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BioMed Research International
Volume 2017, Article ID 3706018, 10 pages
Research Article

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

1Research Department, Asociación para Evitar la Ceguera en México, “Hospital Dr. Luis Sanchez Bulnes” IAP, 04030 México City, Mexico
2Divisón de Ciencias Biológicas de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, Ciudad de México, Mexico
3Neuroscience Division, Institute of Cellular Physiology, UNAM, Ciudad Universitaria, Ciudad de México, Mexico
4Cell Biology Department, Centro de Investigación y de Estudios Avanzados del IPN, Ciudad de México, Mexico
5Department of Biochemistry, School of Medicine, UNAM, Ciudad Universitaria, México City, Mexico

Correspondence should be addressed to Luis Fernando Hernández-Zimbrón; xm.manu@zednanrehfl

Received 4 June 2017; Accepted 9 August 2017; Published 12 September 2017

Academic Editor: Anna Di Vito

Copyright © 2017 Luis Fernando Hernández-Zimbrón et al. 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.


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.