Is There a Causal Link between Inflammation and Dementia?

被引:36
作者
Enciu, Ana-Maria [1 ]
Popescu, Bogdan O. [2 ,3 ]
机构
[1] Carol Davila Univ Med & Pharm, Sch Med, Dept Cellular & Mol Med, Bucharest 050474, Romania
[2] Carol Davila Univ Med & Pharm, Dept Neurol, Colentina Clin Hosp CDPC, Sch Med, Bucharest 020125, Romania
[3] Victor Babes Natl Inst Pathol, Mol Med Lab, Bucharest 050096, Romania
关键词
INTERLEUKIN-1 RECEPTOR ANTAGONIST; MILD COGNITIVE IMPAIRMENT; TRANSGENIC MOUSE MODEL; NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTORS; ALZHEIMERS-DISEASE; CEREBROSPINAL-FLUID; TNF-ALPHA; HUMAN BRAIN; VITAMIN-E;
D O I
10.1155/2013/316495
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
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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页数:6
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