General and dramatic glial reaction in Alzheimer brains
- 1 January 1990
- journal article
- research article
- Published by Wolters Kluwer Health in Neurology
- Vol. 40 (1) , 33
- https://doi.org/10.1212/wnl.40.1.33
Abstract
We quantified glial fibrillary acidic protein (GFAP) using immunoblot techniques and anti-GFAP, in unfractionated homogenates of different brain regions from Alzheimer's disease (AD) patients. The amount of GFAP was significantly higher than in brains from controls and other neurodegenerative disorders (mean of 11 times), even in brain regions usually free of AD lesions such as caudate nucleus, thalamus, cerebellum, or brainstem. This dramatic increase of GFAP is not simply reflective of the astrocytic gliosis usually observed near the neurofibrillary tangles and senile plaques but more likely represents an astrocytic reaction in the whole brain corresponding to an overproduction or an accumulation of GFAP. The significance of such an increase is unknown, but it might be a key element in the pathogenesis of AD.This publication has 15 references indexed in Scilit:
- Neocortical morphometry, lesion counts, and choline acetyltransferase levels in the age spectrum of Alzheimer's diseaseNeurology, 1988
- An immunohistochemical quantification of fibrous astrocytes in the aging human cerebral cortexNeurobiology of Aging, 1987
- Distribution of Glial Fibrillary Acidic Protein in Gliosed Human White MatterJournal of Neurochemistry, 1986
- A glia-derived neurite promoting factor with protease inhibitory activity belongs to the protease nexinsCell, 1986
- Glial fibrillary acidic protein and Alzheimer's diseaseNeurochemical Research, 1985
- Dopaminergic and cholinergic lesions in progressive supranuclear palsyAnnals of Neurology, 1985
- Huntington's disease: Changes in striatal proteins reflect astrocytic gliosisBrain Research, 1982
- Glial fibrillary acidic protein and Alzheimer‐type senile dementiaNeurology, 1980
- TOPOGRAPHY OF SOLUBLE GFA IN AGED HUMAN-BRAIN1979
- Morphometric studies of the neuropathological changes in choreatic diseasesJournal of the Neurological Sciences, 1976