Activation of neuronal extracellular receptor kinase (ERK) in Alzheimer disease links oxidative stress to abnormal phosphorylation

George Perry, Hanno Roder, Akihiko Nunomura, Atsushi Takeda, Avi L. Friedlich, Xiongwei Zhu, Arun K. Raina, Nikki Holbrook, Sandra L. Siedlak, Peggy L.R. Harris, Mark A. Smith

研究成果: Article査読

247 被引用数 (Scopus)

抄録

RESPONSES to increased oxidative stress may be the common mechanism responsible for the varied cytopathology of Alzheimer disease (AD). A possible link in support of this hypothesis is that one of the most striking features of AD, the abnormal accumulation of highly phosphorylated τ and neurofilament proteins, may be brought about by extracellular receptor kinase (ERK) whose activation is a common response to oxidative stress. In this study, we demonstrate that activated ERK is specifically increased in the same vulnerable neurons in AD that are the site of oxidative damage and abnormal phosphorylation. These findings suggest that ERK dysregulation, likely resulting from oxidative stress, could play an important role in the increased phosphorylation of cytoskeletal proteins observed in AD.

本文言語English
ページ(範囲)2411-2415
ページ数5
ジャーナルNeuroReport
10
11
DOI
出版ステータスPublished - 1999 8 2

ASJC Scopus subject areas

  • Neuroscience(all)

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