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α-Synuclein accumulates in Lewy bodies in Parkinson's disease and dementia with Lewy bodies but not in Alzheimer's disease β-amyloid plaque cores

  • Thomas A. Bayer
  • , Pekka Jäkälä
  • , Tobias Hartmann
  • , Laszlo Havas
  • , Catriona McLean
  • , Janetta G. Culvenor
  • , Qiao Xin Li
  • , Colin L. Masters
  • , Peter Falkai
  • , Konrad Beyreuther

Research output: Contribution to journalArticleResearchpeer-review

Abstract

A growing body of evidence suggests that the non-Aβ component of Alzheimer's disease amyloid precursor protein (NACP) or α-synuclein contributes to the neurodegenerative processes in Alzheimer's disease (AD), Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In the present study antisera to the N terminus and the NAC domain of the αsynuclein protein were employed to elucidate the expression pattern in brains of patients with AD, PD, DLB and control specimen, α-Synuclein exhibited an overall punctuate expression profile compatible with a synaptic function. Interestingly, while Lewy bodies were strongly immunoreactive, none of the α-synuclein antisera revealed staining in mature βamyloid plaques in AD. These observations suggest that α-synuclein does not contribute to late neurodegenerative processes in AD brains.

Original languageEnglish
Pages (from-to)213-216
Number of pages4
JournalNeuroscience Letters
Volume266
Issue number3
DOIs
Publication statusPublished - 14 May 1999
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Alzheimer's disease
  • Lewy bodies
  • Parkinson
  • Post-mortem human brain
  • Senile plaques

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