TDP-43 is a key molecule accelerating development of Alzheimer’s disease following traumatic brain injury  

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作  者:Chu Chen 

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

出  处:《Neural Regeneration Research》2024年第5期955-956,共2页中国神经再生研究(英文版)

基  金:supported by National Institutes of Health grants RF1NS076815 and R01AG058621.

摘  要:Currently,more than 55 million people have dementia worldwide and Alzheimer’s disease(AD)is one of the most common causes of dementia in aging.However,no effective therapies are currently available for the prevention and treatment of AD.This is largely due to our limited understanding of the mechanisms underlying the neuropathogenesis of AD.It has widely been recognized that AD is heterogeneous and that multi-factors are contributing to the pathogenesis of AD.Accumulated evidence suggests that traumatic brain injury(TBI)is an important risk factor for the development of AD and dementia later in life(Guo et al.,2000;Johnson et al.,2010).However,the precise mechanism by which TBI contributes to developing AD has yet to be elucidated.

关 键 词:ALZHEIMER TRAUMATIC 

分 类 号:R749.16[医药卫生—神经病学与精神病学]

 

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