A molecular pathway of neurodegeneration linking α-synuclein to ApoE and Aβ peptides

In transgenic mice, α-synuclein induced neurodegeneration involves activation of the ubiquitin/proteasome system, a massive increase in apolipoprotein E levels and accumulation of insoluble mouse Aβ

Gilbert Gallardo; Oliver M Schlüter; Thomas C Südhof

2008

Scholarcy highlights

  • Pathogenic aggregates of α-synuclein are thought to contribute to the development of Parkinson's disease
  • Inclusion bodies containing α-synuclein are present in Parkinson's disease and other neurodegenerative diseases, including Alzheimer's disease
  • Α-synuclein mutations are found in cases of familial Parkinson's disease, and transgenic overexpression of α-synuclein causes neurodegeneration in mice
  • Our data reveal a molecular link between central pathogenic mechanisms implicated in Parkinson's disease and Alzheimer's disease and suggest that intracellular α-synuclein is pathogenic, at least in part, by activation of extracellular signaling pathways involving apolipoprotein E

Need more features? Save interactive summary cards to your Scholarcy Library.