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.
Palmer, Theo D.
中科院分区:
医学1区
文献类型:
--
作者:
Ormerod, Brandi K.;Hanft, Simon J.;Asokan, Aditya;Haditsch, Ursula;Lee, Star W.;Palmer, Theo D.

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疾病对认知的有害影响几乎是每个人都熟悉的。有些影响很快就会消失,而另一些影响可能在疾病消退后仍然存在。我们发现,脂多糖(LPS)刺激的短暂免疫反应损害了海马神经发生,损害了海马依赖的空间记忆。免疫事件导致患病期间产生的神经元数量减少50%,记忆障碍的发生被推迟,与患病期间产生的神经元在海马体中发挥作用的时间一致。广谱非甾体抗炎药可减轻这些作用,但选择性Cox-2抑制无效,而PPARγ激活在保护神经发生和记忆免受lps产生的短暂性疾病的影响方面令人惊讶地有效。这些数据可能突出了慢性炎症和神经炎症发作背后的新机制,这些炎症和神经炎症发作已知会损害海马依赖的学习和记忆形式。
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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