Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.

Type 2 diabetes (T2D) is an important risk factor to suffer dementia, including Alzheimer's disease (AD), and some neuropathological features observed in dementia could be mediated by T2D metabolic alterations. Since brain atrophy and impaired neurogenesis have been observed both T2D and AD we...

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Autores principales:	Juan Jose Ramos-Rodriguez, Sara Molina-Gil, Oscar Ortiz-Barajas, Margarita Jimenez-Palomares, German Perdomo, Irene Cozar-Castellano, Alfonso Maria Lechuga-Sancho, Monica Garcia-Alloza
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3c62cb3d2f9a42008eaeb823fffb8f16
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spelling	oai:doaj.org-article:3c62cb3d2f9a42008eaeb823fffb8f162021-11-18T08:31:44ZCentral proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.1932-620310.1371/journal.pone.0089229https://doaj.org/article/3c62cb3d2f9a42008eaeb823fffb8f162014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24586614/?tool=EBIhttps://doaj.org/toc/1932-6203Type 2 diabetes (T2D) is an important risk factor to suffer dementia, including Alzheimer's disease (AD), and some neuropathological features observed in dementia could be mediated by T2D metabolic alterations. Since brain atrophy and impaired neurogenesis have been observed both T2D and AD we analyzed central nervous system (CNS) morphological alterations in the db/db mice (leptin receptor KO mice), as a model of long-term insulin resistance and T2D, and in C57Bl6 mice fed with high fat diet (HFD), as a model of diet induced insulin resistance and prediabetes. Db/db mice showed an age-dependent cortical and hippocampal atrophy, whereas in HFD mice cortex and hippocampus were preserved. We also detected increased neurogenesis and cell proliferation rates in young db/db mice when compared with control littermates. Our study shows that metabolic parameters serve as predictors of both atrophy and altered proliferation and neurogenesis in the CNS. Moreover in the cortex, atrophy, cell proliferation and neurogenesis were significantly correlated. Our data suggest that T2D may underline some of the pathological features observed in the dementia process. They also support that blood glucose control in elderly patients could help to slow down dementia evolution and maybe, improve its prognosis.Juan Jose Ramos-RodriguezSara Molina-GilOscar Ortiz-BarajasMargarita Jimenez-PalomaresGerman PerdomoIrene Cozar-CastellanoAlfonso Maria Lechuga-SanchoMonica Garcia-AllozaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 2, p e89229 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Juan Jose Ramos-Rodriguez Sara Molina-Gil Oscar Ortiz-Barajas Margarita Jimenez-Palomares German Perdomo Irene Cozar-Castellano Alfonso Maria Lechuga-Sancho Monica Garcia-Alloza Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
description	Type 2 diabetes (T2D) is an important risk factor to suffer dementia, including Alzheimer's disease (AD), and some neuropathological features observed in dementia could be mediated by T2D metabolic alterations. Since brain atrophy and impaired neurogenesis have been observed both T2D and AD we analyzed central nervous system (CNS) morphological alterations in the db/db mice (leptin receptor KO mice), as a model of long-term insulin resistance and T2D, and in C57Bl6 mice fed with high fat diet (HFD), as a model of diet induced insulin resistance and prediabetes. Db/db mice showed an age-dependent cortical and hippocampal atrophy, whereas in HFD mice cortex and hippocampus were preserved. We also detected increased neurogenesis and cell proliferation rates in young db/db mice when compared with control littermates. Our study shows that metabolic parameters serve as predictors of both atrophy and altered proliferation and neurogenesis in the CNS. Moreover in the cortex, atrophy, cell proliferation and neurogenesis were significantly correlated. Our data suggest that T2D may underline some of the pathological features observed in the dementia process. They also support that blood glucose control in elderly patients could help to slow down dementia evolution and maybe, improve its prognosis.
format	article
author	Juan Jose Ramos-Rodriguez Sara Molina-Gil Oscar Ortiz-Barajas Margarita Jimenez-Palomares German Perdomo Irene Cozar-Castellano Alfonso Maria Lechuga-Sancho Monica Garcia-Alloza
author_facet	Juan Jose Ramos-Rodriguez Sara Molina-Gil Oscar Ortiz-Barajas Margarita Jimenez-Palomares German Perdomo Irene Cozar-Castellano Alfonso Maria Lechuga-Sancho Monica Garcia-Alloza
author_sort	Juan Jose Ramos-Rodriguez
title	Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
title_short	Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
title_full	Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
title_fullStr	Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
title_full_unstemmed	Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
title_sort	central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/3c62cb3d2f9a42008eaeb823fffb8f16
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Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.

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