Mohammed T. Abou-Saleh

DEMENTIA AND PARKINSON’S DISEASE 267without dementia. This suggests that the elderly cerebral cortex isvulnerable to the same pathological processes as the substantianigra (and which lead to parkinsonism), whereas the youngercerebral cortex is relatively resistant, so that early-onset PD tendsto be unassociated with dementia. The nature of this age-relatedvulnerability of the cortex is unknown, but it is of interest thatage-related differential vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been demonstrated in primates 26 .CONCLUSIONSThe dementia of PD is entirely distinct from the dementia ofAlzheimer’s disease. In PD dementia is associated with Lewy bodyformation in the cerebral cortex as well as in the substantia nigra;whereas in Alzheimer’s disease neuronal loss and neurofibrillarytangle formation is characteristically in the dorsal raphe nucleiand nucleus basalis of Meynert.The clinical features of the two forms of dementia are usuallydistinguishable. More difficult to distinguish clinically, especiallyin the earlier stages, are the two types of PD. In one the diseasepresents typically in middle life, progresses slowly, responds wellto dopamine agonists and is not associated with dementia;whereas the other (diffuse Lewy body type) presents in late life,progresses more rapidly, responds less well to dopamine agonistsand is associated with dementia. The clinical significance ofmaking this distinction is to define prognosis and also to affectmanagement, in particular the use of dopamine agonists and themanagement of dementia.The cause of PD and of Alzheimer’s disease remains unknownbut there are promising lines of investigation related to thegenetics and molecular biology of the Lewy body and theneurofibrillary tangle, respectively.REFERENCES1. Brown RG, Marsden CD. How common is dementia in Parkinson’sdisease? Lancet 1984; ii: 1262–5.2. Mutch WJ, Dingwall-Fordyce I, Downie AW et al. Parkinson’s diseasein a Scottish city. 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