Overview
- Case Western Reserve researchers identified aberrant binding between alpha‑synuclein and the mitochondrial enzyme ClpP that undermines neuronal health.
- The team designed a decoy compound, CS2, to divert alpha‑synuclein from ClpP and restore mitochondrial function.
- Across human brain tissue, patient‑derived neurons, and mouse models, CS2 improved movement and cognitive measures while reducing brain inflammation.
- The findings were published in Molecular Neurodegeneration in 2025 (DOI: 10.1186/s13024-025-00918-w).
- Researchers are now optimizing the candidate and planning safety, efficacy, and biomarker studies toward possible clinical trials within roughly five years.