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<p>Based on the prevailing α-synuclein “gain-of-function” hypothesis, reducing α-synuclein levels and removing its aggregates is a current focus of disease-modifying therapies for Parkinson’s disease. Emerging evidence of α-synuclein “loss-of-function” suggests that it may be necessary to replenish monomeric α-synuclein levels. We propose a personalized and comprehensive approach for different Parkinson’s subgroups based on whether α-synuclein is likely to contribute to disease pathogenesis through a “gain-of-function”, “loss-of-function”, or both mechanisms.</p>

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A personalised and comprehensive approach is required to suppress or replenish SNCA for Parkinson’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月4日

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  • Dunhui Li,
  • Wai Yan Yau,
  • Shengdi Chen,
  • Steve Wilton,
  • Frank Mastaglia

摘要

Based on the prevailing α-synuclein “gain-of-function” hypothesis, reducing α-synuclein levels and removing its aggregates is a current focus of disease-modifying therapies for Parkinson’s disease. Emerging evidence of α-synuclein “loss-of-function” suggests that it may be necessary to replenish monomeric α-synuclein levels. We propose a personalized and comprehensive approach for different Parkinson’s subgroups based on whether α-synuclein is likely to contribute to disease pathogenesis through a “gain-of-function”, “loss-of-function”, or both mechanisms.