Neurosci Lett. 1992 Jul 6;141(1):16-20.

Preservation of Gi-protein inhibited adenylyl cyclase activity in the brains of patients with Alzheimer's disease.

Cowburn RF, O'Neill C, Ravid R, Winblad B, Fowler CJ.

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Department of Geriatric Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.

Abstract

The coupling of inhibitory guanine nucleotide binding (Gi) proteins to the adenylyl cyclase signal transduction complex was compared in 4 brain regions from a series of Alzheimer's disease and matched control subjects by measuring the inhibition of membrane enzyme activities in response to guanosine 5'-[beta gamma-imido]diphosphate (Gpp[NH]p) and aluminium fluoride (AlF4-). Basal adenylyl cyclase activities were significantly lower in preparations of angular gyrus and frontal and temporal cortices, but not cerebellum, from the Alzheimer's disease cases compared to controls. Gpp[NH]p and AlF4- gave significant inhibitions of adenylyl cyclase activity in all brain regions. The magnitude of these inhibitions, when corrected for altered basal activities, were similar for the Alzheimer's disease and control cases. These results indicate that there is no impairment of Gi-protein mediated inhibition of adenylyl cyclase activity in Alzheimer's disease brain.

PMID:: 1508395; [PubMed - indexed for MEDLINE]

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