非淀粉样蛋白治疗阿尔茨海默病

L. Veng, M. Savage, J. Barrow, C. Zerbinatti
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引用次数: 0

摘要

阿尔茨海默病(AD)大脑是由细胞外淀粉样斑块和细胞内Tau聚集物定义的,它们被认为是导致AD患者神经变性和破坏性认知功能障碍的原因。阿尔茨海默病的治疗主要集中在干预脑淀粉样蛋白水平;然而,由于减少淀粉样蛋白的小分子和免疫治疗方法尚未显示AD患者的认知改善,因此对可以提供额外益处的新干预措施的兴趣正在上升。这篇综述的重点是解决代谢危险因素的治疗方法和减少Tau病理的靶点的发展。关键词:胆固醇;胰岛素;激酶抑制剂;LXR;亚甲蓝;微管;神经原纤维缠结;PPAR;他汀类药物
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Non-amyloid Approaches To Alzheimer's Disease
Alzheimer's disease (AD) brain is defined by extracellular amyloid plaques and intracellular Tau aggregates that are believed to cause the neurodegeneration and devastating cognitive dysfunction of AD patients. AD therapies have focused primarily on intervening at brain amyloid levels; however, since both small molecule and immunotherapy approaches to reduce amyloid have yet to show cognitive improvement in AD patients, interest in new interventions that can provide additional benefits is on the rise. This review focuses on therapeutic approaches addressing metabolic risk factors and development of targets that reduce Tau pathology. Keywords: cholesterol; insulin; kinase inhibitors; LXR; methylene blue; microtubules; neurofibrillary tangles; PPAR; statins
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