Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/4769
Title: Tau phosphorylation in Alzheimer's disease: pathogen or protector?
Authors: Lee, Hyoung-gon 
Perry, George 
Moreira, Paula I. 
Garrett, Matthew R. 
Liu, Quan 
Zhu, Xiongwei 
Takeda, Atsushi 
Nunomura, Akihiko 
Smith, Mark A. 
Issue Date: 2005
Citation: Trends in Molecular Medicine. 11:4 (2005) 164-169
Abstract: During the past decade, hypotheses concerning the pathogenesis of most neurodegenerative diseases have been dominated by the notion that the aggregation of specific proteins and subsequent formation of cytoplasmic and extracellular lesions represent a harbinger of neuronal dysfunction and death. As such, in Alzheimer's disease, phosphorylated tau protein, the major component of neurofibrillary tangles, is considered a central mediator of disease pathogenesis. We challenge this classic notion by proposing that tau phosphorylation represents a compensatory response mounted by neurons against oxidative stress and serves a protective function. This novel concept, which can also be applied to protein aggregates in other neurodegenerative diseases, opens a new window of knowledge with broad implications for both the understanding of mechanisms underlying disease pathophysiology and the design of new therapeutic strategies.
URI: http://hdl.handle.net/10316/4769
Rights: openAccess
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais

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