[Dementia and Parkinson's disease: biochemical and anatomo-clinical correlation].
Intellectual deterioration may be observed in the course of Parkinson's disease. Since it had been reported that central cholinergic systems degenerate in senile dementia and Alzheimer's disease, we measured the activity of choline acetyltransferase (C.A.T.) and the number of muscarinic receptors in various cortical regions of 12 control subjects and 20 patients and compared these biochemical results with clinical and neuropathological data concerning the patients. Thirteen of the parkinsonian patients showed signs of intellectual decline (moderate in 8, severe in 5) and neuropathological examination of the cortex revealed in 10 cases large number of Alzheimer type senile changes extending beyond the hippocampus. C.A.T. activity was decreased in the cerebral cortex in every patient. The decrease was greater in intellectually deteriorated patients and in the group with numerous senile changes in the cortex. The number of muscarinic receptors was increased in patients that had been treated with anticholinergic drugs until they died, but also in those who had not received these drugs, suggesting and underlying denervation hypersensitivity. In the caudate nucleus, however, neither C.A.T. activity nor muscarinic receptor number was altered, indicating that the cortical cholinergic lesion was specific. Although in most cases dementia in Parkinson's disease was of the Alzheimer type, the case of a demented parkinsonian patient in whom cortical C.A.T. activity was severely decreased, in spite of the absence of cortical histopathological evidence characteristic of Alzheimer's disease, suggests that a parkinsonian dementia different from the Alzheimer type also exists. In Parkinson's disease as in Alzheimer's disease the decrease in C.A.T. activity in the cerebral cortex results from degeneration of the cholinergic neurones in the nucleus of Meynert which projects to the cortex. Although the severity of intellectual deterioration seems in relationship with the extent of degeneration, this could already begin before intellectual impairment is apparent.
D000368:Aged; D001921:Brain / Q000473:pathology*; D001923:Brain Chemistry; D002421:Caudate Nucleus / Q000032:analysis; D002540:Cerebral Cortex / Q000032:analysis; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003704:Dementia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006624:Hippocampus / Q000032:analysis; D006801:Humans; D008297:Male; D010300:Parkinson Disease / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D011976:Receptors, Muscarinic / Q000032:analysis
D011976:Receptors, Muscarinic; D002795:Choline O-Acetyltransferase
Démence et maladie de Parkinson: corrélations biochimiques et anatomo-cliniques.