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

Science (New York, N.Y.) | Feb 18, 2000

http://www.ncbi.nlm.nih.gov/pubmed/10678833

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 RIS Download

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

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Associated grants

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

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