Document Detail

Involvement of calpain and p25 of CDK5 pathway in ginsenoside Rb1's attenuation of beta-amyloid peptide25-35-induced tau hyperphosphorylation in cortical neurons.
MedLine Citation:
PMID:  18289510     Owner:  NLM     Status:  MEDLINE    
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.
Xiaochun Chen; Tianwen Huang; Jing Zhang; Jinqiu Song; Limin Chen; Yuangui Zhu
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-03-04
Journal Detail:
Title:  Brain research     Volume:  1200     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-03-17     Completed Date:  2008-07-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  99-106     Citation Subset:  IM    
Department of Neurology, Fujian Institute of Geriatrics, the Affiliated Union Hospital of Fujian Medical University, Fuzhou, Fujian 350001, China.
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MeSH Terms
Alzheimer Disease / drug therapy,  metabolism,  physiopathology
Amyloid beta-Protein / antagonists & inhibitors*,  toxicity
Calcium / metabolism
Calcium Signaling / drug effects,  physiology
Calpain / drug effects*,  metabolism
Cells, Cultured
Cerebral Cortex / drug effects,  metabolism,  pathology
Cytoskeleton / drug effects,  metabolism,  pathology
Drugs, Chinese Herbal / pharmacology,  therapeutic use
Ginsenosides / pharmacology*,  therapeutic use
Microtubules / drug effects,  metabolism,  pathology
Nerve Tissue Proteins / drug effects*,  metabolism
Neurofibrillary Tangles / drug effects,  metabolism,  pathology
Neurons / drug effects*,  metabolism,  pathology
Neuroprotective Agents / pharmacology,  therapeutic use
Peptide Fragments / antagonists & inhibitors*,  toxicity
Rats, Sprague-Dawley
Signal Transduction / drug effects,  physiology
tau Proteins / drug effects*,  metabolism
Reg. No./Substance:
0/Amyloid beta-Protein; 0/Drugs, Chinese Herbal; 0/Ginsenosides; 0/Nerve Tissue Proteins; 0/Neuroprotective Agents; 0/Peptide Fragments; 0/amyloid beta-protein (25-35); 0/ginsenoside Rb1; 0/neuronal Cdk5 activator (p25-p35); 0/tau Proteins; 7440-70-2/Calcium; EC 3.4.22.-/Calpain

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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