Unraveling the molecular mechanisms behind the metabolic basis of sporadic alzheimer's disease

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dc.authorscopusid57211151450
dc.contributor.authorErol, Adnan
dc.date.accessioned2022-05-11T14:39:51Z
dc.date.available2022-05-11T14:39:51Z
dc.date.issued2009
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.description.abstractPeripheral insulin resistance is associated with hyperinsulinemia, which may be associated with brain insulin deficiency that is characteristic of sporadic Alzheimer's disease (sAD). Oxidative insult, which is the result of insulin associated disordered brain energy metabolism, is a significant early event in the pathological cascade of sAD. Aggregation of disease-specific proteins such as amyloid-? and tau may act as a compensatory response against the oxidative insult at the early periods. In the later stages, oxidative stress stimulates c-Jun N-terminal kinase (JNK) activation. The deficient insulin signaling is ultimately linked to protein kinase B (Akt) pathway and subsequently glycogen synthase kinase-3 (GSK3) and forkhead transcription factors (FOXO). Peripheral insulin resistance related intense interactions between JNK, GSK3, FOXO factors, and p53, which may lead to apoptotic neuronal death, are outlined in a postulate. In light of this postulate, the importance of detailed knowledge of these common physiological processes for the opportunities of treatment that could prevent or reduce the onset of sAD is discussed as well. © 2009 - IOS Press and the authors. All rights reserved.
dc.identifier.doi10.3233/JAD-2009-1047
dc.identifier.endpage276
dc.identifier.issn1387-2877
dc.identifier.issue2en_US
dc.identifier.pmid19221404
dc.identifier.scopus2-s2.0-67849110363
dc.identifier.scopusqualityQ1
dc.identifier.startpage267
dc.identifier.urihttps://doi.org/10.3233/JAD-2009-1047
dc.identifier.urihttps://hdl.handle.net/20.500.11776/8759
dc.identifier.volume17
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorErol, Adnan
dc.language.isoen
dc.publisherIOS Press
dc.relation.ispartofJournal of Alzheimer's Disease
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAlzheimer's disease
dc.subjectFOXO
dc.subjectGSK3
dc.subjectInsulin resistance
dc.subjectJNK
dc.subjectP53
dc.subjectamyloid beta protein
dc.subjectforkhead transcription factor
dc.subjectglycogen synthase kinase 3
dc.subjectinsulin
dc.subjectprotein kinase B
dc.subjectprotein p53
dc.subjectstress activated protein kinase
dc.subjecttau protein
dc.subjectAlzheimer disease
dc.subjectapoptosis
dc.subjectbrain metabolism
dc.subjecthyperinsulinemia
dc.subjectinsulin deficiency
dc.subjectinsulin resistance
dc.subjectmetabolic disorder
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein aggregation
dc.subjectreview
dc.titleUnraveling the molecular mechanisms behind the metabolic basis of sporadic alzheimer's disease
dc.typeReview Article

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