Abnormalities in glutamatergic mechanisms in human Huntington's disease.
Of many glutamatergic parameters studied in human Huntington's disease, the following abnormalities were documented in the literature: Decreased glutamate content in cerebrospinal fluid and frontal cortex. Decreased activities of glutamine synthetase, ornithine aminotransferase and aspartate aminotransferase in various brain regions, especially the frontal cortex, caudate nucleus and putamen. Decreased glutamate binding in fibroblast membranes. Although it has been hypothesized that Huntington's disease may have a glutamate-related etiology, presently available evidence is too fragmented and inadequate for any conclusion to be made. However, it is noted that interpretation of these human data is very difficult because of two reasons. Firstly, changes observed in postmortem Huntington's disease brains may only be secondary to the disease instead of being the cause of the disease. Secondly, there is always doubts as to the relevance of data obtained with non-neural tissues such as fibroblasts and platelets.
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D001696:Biomechanical Phenomena; D001921:Brain / Q000201:enzymology / Q000378:metabolism; D005971:Glutamates / Q000378:metabolism / Q000502:physiology* / Q000633:toxicity; D006801:Humans; D006816:Huntington Disease / Q000503:physiopathology*; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter / Q000378:metabolism; D013569:Synapses / Q000378:metabolism
D005971:Glutamates; D017470:Receptors, Glutamate; D017981:Receptors, Neurotransmitter