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阿尔茨海默病的综合综述:病因与治疗。

Comprehensive Review on Alzheimer's Disease: Causes and Treatment.

机构信息

Pharmaceutical Sciences Department, Faculty of Pharmacy, Al-Quds University, Jerusalem 20002, Palestine.

出版信息

Molecules. 2020 Dec 8;25(24):5789. doi: 10.3390/molecules25245789.

Abstract

Alzheimer's disease (AD) is a disorder that causes degeneration of the cells in the brain and it is the main cause of dementia, which is characterized by a decline in thinking and independence in personal daily activities. AD is considered a multifactorial disease: two main hypotheses were proposed as a cause for AD, cholinergic and amyloid hypotheses. Additionally, several risk factors such as increasing age, genetic factors, head injuries, vascular diseases, infections, and environmental factors play a role in the disease. Currently, there are only two classes of approved drugs to treat AD, including inhibitors to cholinesterase enzyme and antagonists to -methyl d-aspartate (NMDA), which are effective only in treating the symptoms of AD, but do not cure or prevent the disease. Nowadays, the research is focusing on understanding AD pathology by targeting several mechanisms, such as abnormal tau protein metabolism, β-amyloid, inflammatory response, and cholinergic and free radical damage, aiming to develop successful treatments that are capable of stopping or modifying the course of AD. This review discusses currently available drugs and future theories for the development of new therapies for AD, such as disease-modifying therapeutics (DMT), chaperones, and natural compounds.

摘要

阿尔茨海默病(AD)是一种导致大脑细胞退化的疾病,是痴呆的主要病因,其特征是思维能力下降和个人日常活动的独立性下降。AD 被认为是一种多因素疾病:提出了两种主要假说作为 AD 的病因,即胆碱能和淀粉样假说。此外,年龄增长、遗传因素、头部损伤、血管疾病、感染和环境因素等多种风险因素也在疾病中发挥作用。目前,仅有两类批准用于治疗 AD 的药物,包括乙酰胆碱酯酶抑制剂和 N-甲基-D-天冬氨酸(NMDA)拮抗剂,这些药物仅对 AD 的症状有效,但不能治愈或预防疾病。如今,研究的重点是通过针对几种机制来了解 AD 的病理,例如异常的 tau 蛋白代谢、β-淀粉样蛋白、炎症反应以及胆碱能和自由基损伤,旨在开发能够阻止或改变 AD 进程的成功疗法。本文综述了目前可用的药物和未来针对 AD 开发新疗法的理论,例如疾病修饰疗法(DMT)、伴侣蛋白和天然化合物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ecf/7764106/41d50f7a4806/molecules-25-05789-g001.jpg

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