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dc.contributor.authorSchuh, Artur Francisco Schumacherpt_BR
dc.contributor.authorRieder, Carlos Roberto de Mellopt_BR
dc.contributor.authorRizzi, Liarapt_BR
dc.contributor.authorChaves, Marcia Lorena Fagundespt_BR
dc.contributor.authorRoriz-Cruz, Matheuspt_BR
dc.date.accessioned2021-08-18T04:44:42Zpt_BR
dc.date.issued2011pt_BR
dc.identifier.issn2090-5513pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/225854pt_BR
dc.description.abstractInsulin and IGF seem to be important players in modulating brain aging. Neurons share more similarities with islet cells than any other human cell type. Insulin and insulin receptors are diffusely found in the brain, especially so in the hippocampus. Caloric restriction decreases insulin resistance, and it is the only proven mechanism to expand lifespan. Conversely, insulin resistance increases with age, obesity, and sedentarism, all of which have been shown to be risk factors for late-onset Alzheimer’s disease (AD). Hyperphagia and obesity potentiate the production of oxidative reactive species (ROS), and chronic hyperglycemia accelerates the formation of advanced glucose end products (AGEs) in (pre)diabetes—both mechanisms favoring a neurodegenerative milieu. Prolonged high cerebral insulin concentrations cause microvascular endothelium proliferation, chronic hypoperfusion, and energy deficit, triggering β-amyloid oligomerization and tau hyperphosphorylation. Insulin-degrading enzyme (IDE) seems to be the main mechanism in clearing β-amyloid from the brain. Hyperinsulinemic states may deviate IDE utilization towards insulin processing, decreasing β-amyloid degradation.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofISRN Neurology. Cairo. Vol. 2011 (2011), 306905, 9 p.pt_BR
dc.rightsOpen Accessen
dc.subjectInsulinapt_BR
dc.subjectDoença de Alzheimerpt_BR
dc.subjectDoenças neurodegenerativaspt_BR
dc.titleMechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s diseasept_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001007611pt_BR
dc.type.originEstrangeiropt_BR


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