Neuronal polo-like kinase in Alzheimer disease indicates cell cycle changes

被引:49
作者
Harris, PLR
Zhu, XW
Pamies, C
Rottkamp, CA
Ghanbari, HA
McShea, A
Feng, Y
Ferris, DK
Smith, MA
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
[2] Panacea Pharmaceut, Rockville, MD 20850 USA
[3] Fred Hutchinson Canc Res Ctr, Program Canc Biol, Seattle, WA 98109 USA
[4] NCI, FCRCD, Frederick, MD 21702 USA
关键词
Alzheimer disease; cell cycle; cytoskeleton; pathogenesis; phosphorylation; polo-like kinase; tau;
D O I
10.1016/S0197-4580(00)00218-9
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 [法学]; 0303 [社会学]; 100203 [老年医学];
摘要
Neurons of adults apparently lack the components necessary to complete the cell division process. Therefore. in Alzheimer disease. the increased expression of cell cycle-related proteins in degenerating neurons likely leads to an interrupted mitotic process associated with cytoskeletal abnormalities and, ultimately, neuronal degeneration. In this study, to further delineate the role of mitotic processes in the pathogenesis of Alzheimer disease, we undertook a study of polo-like kinase (Plk), a protein that plays a crucial role in the cell cycle. Our results show disease-related increases in Plk in susceptible hippocampal and cortical neurons in comparison to young or age-matched controls. An increase in neuronal Plk further implicates aberrations in cell cycle control in the pathogenesis of Alzheimer disease and provides a novel mechanistic basis for therapeutic intervention. (C) 2000 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:837 / 841
页数:5
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