An integrated and unifying hypothesis for the metabolic basis of sporadic Alzheimer's disease

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dc.authorid0000-0002-2741-9755
dc.authorscopusid57211151450
dc.authorwosidErol, Adnan/AAJ-9616-2020
dc.contributor.authorErol, Adnan
dc.date.accessioned2022-05-11T14:39:50Z
dc.date.available2022-05-11T14:39:50Z
dc.date.issued2008
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.description.abstractAcquired disturbances of several aspects of cellular metabolism appear pathologically important in sporadic Alzheimer's disease (SAD). Among these, brain glucose utilization is reduced in the early stages of the disease. Hyperinsulinemia, which is a characteristic finding of insulin resistance, results in a central insulin deficit. Insufficient insulin signaling impairs the intricate balance of nitric oxide regulation of the central nervous system. Reduction in central insulin decreases neuronal nitric oxide synthase and increases inducible synthase activity. This, in turn, decreases astrocytic energy substrates and antioxidant supply of neurons. In addition, an increase in peroxynitrite formation impairs redox balance. Hyperleptinemia and glucose excess, which are the other parameters of insulin resistance, may worsen the reduced astrocytic energy supply and the ongoing inflammation via the inhibition of AMP-activated protein kinase (AMPK). Consequently, energy deficit and inflammation in neuronal tissue may cause neurodegeneration of SAD.
dc.identifier.endpage253
dc.identifier.issn1387-2877
dc.identifier.issn1875-8908
dc.identifier.issue3en_US
dc.identifier.pmid18430992
dc.identifier.scopus2-s2.0-47849121436
dc.identifier.scopusqualityQ1
dc.identifier.startpage241
dc.identifier.urihttps://hdl.handle.net/20.500.11776/8757
dc.identifier.volume13
dc.identifier.wosWOS:000256229900002
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorErol, Adnan
dc.language.isoen
dc.publisherIos Press
dc.relation.ispartofJournal of Alzheimers Disease
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAlzheimer's disease
dc.subjectinflammation
dc.subjectinsulin resistance
dc.subjectketone
dc.subjectneurodegeneration
dc.subjectActivated Protein-Kinase
dc.subjectNitric-Oxide Synthase
dc.subjectAmyloid-Beta-Peptide
dc.subjectGrowth-Factor Expression
dc.subjectCentral-Nervous-System
dc.subjectFactor-Kappa-B
dc.subjectEnergy-Metabolism
dc.subjectInsulin-Resistance
dc.subjectDiabetes-Mellitus
dc.subjectGlucose-Transporter
dc.titleAn integrated and unifying hypothesis for the metabolic basis of sporadic Alzheimer's disease
dc.typeReview Article

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