[Inflammation and neuroregeneration--professor accession].

Brain inflammatory responses exert dual roles leading to acute removal of debris and protracted (secondary) neurodegeneration and apoptosis. Proinflammatory mechanisms involve cytokines, oxidants, enzymes, and toxins that sustain pathology and that impede neural stem cell activation and regeneration. Nevertheless, the phase of secondary damage represents a window of opportunity for neuroprotective intervention. However, agents modulating a single target have failed. The multifaceted pathophysiology points towards a drug with pleiotropic, neuroprotective effects and/or abilities to activate neurogenesis.