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  • 1
    ISSN: 1432-0533
    Keywords: Key word Diffuse Lewy body disease ; Apolipoprotein E gene ; Autosomal dominant ; Parkinson’s disease ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe a Japanese family with parkinsonism and later-onset dementia. The proband developed parkinsonism at the age of 61 years, followed by dementia starting when she was 67. Her uncle, who was also her husband, died at the age of 78 years after 7- and 5-year histories of parkinsonism and dementia, respectively. Pathological examination of these two patients showed marked neuronal loss with Lewy bodies (LBs) in the brain stem pigmented nuclei and numerous cortical LBs and ubiquitin-positive hippocampal CA2/3 neurites were observed. The proband also had many amyloid plaques. Their two sons developed similar parkinsonism at the ages of 39 and 28 years and also suffered later-onset dementia. The apolipoprotein E genotype of the proband, her uncle and one of their sons was ɛ3/4 and that of the other son was ɛ4/4. These findings strongly suggest that this family has autosomal dominant diffuse LB disease.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Apolipoprotein E gene ; Cortical Lewy body ; Amyloid plaque ; Parkinson’s disease ; Dementia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate whether the apolipoprotein E ɛ4 allele (APOE4) affects cortical neuropathology in Parkinson’s disease (PD), we determined APOE genotypes and quantified the densities of cortical Lewy bodies (LBs), amyloid plaques and neurofibrillary tangles in 22 autopsy-proven PD cases (12 with dementia; 10 without dementia) that were not accompanied by Alzheimer’s disease. The APOE4 frequency in the demented patient group was 0.21, which was significantly higher than that in Japanese controls (P 〈 0.04). LB densities in demented PD patients were significantly higher than those in non-demented PD patients, despite the shorter disease duration in the former. Moreover, plaque density in the temporal cortex and LB density in the cingulate cortex were significantly higher in the group with APOE4 than in that without the allele. There was no difference in tangle density between these two groups. These results suggest that APOE4 may influence the increase in the number of cortical LBs and amyloid plaques in PD. It is possible that when PD occurs in individuals with APOE4, concomitantly evolving cortical LB pathology in a proportion of cases results in limbic (transitional) or neocortical-type LB disease.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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