Research Department, Asociación para Evitar la Ceguera en México, "Hospital Dr. Luis Sanchez Bulnes" IAP, 04030 México City, Mexico.
Divisón de Ciencias Biológicas de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, Ciudad de México, Mexico.
Biomed Res Int. 2017;2017:3706018. doi: 10.1155/2017/3706018. Epub 2017 Sep 12.
Aging is the principal risk factor for the development of Alzheimer's disease (AD). The hallmarks of AD are accumulation of the amyloid- peptide 1-42 (A42) and abnormal hyperphosphorylation of Tau (p-Tau) protein in different areas of the brain and, more recently reported, in the visual cortex. Recently, A42 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 A42, p-Tau, glial-acidic fibrillary protein (GFAP), and presenilin-2, one of the main enzymes involved in A42 production. Our results show a significant increase of A42 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 A42 in visual loss due to inflammation present with aging and offer some clues for fruitful avenues for the study of healthy aging.
衰老是阿尔茨海默病（AD）发展的主要风险因素。AD 的特征是在大脑的不同区域积累淀粉样肽 1-42（A42）和 Tau（p-Tau）蛋白异常过度磷酸化，最近有报道称，在视觉皮层也存在这种情况。最近，A42 肽的过度产生与视觉丧失有关。与 AD 相似，在正常衰老过程中，与上述机制的过度激活相关的淀粉样沉积显著增加。然而，年龄引起的视觉皮层损伤导致视觉丧失的相关机制尚不完全清楚。年轻和老年小鼠被用作模型来分析 A42、p-Tau、胶质酸性纤维蛋白（GFAP）和早老素-2 的存在，早老素-2 是参与 A42 产生的主要酶之一。我们的结果表明，在老年小鼠中，以下细胞和/或组织中 A42 的沉积显著增加：视觉皮层的内皮细胞和血管以及神经元；还显示该区域 GFAP 和早老素-2 的表达增加。这些结果为 A42 在衰老引起的炎症导致的视觉丧失中的作用提供了全面的框架，并为健康衰老的研究提供了一些有价值的线索。
