标题:TMP21 in Alzheimer's Disease: Molecular Mechanisms and a Potential Target
作者:Qiu, Kaixin; Zhang, Xiaojie; Wang, Shuai; Li, Chunyan; Wang, Xin; Li, Xuezhi; Wu, Yili
作者机构:[Qiu, Kaixin; Li, Chunyan] Shandong Univ, Cheeloo Coll Med, Jinan, Shandong, Peoples R China.; [Qiu, Kaixin; Wang, Shuai; Li, Chunyan; Wang, Xin; Li 更多
通讯作者:Wu, YL;Wu, YL
通讯作者地址:[Wu, YL]Jining Med Univ, Shandong Collaborat Innovat Ctr Diag Treatment &, Inst Mental Hlth, Jining, Peoples R China;[Wu, YL]Jining Med Univ, Sch Ment 更多
来源:FRONTIERS IN CELLULAR NEUROSCIENCE
出版年:2019
卷:13
DOI:10.3389/fncel.2019.00328
关键词:Alzheimer's disease; TMP21; A beta; Tau phosphorylation; neuronal loss
摘要:Alzheimer's disease (AD) is the most common form of dementia in the elderly, which is characterized by progressive cognitive impairment. Neuritic plaques, neurofibrillary tangles and neuronal loss are the major neuropathological hallmarks in AD brains. TMP21 is a key molecule for protein trafficking in cells. Growing evidence indicates that TMP21 is dysregulated in AD, which plays a pivotal role in neuritic plaque formation. Therefore, we aim to review the dysregulation of TMP21 in AD, the role of TMP21 in neuritic plaque formation and underlying mechanisms. Moreover, the potential role of TMP21 in neurofibrillary tangle formation, synaptic impairment and neuronal loss is discussed. It will provide an outlook into the potential of regulating TMP21 as a therapeutic approach for AD treatment.
收录类别:SCOPUS;SCIE
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85069475744&doi=10.3389%2ffncel.2019.00328&partnerID=40&md5=e69ba7f2471ce2de0de35a29389f25d4
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