AI Article Synopsis
- Over-activated microglia and inflammatory markers are linked to depression, suggesting that targeting microglia could be a new treatment approach.
- The study explores the effects of insulin-like growth factor 2 (IGF2) on microglia activation in response to neuroinflammation, specifically after lipopolysaccharide (LPS) exposure.
- Results indicate that IGF2 treatment reduced microglia over-activation, prevented pro-inflammatory changes, and supported neurogenesis in the hippocampus, offering potential therapeutic strategies for neuropsychiatric disorders.
Article Abstract
Over-activated microglia and inflammatory mediators are found in patients with depression, while manipulation of the microglia function might represent a potential therapeutic strategy. Insulin-like growth factor 2 (IGF2) has been implicated in bacterial infections and autoimmune disorders, but the role of IGF2 on the active phenotype of microglia and neuroinflammation has not been well established. IGF2 influences in modulating microglia responding to neuroinflammation induced by lipopolysaccharide（LPS）challenge will be carefully examined. In the current study, we verified that systemic IGF2 treatment could produce an anti-depression effect in LPS-treated mice. Particularly, we found that systemic IGF2 treatment inhibited microglia over-activation and prevented its transformation to a pro-inflammatory phenotype, thereby protecting hippocampal neurogenesis. Since microglia reactive to neuroinflammation is a common feature of neuropsychiatric disorders, the discoveries from the present study may provide therapeutic innovation for these diseases.
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| http://dx.doi.org/10.1016/j.brainresbull.2023.01.001 | DOI Listing |
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