Can inflammation be resolved in Alzheimer's disease?
Can inflammation be resolved in Alzheimer's disease?
复制标题
阿尔茨海默病的炎症可以得到解决吗？
DOI：
10.1177/1756286418791107
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发表时间：
2018
影响因子：
5.9
通讯作者：
Hjorth E
中科院分区：
文献类型：
--
作者：
Zhu M;Wang X;Sun L;Schultzberg M;Hjorth E
阿尔茨海默病(AD)是一种以进行性记忆丧失和痴呆为特征的神经退行性疾病。越来越多的证据表明，炎症参与了AD的发病机制。流行病学研究表明，抗炎药物的使用与AD的发病率较低有关。然而，抗炎药的临床试验并不成功。最近的研究表明，炎症是通过一组脂质介质介导的过程来解决的，这些介质被称为专门的促分解脂介质(SPM)。与通常涉及抑制炎症介质合成的抗炎策略不同，刺激炎症消退的目的是以与正常生理条件下类似的方式结束炎症。我们之前已经证明，AD患者的解决途径受到损害。此外，我们在体外研究中发现，SPMS可以改善神经元存活，增加小胶质细胞对淀粉样β蛋白(Aβ)的吞噬能力，提示刺激炎症消退可能是AD潜在的治疗靶点。在这篇综述中，我们总结了关于AD炎症消退的最新发现。我们还讨论了刺激AD炎症消退的可能策略，特别是关注信号通路，包括SPM、它们的受体和参与它们形成的酶。
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss and dementia. Accumulating evidence suggests that inflammation is involved in the pathogenesis of AD. Epidemiological studies suggest that use of anti-inflammatory drugs is associated with a lower incidence of AD. However, clinical trials with anti-inflammatory drugs have not been successful. Recent studies have shown that inflammation is resolved by a process that is mediated by a group of lipid mediators, so called specialized pro-resolving lipid mediators (SPMs). Unlike anti-inflammatory strategies, which usually involve inhibition of the synthesis of inflammatory mediators, stimulating the resolution of inflammation is aimed at ending inflammation in a similar fashion as under normal physiological conditions. We have previously shown that pathways of resolution are impaired in AD. Moreover, we found that SPMs can improve neuronal survival and increase microglial phagocytosis of amyloid beta (Aβ) in in vitro studies, indicating that stimulating resolution of inflammation may be a potential therapeutic target in AD. In this review, we summarize recent findings regarding resolution of inflammation in AD. We also discuss possible strategies to stimulate the resolution of inflammation in AD, specifically focusing on signaling pathways, including SPMs, their receptors and enzymes involved in their formation.
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DOI：
10.4049/jimmunol.1600837
发表时间：
2016-12-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Colas RA;Dalli J;Chiang N;Vlasakov I;Sanger JM;Riley IR;Serhan CN
通讯作者：
Serhan CN
DOI：
10.1074/jbc.r117.783076
发表时间：
2017-07-28
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Asatryan A;Bazan NG
通讯作者：
Bazan NG
DOI：
10.1096/fj.201600677rr
发表时间：
2017-01
期刊：
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
影响因子：
--
作者：
Famenini S;Rigali EA;Olivera-Perez HM;Dang J;Chang MT;Halder R;Rao RV;Pellegrini M;Porter V;Bredesen D;Fiala M
通讯作者：
Fiala M
影响因子：
6.3
作者：
COOPER, AL;GIBBONS, L;ROTHWELL, NJ
通讯作者：
ROTHWELL, NJ
影响因子：
168.9
作者：
Cagnin, A;Brooks, DJ;Banati, RB
通讯作者：
Banati, RB