Proposal and Point of View on Targeting α-synuclein for the Treatment of Parkinson's Disease
Issue: 2016 - Volume 6 [Issue 2]
Yong-Peng Yu *
Department of Neurology and Central Laboratory, The Affiliated Weihai Central Hospital of Weifang Medical College, China and Department of Neurology, The Medical College of Qingdao University, China
*Author to whom correspondence should be addressed.
Many scientific studies in the biochemical, genetic fields suggest that there were common mechanisms, such as genes, α-synuclein protein, tau protein, oxidative stress, mitochondrial dysfunction, and iron might be shared in Alzheimer disease (AD) and Parkinson disease (PD). α-synuclein is suggested to have a vital role in the pathogenesis of PD and is a promising therapeutic target. However, gap might always exist between clinical and basic researches. The failure of recent phase III trials of the anti-Amyloid-β (Aβ) monoclonal for AD prompts us to rethink PD therapy strategies. As multiple mechanisms are involved in PD pathogenesis and their relative roles might vary at different stages of this disease. Use of comprehensive prevention strategies and targets at different stages of PD might be a promising way to cure or prevent PD in the future.
Keywords: Alzheimer disease, Parkinson disease, α-synuclein, neurodegeneration, amyloid-β