Inhibition of Neuroinflammation & Neurodegeneration by a Selective Inhibitor of Mitochondrial Pathological Fission

Time: 12:00 pm
day: Day Two


  • Examining mitochondrial dysfunction as a key pathology in ALS
  • Evaluating how excessive mitochondrial fragmentation, seen in patient-derived cells and in a mouse model of the disease, can be blocked by inhibiting the interaction of the mitochondrial fission enzyme, dynamin related protein 1 (Drp1), and one of its adaptors on the mitochondrial surface, Fis1
  • Observing how P110, a heptapeptide inhibitor of this Drp1/Fis1 interaction that we have rationally designed, selectively inhibits mitochondrial fragmentation and dysfunction in the above models, inhibits microglial and astrocytes activation and neuroinflammation and improves the clinical symptoms in ALS mice, without causing any toxicity in healthy mice