Autor: |
Pei JJ; NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA., Tanaka T, Tung YC, Braak E, Iqbal K, Grundke-Iqbal I |
Jazyk: |
angličtina |
Zdroj: |
Journal of neuropathology and experimental neurology [J Neuropathol Exp Neurol] 1997 Jan; Vol. 56 (1), pp. 70-8. |
DOI: |
10.1097/00005072-199701000-00007 |
Abstrakt: |
A number of studies have implicated a proline-directed protein kinase, glycogen synthase kinase-3 (GSK-3) in the hyperphosphorylation of tau in Alzheimer's disease (AD). Toward understanding the role of GSK-3 in the abnormal hyperphosphorylation of tau in AD we have found that GSK-3 is prominently present in neuronal cell bodies and their processes and co-localizes with neurofibrillary changes in AD brain. Furthermore, the levels of GSK-3 as determined by indirect ELISA are approximately 50% increased in the postsynaptosomal supernatant from AD brains as compared to the controls. However, no increase in GSK-3 enzyme activity was detected. In AD brain, with its reduced phosphatase activity, even normal levels of GSK-3 activity might be sufficient for the hyperphosphorylation of tau. |
Databáze: |
MEDLINE |
Externí odkaz: |
|