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Cyclin' toward dementia
Author(s) -
Raina Arun K.,
Zhu Xiongwei,
Rottkamp Catherine A.,
Monteiro Mervyn,
Takeda Atsushi,
Smith Mark A.
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20000715)61:2<128::aid-jnr2>3.0.co;2-h
Subject(s) - neurodegeneration , cyclin , cell cycle , neuroscience , biology , ectopic expression , cell cycle protein , cyclin a , polo like kinase , cyclin d , microbiology and biotechnology , cell , disease , medicine , pathology , genetics , cell culture
Recent evidence has associated the aberrant, proximal re‐expression of various cell cycle control elements with neuronal vulnerability in Alzheimer disease, a chronic neurodegeneration. Such ectopic localization of various cyclins, cyclin‐dependent kinases, and cyclin inhibitors in neurons can be seen as an attempt to re‐enter the cell cycle. Given that primary neurons are terminally differentiated, any attempted re‐entry into the cell division cycle in this postmitotic environment will be dysregulated. Since successful dysregulation of the cell cycle is also the hallmark of a neoplasm, early cell‐cycle pathophysiology in Alzheimer disease may recruit oncogenic signal transduction mechanisms and, hence, can be viewed as an abortive neoplastic transformation. J. Neurosci. Res. 61:128–133, 2000. © 2000 Wiley‐Liss, Inc.