| Literature DB >> 15023356 |
Li-Huei Tsai1, Ming-Sum Lee, Jonathan Cruz.
Abstract
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, beta-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, beta-amyloid plaque and neurofibrillary tangle pathology will be discussed.Entities:
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Year: 2004 PMID: 15023356 DOI: 10.1016/j.bbapap.2003.11.019
Source DB: PubMed Journal: Biochim Biophys Acta ISSN: 0006-3002