LPS-induced neuroinflammatory effects do not recover with time

LPS-induced neuroinflammatory effects do not recover with time
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DOI:
10.1097/00001756-200006050-00032
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发表时间:
2000-06-05
期刊:
影响因子:
1.7
通讯作者:
Wenk, GL
Wenk, GL
中科院分区:
医学4区
文献类型:
--
作者:
Hauss-Wegrzyniak, B;Vraniak, PD;Wenk, GL

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炎症过程发生在与阿尔茨海默病(AD)相关的神经病理标志附近,并可能在疾病的进展及其临床表现中发挥作用。我们之前曾报道,将内毒素长期注入大鼠第四脑室,复制了AD患者大脑中的许多炎症和病理变化。在目前的研究中,我们使用相同的动物模型来研究更长时间注射脂多糖的影响,以及这些影响是否可以随着时间的推移而恢复。结果表明,加倍注射内毒素的时间没有增加炎症反应,也没有产生明显更大的行为损害。停止输注脂多糖后等待37天并未降低激活的小胶质细胞密度,也未改善小鼠在Morris水迷宫中的表现。这些结果表明,炎症可能是AD临床表现的致病机制之一。《神经报告》11:1759-1763(C)2000 Lippincott Williams&Wilkins.
Inflammatory processes develop in the vicinity of the neuropathological hallmarks associated with Alzheimer's disease (AD) and may play a role in the progression of the disease and its clinical expression. We have previously reported that chronic infusion of LPS into the fourth ventricle of rat brains reproduced many of the inflammatory and pathological changes seen in the brain of AD patients. In the current study, we used the same animal model to investigate the effects of longer infusion of LPS and whether these effects could recover over time. The results show that doubling the time of LPS infusion did not increased the inflammatory reaction and did not produce a significantly greater behavioral impairment. Waiting for 37 days after the cessation of the LPS infusion did not decrease the density of activated microglia and did not improve performances in the Morris water maze task. The results suggest that inflammation may contribute to the pathogenic mechanisms that underlie the clinical expression of AD. NeuroReport 11:1759-1763 (C) 2000 Lippincott Williams & Wilkins.