It is clear that the abnormal activation of CDK5 via calpain-mediated cleavage of p35 into the more stable p25 fragment contributes to the pathogenesis of neurodegenerative conditions such as AD and HIVE [4-6,8], however, previous studies have also demonstrated that physiological CDK5 activity is essential for adult neurogenesis [15,16]. This evidence concerns the gene CDK5 and Alzheimer disease.