'Neuroinflammation' differs categorically from inflammation: transcriptomes of Alzheimer's disease, Parkinson's disease, schizophrenia and inflammatory diseases compared

被引:49
作者
Filiou, Michaela D. [1 ]
Arefin, Ahmed Shamsul [2 ]
Moscato, Pablo [2 ]
Graeber, Manuel B. [3 ,4 ]
机构
[1] Max Planck Inst Psychiat, D-80804 Munich, Germany
[2] Univ Newcastle, Ctr Bioinformat Biomarker Discovery & Informat Ba, Hunter Med Res Inst, New Lambton Hts, NSW 2305, Australia
[3] Univ Sydney, Fac Med, Brain & Mind Res Inst, Sydney, NSW 2050, Australia
[4] Univ Sydney, Fac Hlth Sci, Sydney, NSW 2050, Australia
基金
澳大利亚研究理事会;
关键词
Bioinformatics; Inflammation; Microarrays; Microglia; Neurodegeneration; Neuroinflammation; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS PATIENTS; INDUCIBLE CHEMOKINES IP-10; INTERFERON-BETA TREATMENT; CENTRAL-NERVOUS-SYSTEM; REGULATORY T-CELLS; ANTIINFLAMMATORY DRUGS; RECEPTOR EXPRESSION; COMPLEMENT CASCADE; SUBSTANTIA-NIGRA;
D O I
10.1007/s10048-014-0409-x
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
'Neuroinflammation' has become a widely applied term in the basic and clinical neurosciences but there is no generally accepted neuropathological tissue correlate. Inflammation, which is characterized by the presence of perivascular infiltrates of cells of the adaptive immune system, is indeed seen in the central nervous system (CNS) under certain conditions. Authors who refer to microglial activation as neuroinflammation confuse this issue because autoimmune neuroinflammation serves as a synonym for multiple sclerosis, the prototypical inflammatory disease of the CNS. We have asked the question whether a data-driven, unbiased in silico approach may help to clarify the nomenclatorial confusion. Specifically, we have examined whether unsupervised analysis of microarray data obtained from human cerebral cortex of Alzheimer's, Parkinson's and schizophrenia patients would reveal a degree of relatedness between these diseases and recognized inflammatory conditions including multiple sclerosis. Our results using two different data analysis methods provide strong evidence against this hypothesis demonstrating that very different sets of genes are involved. Consequently, the designations inflammation and neuroinflammation are not interchangeable. They represent different categories not only at the histophenotypic but also at the transcriptomic level. Therefore, non-autoimmune neuroinflammation remains a term in need of definition.
引用
收藏
页码:201 / 212
页数:12
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