Neurodegenerative diseases [e.g. MS (multiple sclerosis), ALS (amyotrophic lateral sclerosis), and Alzheimer's disease] and traumatic or ischemic CNS injuries [e.g. SCI (spinal cord injury), stroke, TBI (traumatic brain injury)] all elicit neuroinflammatory cascades. Specifically, the collective effects of activated glia, inflammatory cytokines and chemokines, a compromised blood–brain/spinal cord barrier, and infiltrating leukocytes exacerbate axon damage and demyelination, mitochondrial dysfunction, and glial scar formation. The result is a tissue environment that favors cell death and inhibits mechanisms of endogenous repair (Norenberg et al., 2004; Fleming et al., 2006; Popovich and Longbrake, 2008). Since mature CNS neurons are post-mitotic and regenerate poorly, the destructive effects of trauma, disease and neuroinflammation render affected individuals permanently disabled.
