http://www.sciencedirect.com/science/article/pii/S0889159112004308
Abstract
Before
the 1990s it was widely believed that the adult brain was incapable of
regenerating neurons. However, it is now established that new neurons
are continuously produced in the dentate gyrus of the hippocampus and
olfactory bulb throughout life. The functional significance of adult
neurogenesis is still unclear, but it is widely believed that the new
neurons contribute to learning and memory and/or maintenance of brain
regions by replacing dead or dying cells. Many different factors are
known to regulate adult neurogenesis including immune responses and
signaling molecules released by immune cells in the brain. While immune
activation (i.e., enlargement of microglia, release of cytokines) within
the brain is commonly viewed as a harmful event, the impact of immune
activation on neural function is highly dependent on the form of the
immune response as microglia and other immune-reactive cells in the
brain can support or disrupt brain function depending on the phenotype
and behavior of the cells. For instance, microglia that express an
inflammatory phenotype generally reduce cell proliferation, survival and
function of new neurons whereas microglia displaying an alternative
protective phenotype support adult neurogenesis. The present review
summarizes current understanding of the role of new neurons in cognition
and behavior, with an emphasis on the immune system’s ability to
influence adult hippocampal neurogenesis during both an inflammatory
episode and in the healthy uninjured brain. It has been proposed that
some of the cognitive deficits associated with inflammation may in part
be related to inflammation-induced reductions in adult hippocampal
neurogenesis. Elucidating how the immune system contributes to the
regulation of adult neurogenesis will help in predicting the impact of
immune activation on neural plasticity and potentially facilitate the
discovery of treatments to preserve neurogenesis in conditions
characterized by chronic inflammation.
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