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Article: DNA methylation in the pathology of Alzheimer’s disease: From gene to cognition

TitleDNA methylation in the pathology of Alzheimer’s disease: From gene to cognition
Authors
KeywordsAlzheimer's disease
neuroepigenetics
DNA methylation
amyloid beta
neuroplasticity
Issue Date2020
PublisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0077-8923&site=1
Citation
Annals of the New York Academy of Sciences, 2020, v. 1475 n. 1, p. 15-33 How to Cite?
AbstractAlzheimer’s disease (AD) is a debilitating disorder thatmanifests with amyloid beta plaque deposition, neurofibrillary tangles, neuronal loss, and severe cognitive impairment. Although much effort has been made to decipher the pathogenesis of this disease, the mechanisms causing these detrimental outcomes remain obscure. Over the past few decades, neuroepigenetics has emerged as an important field that, among other things, explores how reversible modifications can change gene expression to control behavior and cognitive abilities. Among epigenetic modifications, DNA methylation requires further elucidation for the conflicting observations from AD research and its pivotal role in learning and memory. In this review, we focus on the essential components of DNA methylation, the effects of aberrant methylation on gene expressions in the amyloidogenic pathway and neurochemical processes, as well as memory epigenetics in Alzheimer’s disease.
Persistent Identifierhttp://hdl.handle.net/10722/284780
ISSN
2020 Impact Factor: 5.691
2015 SCImago Journal Rankings: 2.389
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPoon, CH-
dc.contributor.authorTse, LSR-
dc.contributor.authorLim, LW-
dc.date.accessioned2020-08-07T09:02:32Z-
dc.date.available2020-08-07T09:02:32Z-
dc.date.issued2020-
dc.identifier.citationAnnals of the New York Academy of Sciences, 2020, v. 1475 n. 1, p. 15-33-
dc.identifier.issn0077-8923-
dc.identifier.urihttp://hdl.handle.net/10722/284780-
dc.description.abstractAlzheimer’s disease (AD) is a debilitating disorder thatmanifests with amyloid beta plaque deposition, neurofibrillary tangles, neuronal loss, and severe cognitive impairment. Although much effort has been made to decipher the pathogenesis of this disease, the mechanisms causing these detrimental outcomes remain obscure. Over the past few decades, neuroepigenetics has emerged as an important field that, among other things, explores how reversible modifications can change gene expression to control behavior and cognitive abilities. Among epigenetic modifications, DNA methylation requires further elucidation for the conflicting observations from AD research and its pivotal role in learning and memory. In this review, we focus on the essential components of DNA methylation, the effects of aberrant methylation on gene expressions in the amyloidogenic pathway and neurochemical processes, as well as memory epigenetics in Alzheimer’s disease.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0077-8923&site=1-
dc.relation.ispartofAnnals of the New York Academy of Sciences-
dc.rightsThis is the peer reviewed version of the following article: Annals of the New York Academy of Sciences, 2020, v. 1475 n. 1, p. 15-33, which has been published in final form at https://doi.org/10.1111/nyas.14373. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectAlzheimer's disease-
dc.subjectneuroepigenetics-
dc.subjectDNA methylation-
dc.subjectamyloid beta-
dc.subjectneuroplasticity-
dc.titleDNA methylation in the pathology of Alzheimer’s disease: From gene to cognition-
dc.typeArticle-
dc.identifier.emailLim, LW: limlw@hku.hk-
dc.identifier.authorityLim, LW=rp02088-
dc.description.naturepostprint-
dc.identifier.doi10.1111/nyas.14373-
dc.identifier.pmid32491215-
dc.identifier.scopuseid_2-s2.0-85091237455-
dc.identifier.hkuros311497-
dc.identifier.volume1475-
dc.identifier.issue1-
dc.identifier.spage15-
dc.identifier.epage33-
dc.identifier.isiWOS:000537261600001-
dc.publisher.placeUnited States-
dc.identifier.issnl0077-8923-

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