Cerebral excess release of neurotransmitter amino acids subsequent to reduced cerebral glucose metabolism in early-onset dementia of Alzheimer type.
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.
Hoyer
S
S
Department of Pathochemistry and General Neurochemistry, University of Heidelberg, Federal Republic of Germany.
Nitsch
R
R
D000328:Adult; D000544:Alzheimer Disease / Q000378:metabolism* / Q000503:physiopathology; D000596:Amino Acids / Q000378:metabolism*; D000641:Ammonia / Q000097:blood; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged
D000596:Amino Acids; D000641:Ammonia; D005947:Glucose