Endocannabinoid metabolism and Alzheimer’s disease  

作　　者：Chu Chen 

机构地区：[1]Department of Cellular and Integrative Physiology,School of Medicine,University of Texas Health Science Center at San Antonio,San Antonio,TX,USA

出　　处：《Neural Regeneration Research》2022年第9期1987-1988,共2页中国神经再生研究（英文版）

基　　金：supported by National Institutes of Health grants R01NS076815,R01MH113535,and R01AG058621(to CC).

摘　　要：Alzheimer’s disease(AD)is the most common cause of dementia in the elderly.Unfortunately,there are no effective therapies currently available for prevention and treatment of AD.As it is clear now,the etiology of AD is multifactorial and complex.This means that development of AD is linked to multiple mechanisms or signaling pathways and that a single-target therapy for AD is likely insufficient to achieve therapeutic goals.Therefore,an ideal therapy for AD should be able to modify the disease through multiple signaling pathways.2-Arachidonoylglycerol(2-AG)is an endogenous cannabinoid(endocannabinoid)displayinganti-inflammator y a n d neuroprotective properties,while its metabolites are arachidonic acid(AA)and AA-derived prostaglandins and leukotrienes,which are proinflammatory and neurotoxic(Figure 1).

关 键 词：METABOLISM ALZHEIMER protective 

分 类 号：R749.16[医药卫生—神经病学与精神病学]