Therapeutic effects of telomerase-derived peptide GV1001 in experimental autoimmune encephalomyelitis: inhibiting neuroinflammation and promoting remyelination

GV1001, a peptide derived from human telomerase reverse transcriptase, exhibits anti-cancer and anti-inflammatory actions, yet its impact on experimental autoimmune encephalomyelitis (EAE)—an established mouse model of multiple sclerosis—remains unknown. This study assessed the therapeutic potential and mechanism of GV1001 in EAE. Subcutaneous administration of GV1001 reduced clinical scores, inflammatory cytokine transcripts, and spinal cord pathology in EAE mice. Spinal cord RNA-seq showed that GV1001 suppressed immune and neuroinflammatory genes, particularly in microglia. Experiments in cultured mouse and human glia cells identified microglia as the principal cellular target. Mechanistically, GV1001 increased the NF-κB antagonist PRMT1 and boosted microglial insulin-like growth factor-1, promoting oligodendrocyte progenitor cell survival and maturation. Co-culture assays confirmed that GV1001 blunts microglial neurotoxicity and facilitates remyelination during inflammation. Collectively, the data indicate that GV1001 modulates microglial activity to attenuate neuroinflammation and foster spinal cord repair, underscoring its promise as a multitarget therapy for inflammatory demyelinating diseases such as multiple sclerosis.