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  • Cited by 1
  • Print publication year: 1996
  • Online publication date: July 2010

20 - Temporal lobe immunohistochemical pathology for tangles, plaques and Lewy bodies in diffuse Lewy body disease, Parkinson's disease, and senile dementia of Alzheimer type

from Part two - Pathological issues



Cortical Lewy bodies (LBs), neurofibrillary tangles (NFTs) and senile plaques (SPs) in the limbic and neocortical cortices of the temporal lobe were studied with anti-ubiquitin, anti-tau and anti-β-protein immunohistochemistry in senile dementia of Alzheimer type (SDAT), diffuse Lewy body disease (DLBD), Parkinson's disease (PD) with and without dementia, and normal controls. DLBD was characterized by numerous cortical LBs together with marked senile changes similar to those of SDAT though neocortical NFTs were significantly less than in SDAT. There were rare or no cortical LBs and neocortical NFTs in most PD cases with and without dementia while there were a few cortical LBs and moderate senile changes, in some cases with dementia. These findings suggest that either of the abundant cortical LBs and senile change, or both have produced dementia in DLBD, while the neuropathological background for dementia in PD cases may be heterogeneous and vary among individual cases.


Diffuse Lewy body disease (DLBD) is a neuropathological entity in which abundant Lewy bodies (LBs) are found throughout the cerebral cortex as well as in the brainstem nuclei in the manner identical to Parkinson's disease (Kosaka et al., 1980, 1984). Marked senile changes including abundant senile plaques (SPs) and Alzheimer neurofibrillary tangles (NFTs) are also found in this condition. Immunohistochemical stains with tau and β-protein antibodies respectively demonstrate NFTs and SPs selectively and sensitively. Ubiquitin immunohistochemistry can immunostain LBs of both brainstem and cortical types sensitively (Kuzuhara et al., 1988; Lowe et al., 1988), and detect far more LBs than the conventional techniques (Lennox et al., 1989).