Regular paper

Acta Neuropathologica

, Volume 95, Issue 5, pp 450-454

First online:

Apolipoprotein E ε4 allele and progression of cortical Lewy body pathology in Parkinson’s disease

  • K. WakabayashiAffiliated withBrain Disease Research Center, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan Tel.: 81-25-223-6161, ext. 5221; Fax: 81-25-223-7503; e-mail: koichi@bri.niigata-u.ac.jp
  • , Akiyoshi KakitaAffiliated withDepartment of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Shintaro HayashiAffiliated withDepartment of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Kaoru OkuizumiAffiliated withDepartment of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Osamu OnoderaAffiliated withDepartment of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Hajime TanakaAffiliated withDepartment of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Atsushi IshikawaAffiliated withDepartment of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Shoji TsujiAffiliated withDepartment of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan
  • , Hitoshi TakahashiAffiliated withDepartment of Pathology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951-8585, Japan

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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.

Key words Apolipoprotein E gene Cortical Lewy body Amyloid plaque Parkinson’s disease Dementia