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Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice

Aging is the principal risk factor for the development of Alzheimer's disease (AD). The hallmarks of AD are accumulation of the amyloid-β peptide 1–42 (Aβ42) and abnormal hyperphosphorylation of Tau (p-Tau) protein in different areas of the brain and, more recently reported, in the visual corte...

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Autores principales: Hernández-Zimbrón, Luis Fernando, Perez-Hernández, Montserrat, Torres-Romero, Abigail, Gorostieta-Salas, Elisa, Gonzalez-Salinas, Roberto, Gulias-Cañizo, Rosario, Quiroz-Mercado, Hugo, Zenteno, Edgar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5613629/
https://www.ncbi.nlm.nih.gov/pubmed/29138750
http://dx.doi.org/10.1155/2017/3706018
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author Hernández-Zimbrón, Luis Fernando
Perez-Hernández, Montserrat
Torres-Romero, Abigail
Gorostieta-Salas, Elisa
Gonzalez-Salinas, Roberto
Gulias-Cañizo, Rosario
Quiroz-Mercado, Hugo
Zenteno, Edgar
author_facet Hernández-Zimbrón, Luis Fernando
Perez-Hernández, Montserrat
Torres-Romero, Abigail
Gorostieta-Salas, Elisa
Gonzalez-Salinas, Roberto
Gulias-Cañizo, Rosario
Quiroz-Mercado, Hugo
Zenteno, Edgar
author_sort Hernández-Zimbrón, Luis Fernando
collection PubMed
description Aging is the principal risk factor for the development of Alzheimer's disease (AD). The hallmarks of AD are accumulation of the amyloid-β peptide 1–42 (Aβ42) and abnormal hyperphosphorylation of Tau (p-Tau) protein in different areas of the brain and, more recently reported, in the visual cortex. Recently, Aβ42 peptide overproduction has been involved in visual loss. Similar to AD, in normal aging, there is a significant amyloid deposition related to the overactivation of the aforementioned mechanisms. However, the mechanisms associated with visual loss secondary to age-induced visual cortex affectation are not completely understood. Young and aged mice were used as model to analyze the presence of Aβ42, p-Tau, glial-acidic fibrillary protein (GFAP), and presenilin-2, one of the main enzymes involved in Aβ42 production. Our results show a significant increase of Aβ42 deposition in aged mice in the following cells and/or tissues: endothelial cells and blood vessels and neurons of the visual cortex; they also show an increase of the expression of GFAP and presenilin-2 in this region. These results provide a comprehensive framework for the role of Aβ42 in visual loss due to inflammation present with aging and offer some clues for fruitful avenues for the study of healthy aging.
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spelling pubmed-56136292017-11-14 Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice Hernández-Zimbrón, Luis Fernando Perez-Hernández, Montserrat Torres-Romero, Abigail Gorostieta-Salas, Elisa Gonzalez-Salinas, Roberto Gulias-Cañizo, Rosario Quiroz-Mercado, Hugo Zenteno, Edgar Biomed Res Int Research Article Aging is the principal risk factor for the development of Alzheimer's disease (AD). The hallmarks of AD are accumulation of the amyloid-β peptide 1–42 (Aβ42) and abnormal hyperphosphorylation of Tau (p-Tau) protein in different areas of the brain and, more recently reported, in the visual cortex. Recently, Aβ42 peptide overproduction has been involved in visual loss. Similar to AD, in normal aging, there is a significant amyloid deposition related to the overactivation of the aforementioned mechanisms. However, the mechanisms associated with visual loss secondary to age-induced visual cortex affectation are not completely understood. Young and aged mice were used as model to analyze the presence of Aβ42, p-Tau, glial-acidic fibrillary protein (GFAP), and presenilin-2, one of the main enzymes involved in Aβ42 production. Our results show a significant increase of Aβ42 deposition in aged mice in the following cells and/or tissues: endothelial cells and blood vessels and neurons of the visual cortex; they also show an increase of the expression of GFAP and presenilin-2 in this region. These results provide a comprehensive framework for the role of Aβ42 in visual loss due to inflammation present with aging and offer some clues for fruitful avenues for the study of healthy aging. Hindawi 2017 2017-09-12 /pmc/articles/PMC5613629/ /pubmed/29138750 http://dx.doi.org/10.1155/2017/3706018 Text en Copyright © 2017 Luis Fernando Hernández-Zimbrón et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Hernández-Zimbrón, Luis Fernando
Perez-Hernández, Montserrat
Torres-Romero, Abigail
Gorostieta-Salas, Elisa
Gonzalez-Salinas, Roberto
Gulias-Cañizo, Rosario
Quiroz-Mercado, Hugo
Zenteno, Edgar
Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title_full Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title_fullStr Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title_full_unstemmed Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title_short Markers of Alzheimer's Disease in Primary Visual Cortex in Normal Aging in Mice
title_sort markers of alzheimer's disease in primary visual cortex in normal aging in mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5613629/
https://www.ncbi.nlm.nih.gov/pubmed/29138750
http://dx.doi.org/10.1155/2017/3706018
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