Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications

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dc.citation.volume10
dc.contributor.authorUddin, Md. Sahab
dc.contributor.authorStachowiak, Anna
dc.contributor.authorAl Mamun, Abdullah
dc.contributor.authorTzvetkov, Nikolay T.
dc.contributor.authorTakeda, Shinya
dc.contributor.authorAtanasov, Atanas G.
dc.contributor.authorBergantin, Leandro B. [UNIFESP]
dc.contributor.authorAbdel-Daim, Mohamed M.
dc.contributor.authorStankiewicz, Adrian M.
dc.coverageLausanne
dc.date.accessioned2020-07-08T13:09:51Z
dc.date.available2020-07-08T13:09:51Z
dc.date.issued2018
dc.description.abstractAlzheimer's disease (AD) is the most common cause of progressive dementia in the elderly. It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid beta (A beta), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans. In brains of AD patients the metabolism of A beta is dysregulated, which leads to the accumulation and aggregation of A beta. Metabolism of A beta and tau proteins is crucially influenced by autophagy. Autophagy is a lysosome-dependent, homeostatic process, in which organelles and proteins are degraded and recycled into energy. Thus, dysfunction of autophagy is suggested to lead to the accretion of noxious proteins in the AD brain. In the present review, we describe the process of autophagy and its importance in AD. Additionally, we discuss mechanisms and genes linking autophagy and AD, i.e., the mTOR pathway, neuroinflammation, endocannabinoid system, ATG7, BCL2, BECN1, CDK5, CLU, CTSD, FOXO1, GFAP, ITPR1, MAPT, PSEN1, SNCA, UBQLN1, and UCHL1. We also present pharmacological agents acting via modulation of autophagy that may show promise in AD therapy. This review updates our knowledge on autophagy mechanisms proposing novel therapeutic targets for the treatment of AD.en
dc.description.affiliationSoutheast Univ, Dept Pharm, Dhaka, Bangladesh
dc.description.affiliationPolish Acad Sci, Inst Genet & Anim Breeding, Dept Expt Embryol, Magdalenka, Poland
dc.description.affiliationBulgarian Acad Sci, Inst Mol Biol Roumen Tsanev, Dept Mol Biol & Biochem Pharmacol, Sofia, Bulgaria
dc.description.affiliationTottori Univ, Grad Sch Med Sci, Dept Clin Psychol, Tottori, Japan
dc.description.affiliationPolish Acad Sci, Inst Genet & Anim Breeding, Dept Mol Biol, Magdalenka, Poland
dc.description.affiliationUniv Vienna, Dept Pharmacognosy, Vienna, Austria
dc.description.affiliationUniv Fed Sao Paulo, Dept Pharmacol, Sao Paulo, Brazil
dc.description.affiliationSuez Canal Univ, Dept Pharmacol, Ismailia, Egypt
dc.description.affiliationYokohama City Univ, Dept Ophthalmol & Microtechnol, Yokohama, Kanagawa, Japan
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Pharmacol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipPolish KNOW (Leading National Research Centre) Scientific Consortium "Healthy Animal-Safe Food" decision of Ministry of Science and Higher Education
dc.description.sponsorshipIDPolish KNOW: 05-1/KNOW2/2015
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.3389/fnagi.2018.00004
dc.identifier.citationFrontiers In Aging Neuroscience. Lausanne, v. 10, p. -, 2018.
dc.identifier.doi10.3389/fnagi.2018.00004
dc.identifier.issn1663-4365
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/54248
dc.identifier.wosWOS:000423548600001
dc.language.isoeng
dc.publisherFrontiers Media Sa
dc.relation.ispartofFrontiers In Aging Neuroscience
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectautophagyen
dc.subjectAlzheimer's diseaseen
dc.subjectamyloid betaen
dc.subjecttauen
dc.titleAutophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implicationsen
dc.typeinfo:eu-repo/semantics/article
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