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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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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. |
format | Online Article Text |
id | pubmed-5613629 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
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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