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阿尔茨海默病的分子发病机制:最新进展

Molecular Pathogenesis of Alzheimer's Disease: An Update.

作者信息

Sanabria-Castro Alfredo, Alvarado-Echeverría Ileana, Monge-Bonilla Cecilia

机构信息

Research Unit, Hospital San Juan de Dios, Costa Rican Social Security Fund (CCSS), San José, Costa Rica.

出版信息

Ann Neurosci. 2017 May;24(1):46-54. doi: 10.1159/000464422. Epub 2017 Apr 21.

Abstract

Dementia is a chronic or progressive syndrome, characterized by impaired cognitive capacity beyond what could be considered a consequence of normal aging. It affects the memory, thinking process, orientation, comprehension, calculation, learning ability, language, and judgment; although awareness is usually unaffected. Alzheimer's disease (AD) is the most common form of dementia; symptoms include memory loss, difficulty solving problems, disorientation in time and space, among others. The disease was first described in 1906 at a conference in Tubingen, Germany by Alois Alzheimer. One hundred and ten years since its first documentation, many aspects of the pathophysiology of AD have been discovered and understood, however gaps of knowledge continue to exist. This literature review summarizes the main underlying neurobiological mechanisms in AD, including the theory with emphasis on amyloid peptide, cholinergic hypothesis, glutamatergic neurotransmission, the role of tau protein, and the involvement of oxidative stress and calcium.

摘要

痴呆是一种慢性或进行性综合征,其特征是认知能力受损,超出了正常衰老可能导致的范围。它会影响记忆、思维过程、定向、理解、计算、学习能力、语言和判断力;尽管意识通常不受影响。阿尔茨海默病(AD)是最常见的痴呆形式;症状包括记忆力丧失、解决问题困难、时空定向障碍等。该疾病于1906年在德国图宾根的一次会议上由阿洛伊斯·阿尔茨海默首次描述。自首次记录以来的110年里,AD病理生理学的许多方面已被发现和理解,但知识空白仍然存在。这篇文献综述总结了AD主要的潜在神经生物学机制,包括强调淀粉样肽的理论、胆碱能假说、谷氨酸能神经传递、tau蛋白的作用以及氧化应激和钙的参与。

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