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首页> 外文期刊>Journal of neuroimmune pharmacology: the official journal of the Society on NeuroImmune Pharmacology >Non-steroidal anti-inflammatory drugs and cognitive function: Are prostaglandins at the heart of cognitive impairment in dementia and delirium?
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Non-steroidal anti-inflammatory drugs and cognitive function: Are prostaglandins at the heart of cognitive impairment in dementia and delirium?

机译:非甾体类抗炎药和认知功能:前列腺素是否在痴呆和ir妄的认知障碍中处于核心地位?

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Studies of non-steroidal anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis imply that inflammation is important in the development of Alzheimer's disease (AD). However, these drugs have not alleviated the symptoms of AD in those who have already developed dementia. This suggests that the primary mediator targeted by these drugs, PGE2, is not actively suppressing memory function in AD. Amyloid-β oligomers appear to be important for the mild cognitive changes seen in AD transgenic mice, yet amyloid immunotherapy has also proven unsuccessful in clinical trials. Collectively, these findings indicate that NSAIDs may target a prodromal process in mice that has already passed in those diagnosed with AD, and that synaptic and neuronal loss are key determinants of cognitive dysfunction in AD. While the role of inflammation has not yet become clear, inflammatory processes definitely have a negative impact on cognitive function during episodes of delirium during dementia. Delirium is an acute and profound impairment of cognitive function frequently occurring in aged and demented patients exposed to systemic inflammatory insults, which is now recognised to contribute to longterm cognitive decline. Recent work in animal models is beginning to shed light on the interactions between systemic inflammation and CNS pathology in these acute exacerbations of dementia. This review will assess the role of prostaglandin synthesis in the memory impairments observed in dementia and delirium and will examine the relative contribution of amyloid, synaptic and neuronal loss. We will also discuss how understanding the role of inflammatory mediators in delirious episodes will have major implications for ameliorating the rate of decline in the demented population.
机译:类风湿关节炎中非甾体类抗炎药(NSAIDs)的研究表明,炎症在阿尔茨海默氏病(AD)的发展中很重要。但是,这些药物并没有减轻痴呆症患者的AD症状。这表明这些药物靶向的主要介质PGE2并未积极抑制AD的记忆功能。淀粉样蛋白-β寡聚物似乎对AD转基因小鼠所见的轻度认知变化很重要,但是淀粉样蛋白免疫疗法在临床试验中也被证明是不成功的。总的来说,这些发现表明,NSAIDs可能靶向已经诊断患有AD的小鼠中已经通过的小鼠的前驱过程,并且突触和神经元丢失是AD认知功能障碍的关键决定因素。尽管炎症的作用尚未明确,但炎症过程无疑会对痴呆症中ir妄发作期间的认知功能产生负面影响。 r妄是急性和严重的认知功能损害,常发生于遭受全身性炎症损害的老年和痴呆患者中,现已公认可导致长期的认知功能下降。在动物模型中的最新工作开始阐明在这些急性痴呆症中全身性炎症与中枢神经系统病理之间的相互作用。这项审查将评估前列腺素合成在痴呆和del妄中观察到的记忆障碍中的作用,并将检查淀粉样蛋白,突触和神经元丢失的相对作用。我们还将讨论理解炎症介质在精神错乱发作中的作用将如何对改善痴呆人群的下降速度产生重大影响。

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