Cdk5, a therapeutic target for Alzheimer's disease?

✍ Scribed by Li-Huei Tsai; Ming-Sum Lee; Jonathan Cruz

• Publisher: Elsevier Science
• Year: 2004
• Tongue: English
• Weight: 124 KB
• Volume: 1697
• Category: Article
• ISSN: 1570-9639
• DOI: 10.1016/j.bbapap.2003.11.019

✦ Synopsis

Alzheimer's disease (AD) represents the leading cause for senile dementia affecting more than 4 million people worldwide. AD patients display a triad of pathological features including brain atrophy caused by neuronal loss, h-amyloid plaque and neurofibrillary tangles. We previously show that Cyclin-dependent kinase 5 (Cdk5) is deregulated in AD brains and may contribute to the pathogenesis of AD. In AD brains, a calpain cleavage product of its physiological regulator p35, p25 is elevated. p25 causes prolonged activation of Cdk5 and alteration of its substrate specificity. The implications of p25/Cdk5 in neurotoxicity, h-amyloid plaque and neurofibrillary tangle pathology will be discussed.