期刊
RADIATION RESEARCH
卷 173, 期 1, 页码 49-61出版社
RADIATION RESEARCH SOC
DOI: 10.1667/RR1821.1
关键词
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资金
- NIH [AG11370, CA133483, NS056678, CA122318]
- H. Parker Neuroscience Fund of Wake Forest University Health Sciences
- Elekta, Inc.
- NATIONAL CANCER INSTITUTE [R01CA133483, R01CA122318] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [F31NS056678] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG011370] Funding Source: NIH RePORTER
Cognitive dysfunction develops in approximately 50% of patients who receive fractionated whole-brain irradiation and survive 6 months or more. The mechanisms underlying these deficits are unknown. A recent study demonstrated that treatment with the angiotensin 11 type I receptor antagonist (AT(1)RA) L-158,809 before, during and after fractionated whole-brain irradiation prevents or ameliorates radiation-induced cognitive deficits in adult rats. Given that (1) AT(1)RAs may function as anti-inflammatory drugs, (2) inflammation is thought to contribute to radiation injury, and (3) radiation-induced inflammation alters progenitor cell populations, we tested whether the cognitive benefits of L-158,809 treatment were associated with amelioration of the sustained neuroinflammation and changes in neurogenesis that are induced by fractionated whole-brain irradiation. In rats examined 28 and 54 weeks after irradiation, L-158,809 treatment did not alter the effects of radiation on the number and activation of microglia in the perirhinal cortex and hippocampus, nor did it prevent the radiation-induced decrease in proliferating cells and immature neurons in the hippocampus. These findings suggest that L-158,809 does not prevent or ameliorate radiation-induced cognitive deficits by modulation of chronic inflammatory mechanisms, but rather may reduce radiation-induced changes that occur earlier in the postirradiation period and that lead to cognitive dysfunction. (C) 2010 by Radiation Research Society
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