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Cerebral excess release of neurotransmitter amino acids subsequent to reduced cerebral glucose metabolism in early-onset dementia of Alzheimer type

Journal of Neural Transmission volume 75, pages 227–232 (1989)Cite this article

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Summary

A massive cerebral release of amino acids and ammonia was found in early-onset dementia of Alzheimer type. Aspartate and glycine were liberated in high concentrations, whereas glutamate remained rather unchanged. This excess cerebral protein catabolism is due to a 44% reduction in cerebral glucose metabolism. Whereas glutamate and other glucoplastic amino acids may substitute glucose, elevated aspartate may contribute to neuronal damage. The results are discussed with respect to a possible neuronal insulin/insulin receptor deficiency.

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Author notes

  1. S. Hoyer

    Present address: Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany

Authors and Affiliations

  1. Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Heidelberg, Germany

    R. Nitsch

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  1. S. Hoyer
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  2. R. Nitsch
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Hoyer, S., Nitsch, R. Cerebral excess release of neurotransmitter amino acids subsequent to reduced cerebral glucose metabolism in early-onset dementia of Alzheimer type. J. Neural Transmission 75, 227–232 (1989). https://doi.org/10.1007/BF01258634

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  • DOI: https://doi.org/10.1007/BF01258634

Keywords

  • Dementia of Alzeimer type
  • amino acids
  • neurotoxic effect
  • neuronal damage
  • insulin receptor