Neuroinflammation as a Potential Therapeutic Target in Alzheimer?s Disease

被引:44
作者
Liu, Ping [1 ]
Wang, Yunyun [1 ,2 ]
Sun, Yan [1 ]
Peng, Guoping [1 ]
机构
[1] Zhejiang Univ, Affiliated Hosp 1, Dept Neurol, Sch Med, 79 Qingchun Rd, Hangzhou 310003, Zhejiang, Peoples R China
[2] Shengzhou Peoples Hosp, Dept Neurol, Shaoxing, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer?s disease; neuroinflammation; disease-modifying therapy; anti-inflammatory treatment; ATTENUATES SYNAPTIC DYSFUNCTION; CEREBROSPINAL-FLUID; COMMON VARIANTS; DOUBLE-BLIND; MOUSE MODEL; CD33; YKL-40; MEMORY; NSAID; RISK;
D O I
10.2147/CIA.S357558
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Although amyloid-?? (A??) peptide accumulation is considered as a key early event in the pathogenesis of Alzheimer???s disease (AD), the precise pathophysiology of this deadly illness remains unclear and no effective remedies capable of inhibiting disease progression have been discovered. In addition to deposition of extracellular A?? plaques and intracellular neurofibrillary tangles, neuroinflammation has been identified as the third core characteristic crucial in the pathogenesis of AD. More and more evidence from laboratory and clinical studies have suggested that anti-inflammatory treatments could defer or prevent the occurrence of AD. In this review, we will discuss multifaceted evidence of neuroinflammation presented in AD and the newly emerged anti-both in pre-clinical and clinical AD.
引用
收藏
页码:665 / 674
页数:10
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