November 11, 2003 | Christine T. Ekdahl*, Jan-Hendrik Claassen*, Sara Bonde*, Zaal Kokaia*, and Olle Lindvall**
The study by Ekdahl et al. investigates the detrimental effects of inflammation on neurogenesis in the adult hippocampus. They demonstrate that lipopolysaccharide (LPS)-induced inflammation, which activates microglia in the area where new neurons are generated, significantly impairs basal hippocampal neurogenesis in rats. This impairment is also observed when neurogenesis is triggered by a brain insult, such as status epilepticus (SE). The number of new neurons is reduced by 85% in the subgranular zone (SGZ) of the dentate gyrus (DG) due to inflammation. Systemic administration of minocycline, a microglia-specific inhibitor, effectively restores neurogenesis suppressed by inflammation. The study suggests that activated microglia may contribute to cognitive dysfunction in conditions like aging, dementia, and epilepsy by suppressing hippocampal neurogenesis.The study by Ekdahl et al. investigates the detrimental effects of inflammation on neurogenesis in the adult hippocampus. They demonstrate that lipopolysaccharide (LPS)-induced inflammation, which activates microglia in the area where new neurons are generated, significantly impairs basal hippocampal neurogenesis in rats. This impairment is also observed when neurogenesis is triggered by a brain insult, such as status epilepticus (SE). The number of new neurons is reduced by 85% in the subgranular zone (SGZ) of the dentate gyrus (DG) due to inflammation. Systemic administration of minocycline, a microglia-specific inhibitor, effectively restores neurogenesis suppressed by inflammation. The study suggests that activated microglia may contribute to cognitive dysfunction in conditions like aging, dementia, and epilepsy by suppressing hippocampal neurogenesis.