Regulation of amyloid precursor protein cleavage

被引:203
作者
Mills, J [1 ]
Reiner, PB [1 ]
机构
[1] Univ British Columbia, Kinsmen Lab Neurol Res, Grad Program Neurosci, Vancouver, BC V6T 1Z3, Canada
关键词
amyloid precursor protein; beta-amyloid; Alzheimer's disease; second messengers;
D O I
10.1046/j.1471-4159.1999.0720443.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Multiple lines of evidence suggest that increased production and/or deposition of the beta-amyloid peptide, derived from the amyloid precursor protein, contributes to Alzheimer's disease. A growing list of neurotransmitters, growth factors, cytokines, and hormones have been shown to regulate amyloid precursor protein processing. Although traditionally thought to be mediated by activation of protein kinase C, recent data have implicated other signaling mechanisms in the regulation of this process. Moreover, novel mechanisms of regulation involving cholesterol-, apolipoprotein E-, and stress-activated pathways have been identified. As the phenotypic changes associated with Alzheimer's disease encompass many of these signaling systems, it is relevant to determine how altered cell signaling may be contributing to increasing brain amyloid burden. We review the myriad ways in which first messengers regulate amyloid precursor protein catabolism as well as the signal transduction cascades that give rise to these effects. Key Words: Amyloid precursor protein-beta-Amyloid-Alzheimer's disease-Second messengers.
引用
收藏
页码:443 / 460
页数:18
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