Meraz-Ríos Marco Antonio, Franco-Bocanegra Diana, Toral Rios Danira, Campos-Peña Victoria
Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Instituto Politécnico Nacional 2508, 07360 Mexico City, Mexico.
Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México, Universidad 3000, Coyoacan, 04510 Mexico City, Mexico.
Oxid Med Cell Longev. 2014;2014:375968. doi: 10.1155/2014/375968. Epub 2014 Jan 14.
Alzheimer's disease (AD) is the most common cause of dementia in elderly adults. It is estimated that 10% of the world's population aged more than 60-65 years could currently be affected by AD, and that in the next 20 years, there could be more than 30 million people affected by this pathology. One of the great challenges in this regard is that AD is not just a scientific problem; it is associated with major psychosocial and ethical dilemmas and has a negative impact on national economies. The neurodegenerative process that occurs in AD involves a specific nervous cell dysfunction, which leads to neuronal death. Mutations in APP, PS1, and PS2 genes are causes for early onset AD. Several animal models have demonstrated that alterations in these proteins are able to induce oxidative damage, which in turn favors the development of AD. This paper provides a review of many, although not all, of the mutations present in patients with familial Alzheimer's disease and the association between some of these mutations with both oxidative damage and the development of the pathology.
阿尔茨海默病(AD)是老年人痴呆最常见的病因。据估计,目前全球60 - 65岁以上人口中有10%可能受AD影响,且在未来20年,受这种病症影响的人数可能超过3000万。在这方面的一大挑战是,AD不仅是一个科学问题;它还与重大的社会心理和伦理困境相关,并且对国家经济有负面影响。AD中发生的神经退行性过程涉及特定的神经细胞功能障碍,这会导致神经元死亡。APP、PS1和PS2基因的突变是早发性AD的病因。多种动物模型已证明,这些蛋白质的改变能够诱导氧化损伤,进而促进AD的发展。本文综述了家族性阿尔茨海默病患者中存在的许多(尽管不是全部)突变,以及其中一些突变与氧化损伤和病症发展之间的关联。