辐射与阿尔茨海默病(AD)

F. Tang
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引用次数: 3

摘要

表明电离辐射是阿尔茨海默病的危险因素。鼻内吸入氡气可使鼻脑和海马受到损伤性辐射,从而引发AD[8]。阿尔茨海默氏神经原纤维缠结由tau蛋白组成,这是AD最常见的病理标志之一,在Braak期11(6个Braak期中)及以上的tau聚集病理影响50%的45岁以上人群[9-11]。我们最近回顾了产前和产后辐射对动物模型和人类研究的影响,发现阿尔茨海默病与早期辐射暴露引起的神经心理障碍在海马神经病理学、认知障碍和相关分子机制上有许多相似之处[12-16]。这表明,在人类生命早期对大脑进行照射可能会引发从40岁和50岁时的tau聚集开始的异常发育事件,从而导致人类生命后期患上阿尔茨海默病。在分子水平上,产前产后辐照诱导脑氧化应激[15]、神经炎症反应[16,17]、毛细血管损失或损伤
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Radiation and Alzheimer's Disease (AD)
radiation suggested that ionizing radiation was a risk factor for AD. Intranasal inhalation of radon gas could subject the rhinencephalon and hippocampus to damaging radiation that initiated AD [8]. The Alzheimer neurofibrillary tangle is composed of tau, which is one of the most common pathological hallmarks of AD and tau aggregation pathology at Braak stage 1 1 (out of 6 Braak stages) or beyond affects 50% of the population over the age of 45 [9-11]. Our recent review of the effect of the preand post-natal irradiation on animal models and human studies indicated many similarities in hippocampal neuropathology, cognitive impairment and relevant molecular mechanisms between Alzheimer’s disease and early life radiation exposure-induced neuropsychological disorders [12-16]. It suggests that irradiation of the brain in early human life may set abnormal developmental events into motion that starts from tau aggregation at the ages of 40s and 50s, leading to the development of Alzheimer’s Disease at the late stages of human life. At molecular level, preor post-natal irradiation induced brain oxidative stress [15], neuroinflammatory response [16,17], capillary loss or impairment of
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