Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/225854 |
Resumo: | Insulin 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. |
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Schuh, Artur Francisco SchumacherRieder, Carlos Roberto de MelloRizzi, LiaraChaves, Marcia Lorena FagundesRoriz-Cruz, Matheus2021-08-18T04:44:42Z20112090-5513http://hdl.handle.net/10183/225854001007611Insulin 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.application/pdfengISRN Neurology. Cairo. Vol. 2011 (2011), 306905, 9 p.InsulinaDoença de AlzheimerDoenças neurodegenerativasMechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s diseaseEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001007611.pdf.txt001007611.pdf.txtExtracted Texttext/plain57874http://www.lume.ufrgs.br/bitstream/10183/225854/2/001007611.pdf.txt5235b0d19f60ddd61ca74b79e2ac09d1MD52ORIGINAL001007611.pdfTexto completo (inglês)application/pdf1272424http://www.lume.ufrgs.br/bitstream/10183/225854/1/001007611.pdf2bd2bb9adbd5e82cc76ec7b93751eeccMD5110183/2258542021-08-18 05:21:31.467oai:www.lume.ufrgs.br:10183/225854Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2021-08-18T08:21:31Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
title |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
spellingShingle |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease Schuh, Artur Francisco Schumacher Insulina Doença de Alzheimer Doenças neurodegenerativas |
title_short |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
title_full |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
title_fullStr |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
title_full_unstemmed |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
title_sort |
Mechanisms of brain aging regulation by insulin : implications for neurodegeneration in late-onset Alzheimer’s disease |
author |
Schuh, Artur Francisco Schumacher |
author_facet |
Schuh, Artur Francisco Schumacher Rieder, Carlos Roberto de Mello Rizzi, Liara Chaves, Marcia Lorena Fagundes Roriz-Cruz, Matheus |
author_role |
author |
author2 |
Rieder, Carlos Roberto de Mello Rizzi, Liara Chaves, Marcia Lorena Fagundes Roriz-Cruz, Matheus |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Schuh, Artur Francisco Schumacher Rieder, Carlos Roberto de Mello Rizzi, Liara Chaves, Marcia Lorena Fagundes Roriz-Cruz, Matheus |
dc.subject.por.fl_str_mv |
Insulina Doença de Alzheimer Doenças neurodegenerativas |
topic |
Insulina Doença de Alzheimer Doenças neurodegenerativas |
description |
Insulin 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. |
publishDate |
2011 |
dc.date.issued.fl_str_mv |
2011 |
dc.date.accessioned.fl_str_mv |
2021-08-18T04:44:42Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10183/225854 |
dc.identifier.issn.pt_BR.fl_str_mv |
2090-5513 |
dc.identifier.nrb.pt_BR.fl_str_mv |
001007611 |
identifier_str_mv |
2090-5513 001007611 |
url |
http://hdl.handle.net/10183/225854 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.pt_BR.fl_str_mv |
ISRN Neurology. Cairo. Vol. 2011 (2011), 306905, 9 p. |
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info:eu-repo/semantics/openAccess |
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openAccess |
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