Is there a causal link between inflammation and dementia?

Is there a causal link between inflammation and dementia?
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DOI:
10.1155/2013/316495
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发表时间:
2013
影响因子:
--
通讯作者:
Popescu BO
Popescu BO
中科院分区:
生物学3区
文献类型:
--
作者:
Enciu AM;Popescu BO

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神经炎症是阿尔茨海默病(AD)的常见病,但目前的知识不足以说明炎症是病因、促进因素,还是仅仅是这种不可避免的进行性疾病的次要现象。在当前的论文中,我们回顾了研究数据,表明炎症不是痴呆发病的先决条件,尽管它可能会恶化疾病的进程,但最近的证据表明,慢性抑制炎症通路并不一定对患者有益。抗炎药物的前瞻性临床试验未能阻止疾病进展,患者血清和脑脊液中炎症标志物的测量结果相互矛盾,最近的实验室研究无疑证明了神经炎症也有保护作用。tnfr或ILRs的敲除动物模型似乎不能预防病理或认知能力下降,但恰恰相反。在AD中,对炎症通路的治疗干预仍有研究前景,但其目标可能需要重新评估。
Neuroinflammation is a constant event in Alzheimer's disease (AD), but the current knowledge is insufficient to state whether inflammation is a cause, a promoter, or simply a secondary phenomenon in this inexorably progressive ailment. In the current paper, we review research data showing that inflammation is not a prerequisite for onset of dementia, and, although it may worsen the course of the disease, recent evidence shows that chronic inhibition of inflammatory pathways is not necessarily beneficial for patients. Prospective clinical trials with anti-inflammatory drugs failed to stop disease progression, measurements of inflammatory markers in serum and cerebrospinal fluid of patients yielded contradictory results, and recent bench research proved undoubtedly that neuroinflammation has a protective side as well. Knockout animal models for TNFRs or ILRs do not seem to prevent the pathology or the cognitive decline, but quite the contrary. In AD, the therapeutic intervention on inflammatory pathways still has a research future, but its targets probably need reevaluation.
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