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Pathological changes in dopaminergic nerve cells of the substantia nigra and olfactory bulb in mice transgenic for truncated human alpha-synuclein(1-120): implications for Lewy body disorders.

Dysfunction of the 140 aa protein alpha-synuclein plays a central role in Lewy body disorders, including Parkinson's disease, as well as in multiple system atrophy. Here, we show that the expression of truncated human alpha-synuclein(1-120), driven by the rat tyrosine hydroxylase promoter on a mouse alpha-synuclein null background, leads to the formation of pathological inclusions in the substantia nigra and olfactory bulb and to a reduction in striatal dopamine levels. At the behavioral level, the transgenic mice showed a progressive reduction in spontaneous locomotion and an increased response to amphetamine. These findings suggest that the C-terminal of alpha-synuclein is an important regulator of aggregation in vivo and will help to understand the mechanisms underlying the pathogenesis of Lewy body disorders and multiple system atrophy.

Pubmed ID: 16611810


  • Tofaris GK
  • Garcia Reitböck P
  • Humby T
  • Lambourne SL
  • O'Connell M
  • Ghetti B
  • Gossage H
  • Emson PC
  • Wilkinson LS
  • Goedert M
  • Spillantini MG


The Journal of neuroscience : the official journal of the Society for Neuroscience

Publication Data

April 12, 2006

Associated Grants

  • Agency: Parkinson's UK, Id: G-4039
  • Agency: Medical Research Council, Id: MC_U105184291
  • Agency: NIA NIH HHS, Id: P30 AG10133

Mesh Terms

  • Animals
  • Dopamine
  • Humans
  • Lewy Bodies
  • Lewy Body Disease
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Transgenic
  • Neurons
  • Olfactory Bulb
  • Parkinson Disease
  • Promoter Regions, Genetic
  • Rats
  • Substantia Nigra
  • Tyrosine 3-Monooxygenase
  • alpha-Synuclein