Abstract：
:Increasing evidence have shown that beta-amyloid (Abeta) induced hyperphosphorylation of tau, which eventually resulted in the disruption of microtubule (MT) integrity. Cyclin-dependent kinase 5 (CDK5) and its activator p35 are required for neurite outgrowth. The cleavage of p35 to p25, mediated by calpain and calcium, caused CDK5 dislocation and subsequently p25/CDK5-induced tau hyperphosphorylation, which disrupted the cytoskeleton and resulted in neuronal death. In the present study we investigated the effects of ginsenoside Rb1 on fibrillar Abeta(25-35)-induced tau hyperphosphorylation in primary cultured cortical neurons and also the potential involvement of Ca(2+)-calpain-CDK5 signal pathway. The present study suggests that Ca(2+), calpain, and p25 in CDK5 pathway may play important roles in Abeta(25-35)-induced tau hyperphosphorylation.
journal_name
Brain Resjournal_title
Brain researchauthors
Chen X,Huang T,Zhang J,Song J,Chen L,Zhu Ydoi
10.1016/j.brainres.2007.12.029subject
Has Abstractpub_date
2008-03-20 00:00:00pages
99-106eissn
0006-8993issn
1872-6240pii
S0006-8993(07)02964-2journal_volume
1200pub_type
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