Review

Neuroscience Bulletin

, Volume 30, Issue 2, pp 359-366

Tau hyperphosphorylation induces apoptotic escape and triggers neurodegeneration in Alzheimer’s disease

  • Jian-Zhi WangAffiliated withDepartment of Pathology and Pathophysiology, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology Email author 
  • , Zhi-Hao WangAffiliated withDepartment of Pathology and Pathophysiology, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology
  • , Qing TianAffiliated withDepartment of Pathology and Pathophysiology, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology

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Abstract

Since abnormal post-translational modifications or gene mutations of tau have been detected in over twenty neurodegenerative disorders, tau has attracted widespread interest as a target protein. Among its various post-translational modifications, phosphorylation is the most extensively studied. It is recognized that tau hyperphosphorylation is the root cause of neurodegeneration in Alzheimer’s disease (AD); however, it is not clear how it causes neurodegeneration. Based on the findings that tau hyperphosphorylation leads to the escape of neurons from acute apoptosis and simultaneously impairs the function of neurons, we have proposed that the nature of AD neurodegeneration is the consequence of aborted apoptosis induced by tau phosphorylation. Therefore, proper manipulation of tau hyperphosphorylation could be promising for arresting AD neurodegeneration. In this review, the neuroprotective and neurodegenerative effects of tau hyperphosphorylation and our thoughts regarding their relationship are presented.

Keywords

Alzheimer’s disease microtubule-associated protein tau hyperphosphorylation apoptosis neurodegeneration