Journal
SCIENCE
Volume 287, Issue 5456, Pages 1265-1269Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.287.5456.1265
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- NIA NIH HHS [AG5131, AG10689, AG11385] Funding Source: Medline
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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.
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