文献类型：期刊文献

英文题名：Psychosocial stress on neuroinflammation and cognitive dysfunctions in Alzheimer's disease: the emerging role for microglia?

作者：Piirainen, Sami[1];Youssef, Andrew[1];Song, Cai[2,3];Kalueff, Allan V.[2,4,5,6];Landreth, Gary E.[7];Malm, Tarja[8];Tian, Li[1,9,10]

机构：[1]Univ Helsinki, Neurosci Ctr, HiLIFE, Viikinkaari 4, FIN-00014 Helsinki, Finland;[2]Guangdong Ocean Univ, Coll Food Sci & Technol, Key Lab Aquat Prod Proc & Safety, Res Inst Marine Drugs & Nutr, Zhanjiang 524088, Peoples R China;[3]Dalhousie Univ, Dept Psychol & Neurosci, Life Sci Ctr, 1355 Oxford St, Halifax, NS B3H4R2, Canada;[4]St Petersburg State Univ, Inst Translat Biomed, St Petersburg 199034, Russia;[5]Ural Fed Univ, Ekaterinburg 620002, Russia;[6]ZENEREI Res Ctr, Slidell, LA 70458 USA;[7]Case Western Reserve Univ, Sch Med, Dept Neurosci, Alzheimer Res Lab, Cleveland, OH 44106 USA;[8]Univ Eastern Finland, AI Virtanen Inst Mol Sci, Neulaniementie 2, Kuopio 70150, Finland;[9]Zhejiang Univ Univ Edinburgh Joint Inst, 718 East Haizhou Rd, Haining 314400, Zhejiang, Peoples R China;[10]Peking Univ, Beijing Huilongguan Hosp, Psychiat Res Ctr, Beijing 100096, Peoples R China

年份：2017

卷号：77

起止页码：148

外文期刊名：NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS

收录：SSCI(收录号：WOS:000401973800012)、SCI-EXPANDED(收录号：WOS:000401973800012)、、Scopus(收录号：2-s2.0-85016435120)、WOS

基金：LT is supported by the Academy of Finland projects 1273108 and 1283085, National Natural Science Foundation of China project 81461130016, European Commission FP7/Cooperation sub-programme/HEALTH-2013-Innovation Grant 602919 and Magnus Ehrnrooth Foundation. SP is supported by the Brain & Mind doctoral program of the University of Helsinki. AY is supported by the Centre for International Mobility (CIMO) fellowship. TM is supported by the Academy of Finland and Emil Aaltonen foundation. CS is supported by National Natural Science Foundation of China project 81471223 and 81171118, as well as Taiwan MOST 103-2320-B-039-041-MY3. AVK is the President of the International Stress and Behavior Society (ISBS), and his lab is supported by St. PetersburgState University internal funds. His research is supported by the Russian Foundation for Basic Research (RFBR) grant 16-04-00851. GL is supported by NIH R01 AG043522. The authors did not receive any specific grants from funding agencies for preparation of this manuscript.

语种：英文

外文关键词：Late-onset Alzheimer's disease; Psychosocial stress; Microglia; Amyloid clearance; Dementia

外文摘要：Chronic psychosocial stress is increasingly recognized as a risk factor for late-onset Alzheimer's disease (LOAD) and associated cognitive deficits. Chronic stress also primes microglia and induces inflammatory responses in the adult brain, thereby compromising synapse-supportive roles of microglia and deteriorating cognitive functions during aging. Substantial evidence demonstrates that failure of microglia to clear abnormally accumulating amyloid-beta (A beta) peptide contributes to neuroinflammation and neurodegeneration in AD. Moreover, genome-wide association studies have linked variants in several immune genes, such as TREM2 and CD33, the expression of which in the brain is restricted to microglia, with cognitive dysfunctions in LOAD. Thus, inflammation-promoting chronic stress may create a vicious cycle of aggravated microglial dysfunction accompanied by increased A beta accumulation, collectively exacerbating neurodegeneration. Surprisingly, however, little is known about whether and how chronic stress contributes to microglia-mediated neuroinflammation that may underlie cognitive impairments in AD. This review aims to summarize the currently available clinical and preclinical data and outline potential molecular mechanisms linking stress, microglia and neurodegeneration, to foster future research in this field. (C) 2017 Elsevier Ltd. All rights reserved.