APOLIPOPROTEIN-E EPSILON-4 ALLELE AND PROGRESSION OF CORTICAL LEWY BODY PATHOLOGY IN PARKINSONS-DISEASE

Citation
K. Wakabayashi et al., APOLIPOPROTEIN-E EPSILON-4 ALLELE AND PROGRESSION OF CORTICAL LEWY BODY PATHOLOGY IN PARKINSONS-DISEASE, Acta Neuropathologica, 95(5), 1998, pp. 450-454
Citations number
42
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
95
Issue
5
Year of publication
1998
Pages
450 - 454
Database
ISI
SICI code
0001-6322(1998)95:5<450:AEAAPO>2.0.ZU;2-N
Abstract
To elucidate whether the apolipoprotein E epsilon 4 allele (APOE4) aff ects cortical neuropathology in Parkinson's disease (PD), we determine d APOE genotypes and quantified the densities of cortical Lewy bodies (LBs), amyloid plaques and neurofibrillary tangles in 22 autopsy-prove n PD cases (12 with dementia; 10 without dementia) that were not accom panied by Alzheimer's disease. The APOE4 frequency in the demented pat ient group was 0.21, which was significantly higher than that in Japan ese controls (P < 0.04). LB densities in demented PD patients were sig nificantly higher than those in non-demented PD patients, despite the shorter disease duration in the former. Moreover, plaque density in th e temporal cortex and LB density in the cingulate cortex were signific antly higher in the group with APOE4 than in that without the allele. There was no difference in tangle density between these two groups. Th ese results suggest that APOE4 may influence the increase in the numbe r 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) o r neocortical-type LB disease.