Induction of p21ras in Alzheimer pathology.
Changes in the expression of the small G-protein p21ras, a critical regulator of cell proliferation and differentiation, were investigated by immunohistochemical methods in the temporal cortex of patients with Alzheimer's disease. In both normal brain and in Alzheimer's disease, the H-ras, K-ras and N-ras gene products were equally detected in almost all neurones and occasionally also in glial cells. In Alzheimer's disease an increased expression of p21ras was observed within neuritic plaques as well as in neurones and glial cells closely associated with plaques. Neurones containing tangle-bearing material also showed a high level of expression. It is suggested that activation of p21ras dependent signalling pathways are involved in the processes of neurodegeneration and/or aberrant repair in Alzheimer's disease.
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D015153:Blotting, Western; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D019204:GTP-Binding Proteins / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000473:pathology; D009473:Neuronal Plasticity / Q000502:physiology; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis*; D020668:rap GTP-Binding Proteins
D011518:Proto-Oncogene Proteins; D019204:GTP-Binding Proteins; D020668:rap GTP-Binding Proteins