Brain Inflammation and the Neuronal Fate: from Neurogenesis to Neurodegeneration

Abstract Inflammation is a self-defensive reaction that may develop into a chronic state and become a causative factor in the pathogenesis of a broad range of disabling diseases. Similar to peripheral inflammation, brain inflammation is increasingly being viewed as a target for treating neurological diseases, not only infectious and immune-mediated disorders such as meningitis or multiple sclerosis but also stroke, trauma, and neurodegenerative diseases that were originally not considered to be inflammatory. Microglial cells, the resident macrophages of brain parenchyma, are generally viewed as major sources of pro-inflammatory and potentially neurotoxic molecules in the damaged brain, However, a direct link between activated microglia and tissue damage has not been univocally demonstrated in vivo, and recent studies have rather documented exacerbation of injury following selective microglial ablation or anti-inflammatory treatments. Recent studies have implicated inflammation in the regulation of adult neurogenesis, thus broadening the therapeutic potential of strategies aimed at controlling neuroinflammation. This chapter summarizes the main evidence supporting both detrimental and protective roles of inflammation in acute and chronic brain diseases.