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Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders.

To elucidate the role of the synaptic protein alpha-synuclein in neurodegenerative disorders, transgenic mice expressing wild-type human alpha-synuclein were generated. Neuronal expression of human alpha-synuclein resulted in progressive accumulation of alpha-synuclein-and ubiquitin-immunoreactive inclusions in neurons in the neocortex, hippocampus, and substantia nigra. Ultrastructural analysis revealed both electron-dense intranuclear deposits and cytoplasmic inclusions. These alterations were associated with loss of dopaminergic terminals in the basal ganglia and with motor impairments. These results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions.

Pubmed ID: 10678833


  • Masliah E
  • Rockenstein E
  • Veinbergs I
  • Mallory M
  • Hashimoto M
  • Takeda A
  • Sagara Y
  • Sisk A
  • Mucke L


Science (New York, N.Y.)

Publication Data

February 18, 2000

Associated Grants

  • Agency: NIA NIH HHS, Id: AG10689
  • Agency: NIA NIH HHS, Id: AG11385
  • Agency: NIA NIH HHS, Id: AG5131

Mesh Terms

  • Animals
  • Brain
  • Dopamine
  • Humans
  • Inclusion Bodies
  • Lewy Bodies
  • Lewy Body Disease
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Mice, Transgenic
  • Microscopy, Electron
  • Motor Activity
  • Nerve Tissue Proteins
  • Neurodegenerative Diseases
  • Neurons
  • Substantia Nigra
  • Synucleins
  • Tyrosine 3-Monooxygenase
  • Ubiquitins
  • alpha-Synuclein