PPARγ activation prevents impairments in spatial memory and neurogenesis following transient illness.
PPARγ activation prevents impairments in spatial memory and neurogenesis following transient illness.
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DOI:
10.1016/j.bbi.2012.10.017
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发表时间:
2013-03
影响因子:
15.1
通讯作者:
Palmer, Theo D.
中科院分区:
文献类型:
--
作者:
Ormerod, Brandi K.;Hanft, Simon J.;Asokan, Aditya;Haditsch, Ursula;Lee, Star W.;Palmer, Theo D.
关键词:
The detrimental effects of illness on cognition are familiar to virtually everyone. Some effects resolve quickly while others may linger after the illness resolves. We found that a transient immune response stimulated by lipopolysaccharide (LPS) compromised hippocampal neurogenesis and impaired hippocampus-dependent spatial memory. The immune event caused a 50% reduction in the number of neurons generated during the illness and the onset of the memory impairment was delayed and coincided with the time when neurons generated during the illness would have become functional within the hippocampus. Broad spectrum non-steroidal anti-inflammatory drugs attenuated these effects but selective Cox-2 inhibition was ineffective while PPARγ activation was surprisingly effective at protecting both neurogenesis and memory from the effects of LPS-produced transient illness. These data may highlight novel mechanisms behind chronic inflammatory and neuroinflammatory episodes that are known to compromise hippocampus-dependent forms of learning and memory.
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DOI:
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影响因子:
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