science
Preprint identifies NaV1.7 pathway behind pain in Parkinson’s model
A bioRxiv preprint reports that brain-originating dopaminergic neurodegeneration can produce persistent NaV1.7-dependent hyperexcitability in peripheral sensory neurons in a preclinical Parkinson’s model. Blocking NaV1.7 or disrupting its CRMP2 regulation reduced pain-like behaviours, while human Parkinson’s DRG profiling found related excitability-gene changes.