Abstract
The link between peripheral inflammation and neuropsychiatric disorders has gained momentum in the recent past. Although the sequalae of peripheral inflammation leading to clinical symptomology is unclear, it is becoming apparent that microglia and neuroinflammation play a critical role in the pathophysiology of such disorders. To model the consequences of elevated inflammation, we challenged mice peripherally with LPS and polyI:C to study effects on brain neuroinflammation.
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