期刊论文详细信息
Research and Practice in Thrombosis and Haemostasis
The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy
Sidney Strickland1  Pradeep K. Singh1  Ana Badimon1  Erin H. Norris1  Zu‐Lin Chen1 
[1] Patricia and John Rosenwald Laboratory of Neurobiology and Genetics The Rockefeller University New York NY USA;
关键词: Alzheimer's disease;    beta‐amyloid;    blood‐brain barrier;    coagulation factors;    contact system;    dementia;   
DOI  :  10.1002/rth2.12504
来源: DOAJ
【 摘 要 】

Abstract Alzheimer's disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. Extracellular beta‐amyloid (Aβ) plaques and neurofibrillary tau tangles are classical hallmarks of AD pathology and thus are the prime targets for AD therapeutics. However, approaches to slow or stop AD progression and dementia by reducing Aβ production, neutralizing toxic Aβ aggregates, or inhibiting tau aggregation have been largely unsuccessful in clinical trials. The contribution of dysregulated vascular components and inflammation is evident in AD pathology. Vascular changes are detectable early in AD progression, so treatment of vascular defects along with anti‐Aβ/tau therapy could be a successful combination therapeutic strategy for this disease. Here, we explain how vascular dysfunction mechanistically contributes to thrombosis as well as inflammation and neurodegeneration in AD pathogenesis. This review provides evidence that addressing vascular dysfunction in people with AD could be a promising therapeutic strategy.

【 授权许可】

Unknown   

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