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Cdk5, a therapeutic target for Alzheimer's disease?
Li-Huei Tsai1, Ming-Sum Lee, Jonathan Cruz
1Department of Pathology, Harvard Medical School, Howard Hughes Medical Institute, 200 Longwood Avenue, Boston, MA 02115, USA. li-huei_tesai@hms.harvard.edu
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.