Neuroinflammation in Alzheimer's disease.
Neuroinflammation in Alzheimer's disease.
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DOI：
10.1016/s1474-4422(15)70016-5
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发表时间：
2015-04
期刊：
影响因子：
--
通讯作者：
Kummer MP
中科院分区：
文献类型：
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作者：
Heneka MT;Carson MJ;El Khoury J;Landreth GE;Brosseron F;Feinstein DL;Jacobs AH;Wyss-Coray T;Vitorica J;Ransohoff RM;Herrup K;Frautschy SA;Finsen B;Brown GC;Verkhratsky A;Yamanaka K;Koistinaho J;Latz E;Halle A;Petzold GC;Town T;Morgan D;Shinohara ML;Perry VH;Holmes C;Bazan NG;Brooks DJ;Hunot S;Joseph B;Deigendesch N;Garaschuk O;Boddeke E;Dinarello CA;Breitner JC;Cole GM;Golenbock DT;Kummer MP
越来越多的证据表明，阿尔茨海默病的发病机制并不局限于神经元区室，但强烈的相互作用与免疫机制在大脑中。错误折叠和聚集的蛋白质与微胶质细胞和星形胶质细胞上的模式识别受体结合，并触发先天免疫反应，其特征在于释放炎症介质，这有助于疾病的进展和严重程度。全基因组分析表明，几个基因，这增加了散发性阿尔茨海默病的风险编码因子，调节胶质细胞清除错误折叠的蛋白质和炎症反应。包括全身性炎症和肥胖在内的外部因素可能会干扰大脑的免疫过程，并进一步促进疾病进展。这一回顾提供了对当前知识的概述，并侧重于最新和令人兴奋的发现。风险因素的调节和所述免疫机制的干预可能会导致未来阿尔茨海默病的预防或治疗策略。
Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment but strongly interacts with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on micro- and astroglia and trigger an innate immune response, characterized by the release of inflammatory mediators, which contribute to disease progression and severity. Genome wide analysis suggests that several genes, which increase the risk for sporadic Alzheimer's disease en-code for factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity are likely to interfere with the immunological processes of the brain and further promote disease progression. This re-view provides an overview on the current knowledge and focuses on the most recent and exciting findings. Modulation of risk factors and intervention with the described immune mechanisms are likely to lead to future preventive or therapeutic strategies for Alzheimer's disease.