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作 者:Jiying Hu Liqiang Wang Jie Chen Yi Liang
机构地区:[1]Hubei Key Laboratory of Cell Homeostasis,College of Life Sciences,TaiKang Center for Life and Medical Sciences,Wuhan University,Wuhan 430072,China [2]Office of Core Facility,Shenzhen Bay Laboratory,Shenzhen 518000,China
出 处:《Acta Biochimica et Biophysica Sinica》2024年第7期1085-1088,共4页生物化学与生物物理学报(英文版)
基 金:supported by the grants from the National Natural Science Foundation of China(Nos.32271326,32071212,and 31770833 to Y.L.and No.32201040 to L.W.);the Key Project of Basic Research,Science and Technology R&D Fund of Shenzhen(No.JCYJ20200109144418639 to Y.L.).
摘 要:A pathological hallmark of Alzheimer’s disease(AD),the most common neurodegenerative disease in elderly people,is the formation of neurofibrillary tangles(NFTs),which are mainly composed of bundles of amyloid fibrils formed by abnormal deposition of hyperphosphorylated full-length human Tau protein[1–3].Recent studies have shown that AD-related cognitive decline and brain atrophy are closely correlated with Tau PET signal,further supporting the link between Tau pathology and AD symptomatology[4,5].Despite the high incidence and severe burden to patients,caregivers,and health systems caused by AD,there are few disease-modifying therapies available.
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