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Faculté de Médecine, Laboratory of Neurosciences, Unité INSERM 16, Lille, France.
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.
Address correspondence and reprint requests to Dr. André Delacourte, Unité INSERM 16, Laboratory of Neurosciences, Faculté de Médecine, 59045 Lille, France.
Supported by grants from MRES (88.C.0710), CNMATS/INSERM, and ADERMA.
Received March 2, 1989. Accepted for publication in final form June 28, 1989.
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