發(fā)布時間：2020-12-04 13:31

　　阿爾茨海默病(Alzheimer’s disease,AD)是最常見的中樞神經(jīng)系統(tǒng)退行性疾病,其發(fā)病機制復(fù)雜,至今仍未完全闡明.最近的研究表明,小膠質(zhì)細胞過度激活、炎癥因子的過度產(chǎn)生與AD的發(fā)病密切相關(guān).小膠質(zhì)細胞受體及下游通路的異常調(diào)節(jié)可導(dǎo)致AD患者及AD實驗動物的免疫失衡.天然小分子化合物通過激活小膠質(zhì)細胞的抑炎受體,抑制促炎受體或調(diào)節(jié)Aβ清除受體,可逆轉(zhuǎn)免疫失衡.本文綜述了小膠質(zhì)細胞在AD慢性炎癥中的作用機制,并總結(jié)天然小分子化合物通過調(diào)節(jié)小膠質(zhì)細胞受體及其下游通路在AD免疫穩(wěn)態(tài)中的有益作用. 

【文章來源】：生物化學與生物物理進展. 2020年08期 第712-728頁 北大核心

【文章頁數(shù)】：17 頁

【文章目錄】：
1 The inflammatory response is a key factor in the pathogenesis of Alzheimer’s disease
2 Improper regulation of microglial receptors and their downstream pathways impair immune homeostasis in AD
    2.1 Increase release of inflammatory cytokines via activation of microglial pro-inflammatory receptors and their downstream pathways in AD
    2.2 Decrease expression of anti-inflammatory receptors in microglia aggravate the imbalance of inflammatory cytokines in AD
    2.3 Improper regulation of the Aβclearance receptor in microglia promote the progress of AD
3 Natural small-molecule compounds regulate the pathological process of Alzheimer’s disease by maintaining immune homeostasis
    3.1 Natural small-molecule compounds inhibit the activation of microglial pro-inflammatory receptors and their downstream pathways in AD
    3.2 Natural small-molecule compounds activate microglial anti-inflammatory receptors and its downstream pathways in AD
    3.3 Natural small-molecule compounds show its benefit effects through regulate the receptors involved in Aβclearance in AD
4 Summary and prospect


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碩士論文
[1]Trem2激活促進抗炎和自噬改善阿爾茨海默病行為學的研究[D]. 辜敏.重慶醫(yī)科大學 2016
[2]吳茱萸堿對阿爾茨海默病模型大鼠HMGB1/TLR4/NF-κB信號通路的研究[D]. 孫文蕾.河北醫(yī)科大學 2015
[3]蛇床子素對阿爾茨海默病模型大鼠認知障礙的神經(jīng)保護作用及其機制研究[D]. 鄭為娜.河北醫(yī)科大學 2015



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