Recent evidence has associated the aberrant, proximal re-expression of vari
ous cell cycle control elements with neuronal vulnerability in Alzheimer di
sease, a chronic neurodegeneration. Such ectopic localization of various cy
clins, cyclin-dependent kinases, and cyclin inhibitors in neurons can be se
en as an attempt to re-enter the cell cycle. Given that primary neurons are
terminally differentiated. any attempted re-entry into the cell division c
ycle 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 signa
l transduction mechanisms and, hence, can be viewed as an abortive neoplast
ic transformation. (C) 2000 Wiley-Liss, Inc.