Abstract
AbstractRecent investigations into the etiology and pathogenesis of Alzheimer’s disease (AD) in the past few years have expanded to include previously unexplored and/or disconnected aspects of AD and related conditions at both the cellular and systemic levels of organization. These include how AD-associated abnormalities affect the cell cycle and neuronal differentiation state and how they recruit signal transduction, membrane trafficking and protein transcytosis mechanisms to produce a neurotoxic syndrome capable of spreading itself throughout the brain. The recent expansion of AD research into intercellular and new aspects of cellular degenerative mechanisms is causing a systemic re-evaluation of AD pathogenesis, including the roles played by well-studied elements, such as the generation of Aβ and tau protein aggregates. It is also changing our view of neurodegenerative diseases as a whole. Here we propose a conceptual framework to account for some of the emerging aspects of the role of tau in AD pathogenesis.
Reference264 articles.
1. Alzheimer A., Über eine eigenartige Erkrankung der Hirnrinde, Allg. Z. Psychiatr., 1907, 64, 146–148
2. Lowenberg K., Waggoner R., Familial organic psychosis (Alzheimer’s type), Arch. Neurol., 1934, 31, 737–754
3. Blessed G., Tomlinson B.E., Roth M., The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects, Br. J. Psychiatry, 1968, 114, 797–811
4. Olson M.I., Shaw C.M., Presenile dementia and Alzheimer’s disease in mongolism, Brain, 1969, 92, 147–156
5. Cook R., Ward B., Austin J., Studies in aging of the brain: IV. Familial Alzheimer’s disease: relationship to transmissible dementia, aneuploidy and microtubular defects, Neurology, 1979, 29, 1402–1412
Cited by
10 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献