Robustness of G Proteins in Alzheimer's Disease: An Immunoblot Study

Authors

  • Mark McLaughlin,

    Corresponding author
    1. Department of Biochemistry, Welcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Glasgow, Scotland
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  • Brian M. Ross,

    1. Department of Biochemistry, Welcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Glasgow, Scotland
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  • Graeme Milligan,

    1. Department of Biochemistry, Welcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Glasgow, Scotland
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  • James McCulloch,

    1. Department of Biochemistry, Welcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Glasgow, Scotland
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  • John T. Knowler

    1. Department of Biochemistry, Welcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Glasgow, Scotland
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Address correspondence and reprint requests to Mr. M. McLaughlin at Wellcome Surgical Institute and Hugh Fraser Neuroscience Laboratories. University of Glasgow, Garscube Estate, Bearsden Road. Glasgow G61 1QH. U.K.

Abstract

Abstract: Many of the neurotransmitter systems that are altered in senile dementia of the Alzheimer type are known to mediate their effects via G proteins, yet the integrity of guanine nucleotide-binding proteins (G proteins) in Alzheimer's diseased brains has received minimal investigation. The aim of this study was to establish whether the level of Gα subunits of five G proteins was altered in Alzheimer's disease. We used immunoblotting (Western blotting) to compare the amounts of Gi1, Gi2, GsH (heavy molecular weight), GSL (light molecular weight), and Go in the frontal cortex and hippocampus, two regions severely affected by the disease, and the cerebellum, which is less severely affected. The number of senile plaques was also quantified. We report that there was no significant difference in the level of these Gα subunits between Alzheimer's diseased and age-matched postmortem brains. These results suggest that alterations in the amount of G protein α subunits are not a feature of Alzheimer's disease.

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