What excitotoxin kills striatal neurons in Huntington's disease? Clues from neurochemical studies
1990; Lippincott Williams & Wilkins; Volume: 40; Issue: 1 Linguagem: Inglês
10.1212/wnl.40.1.20
ISSN1526-632X
AutoresThomas L. Perry, Shirley Hansen,
Tópico(s)Mitochondrial Function and Pathology
ResumoAmino acid analyses of both caudate nucleus and putamen obtained at autopsy from patients dying with Huntington9s disease (HD), and from control subjects, showed significantly decreased mean glutamate contents in the HD patients. In addition, the mean glutamate concentration was significantly increased in the CSF of living HD patients as compared with controls. Neurochemical studies also showed that neither aspartic acid, proline, 5-oxoproline, nor homocysteic acid is likely to act as a causative excitotoxin in HD. Excessive striatal glycine content, or deficient glutathione content, is unlikely to contribute to the effects of a causative excitotoxin in HD. We suggest that glutamic acid may be the proximate causative neurotoxin in the striatum in HD, as a result of an unexplained failure in the reuptake mechanism for glutamate released there as an excitatory neurotransmitter.
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