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Robert Perry, Department of Neuropathology, Newcastle General Hospital,Ian McKeith, University of Newcastle upon Tyne,Elaine Perry, MRC Neurochemical Pathology Unit, Newcastle General Hospital
Two alternative hypotheses – that there is either a unitary or a multiple neuropathological basis for dementia in diseases associated with Lewy bodies – are considered in relation to Parkinson's disease (PD) and Lewy body dementia (LBD including senile dementia of Lewy body type, SDLT). Densities of limbic (cingulate) cortical Lewy bodies, neocortical Lewy bodies, neocortical plaques, neocortical tangles, Braak staging, and Apo E frequency have been quantified in PD (demented and nondemented), SDLT, and Alzheimer's disease (AD with presenile and senile onset). Of these parameters the mean density of cingulate Lewy bodies is significantly greater in SDLT compared with all PD cases. There is no obvious correlation between Lewy body density and cognitive impairment assessed using a simple test of mental ability, and other measures of mental function in LBD may need to be considered. Since there is no absolute density of limbic Lewy bodies that clearly differentiates SDLT or demented PD cases from all nondemented PD cases, neuropathological criteria may need to incorporate severity of Alzheimer-type pathology as an additional optional factor. Mean neocortical plaque density is significantly lower in SDLT compared with AD cases but it is also significantly higher than in demented and nondemented PD cases, and higher than densities in normals. Even so, neocortical plaque density does not itself differentiate all SDLT cases from the normal. It is likely that the biological basis for dementia or psychoses in LBD, a cardinal feature of which is fluctuating symptomatology, is in part a functional or neurochemical abnormality.
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