摘要

The discovery of mutations in hereditary forms of Parkinson's disease has implicated aggregation of alpha-synuclein, dysfunction of protein turnover and mitochondrial dysfunction as important mediators in the pathogenesis of Parkinson's disease. Subsequent studies have shown that these factors also represent hallmarks of idiopathic Parkinson's disease. Cell death mechanisms include excitotoxicity, calcium overload, apoptosis and autophagia. Here, I will briefly review the molecular mechanisms of neurodegeneration in Parkinson's disease and point out potential treatment options.

  • 出版日期2007