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Cranial radiation therapy causes a progressive decline in cognitivefunction that is linked to impaired neurogenesis. Chronic inflammationaccompanies radiation injury, suggesting that inflammatory processesmay contribute to neural stem cell dysfunction. Here, we showthat neuroinflammation alone inhibits neurogenesis and thatinflammatory blockade with indomethacin, a common nonsteroidalanti-inflammatory drug, restores neurogenesis after endotoxin-inducedinflammation and augments neurogenesis after cranial irradiation.
Stanford University, Department of Neurosurgery, MSLS P309, Mail Code 5487, 1201 Welch Road, Stanford, CA 943055487, USA.
* To whom correspondence should be addressed. E-mail: tpalmer{at}stanford.edu
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