Late phase cell cycle proteins in Alzheimer’s disease: a possible target for therapy?

Abstract

Alzheimer's disease (AD) is represented by neuronal loss and this loss is correlated to a constant state of neuronal instability induced by intrinsic and extrinsic factors. In this paper data is presented regarding the possible roles of late phase cell cycle proteins in normal and affected neurons with the goal that understanding the mechanisms involved in the regulation of these proteins may represent a novel strategy for AD treatment. The results demonstrate a relative differential pattern of expression of certain proteins (APC/C, Mad1 and Mad2, Bub R1, Bub1, CDK 11, cohesin subunit Rad 21 and astrin) in the AD brain versus age matched controls, and it is suggested that targeting these proteins might translate into potential treatments for AD. Although the data presented here is of some interest, the ability to translate such information into clinical applications is often a challenge.

Combined markers for predicting cognitive deficit in patients with Alzheimer’s disease

“…So, we combined the neurophysiological markers with a genetic marker in a trial to reach reliable findings. Bajic et al [8] clarified that there is an increasing interest in the evaluation of DNA damage markers in individuals liable to develop AD. These biomarkers may identify individuals at early stages of neurodegeneration.…”

“…Genomic instability is the earliest neuropathological event detected at the preclinical phase of the disease [6][7][8].…”