| Summary: | Nerve growth factor (NGF) represents a new therapeutic strategy for multiple sclerosis (MS) because of its immunomodulatory and neuroprotective activity. To analyze changes in NGF expression experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats. In the dorsal root ganglia (DRG) of animals with EAE, NGF mRNA and protein increased between 18 - 24 days post induction (dpi) during complete neurological recovery. In the spinal cord (SC) of animals with EAE, NGF mRNA and protein expression increased at 15 dpi and 12 dpi, respectively, to reduce EAE-induced disability. We identified the 25 kDa pro-NGF as a biologically active isoform during EAE. EAE SC axons demonstrate a loss or thinning of myelin which correlated with maximal neurological disability. NGF plays a role in minimizing EAE-induced inflammation and myelin damage to promote neurological recovery. NGF may be an “off switch” for a cytokine-neurotrophin signaling triad to govern the extent of myelin damage.
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