Aβ deposition is associated with enhanced cortical α-synuclein lesions in Lewy body diseases

Olga Pletnikova, Neva West, Michael K. Lee, Gay L. Rudow, Richard L. Skolasky, Ted M. Dawson, Laura Marsh, Juan C. Troncoso

Research output: Contribution to journalArticlepeer-review

169 Scopus citations


In order to understand better the neuropathological substrate of dementia in Parkinson's disease (PD) and to examine its interactions with Alzheimer's disease (AD), we examined autopsy brains from 21 cases of PD and Lewy body disease (LBD) with dementia. We separated brains in two groups according to the presence of Aβ deposits. In brains without Aβ, we found few or no Lewy bodies (LB) in the cerebral cortex. By contrast, in brains with Aβ, we observed significant increases in LB in the cerebral cortex (p < 0.01) and α-synuclein immunoreactive lesions in the cingulate cortex (p < 0.01). Immunoblots of α-synuclein from cingulate cortex in brains with Aβ showed significantly higher levels of insoluble α-synuclein compared to brains without Aβ. Our observations indicate that in cases of PD with dementia, the neocortex is not necessarily involved by LB. Furthermore, the presence of Aβ deposits in the cerebral cortex was associated with extensive α-synuclein lesions and higher levels of insoluble α-synuclein. This suggests that Aβ enhances the development of cortical α-synuclein lesions in cases of PD.

Original languageEnglish (US)
Pages (from-to)1183-1192
Number of pages10
JournalNeurobiology of aging
Issue number8
StatePublished - Aug 2005


  • Alzheimer's
  • Dementia
  • LBD
  • Lewy body disease
  • Lewy neurites
  • PD
  • Parkinson's disease

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology


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