full textHameed, Abdul G., Sheila E. Francis, David C. Crossman, and Allan Lawrie. "TRAIL Deficiency Protects Fat-fed ApoE-/- Mice From Pulmonary Arterial Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2283.
Full textMauderly, Joe L., Steven Seilkop, Jacob D. McDonald, Amie Lund, and Matthew Campen. "Identification Of Combustion Product Components Causing Vascular Responses In ApoE-/- Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3233.
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