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
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.