Papel del estrés oxidativo en el desarrollo del deterioro cognitivo y su progresión a enfermedad de Alzheimer

J. CRUZ-RODRÍGUEZ, Gabriel BETANZOS-CABRERA, B. H. CAMACHO-DÍAZ, María Araceli Ortiz-Rodríguez
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Abstract

This review aims to provide scientific evidence of the role of oxidative stress in the development of cognitive impairment and its progression to Alzheimer's disease. Oxidative stress originates when there is an uncontrolled production of free radicals that disrupts the balance between oxidants and antioxidants, favoring oxidants. It has been associated with oxidative stress with the pathogenesis of brain aging, cognitive impairment and some neurological diseases. The cells of the central nervous system produce a high amount of free radicals since their energy demand is high, this coupled with a low antioxidant capacity, favors the appearance of a pro-oxidant environment that contributes to neurodegeneration and neuronal death. Alzheimer's disease is the most frequent form of dementia, it is characterized by neurodegenerative changes that occur with cognitive impairment, progressive impairment of memory and thought, until preventing the performance of daily life activities. Neuropathologically, it is characterized by the presence of extracellular deposits of β-amyloid peptide in the form of neurofibrillar plaques and clews; lesions capable of generating damage and neuronal death that lead to cognitive failure through the generation of more free radicals
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氧化应激在认知障碍发展和阿尔茨海默病进展中的作用
本综述旨在提供氧化应激在认知障碍发展及其发展为阿尔茨海默病中的作用的科学证据。当自由基的产生不受控制,破坏了氧化剂和抗氧化剂之间的平衡,有利于氧化剂时,氧化应激就产生了。氧化应激与脑老化、认知障碍和某些神经系统疾病的发病机制有关。中枢神经系统的细胞产生大量自由基,因为它们的能量需求高,加上抗氧化能力低,有利于促氧化环境的出现,导致神经变性和神经元死亡。阿尔茨海默病是最常见的痴呆症形式,其特征是神经退行性变化,伴有认知障碍,记忆和思维的进行性损害,直到无法进行日常生活活动。神经病理学上,其特征是细胞外以神经纤维斑块和提示形式存在β-淀粉样肽沉积;能够产生损伤和神经元死亡的病变,通过产生更多自由基导致认知功能衰竭
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