Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis

Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression sig...
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Autor*in:	Holtman, Inge R [verfasserIn] Raj, Divya D Miller, Jeremy A Schaafsma, Wandert Yin, Zhuoran Brouwer, Nieske Wes, Paul D Möller, Thomas Orre, Marie Kamphuis, Willem Hol, Elly M Boddeke, Erik W G M Eggen, Bart J L

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	Amyotrophic Lateral Sclerosis Primed Microglia Module Membership rTg4510 Mouse Consensus Network

Anmerkung:	© Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: Acta Neuropathologica Communications - London : Biomed Central, 2013, 3(2015), 1 vom: 23. Mai
Übergeordnetes Werk:	volume:3 ; year:2015 ; number:1 ; day:23 ; month:05

Links:	Volltext

DOI / URN:	10.1186/s40478-015-0203-5

Katalog-ID:	SPR036509515

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520			\|a Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects.
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allfields	10.1186/s40478-015-0203-5 doi (DE-627)SPR036509515 (SPR)s40478-015-0203-5-e DE-627 ger DE-627 rakwb eng Holtman, Inge R verfasserin aut Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213 Raj, Divya D aut Miller, Jeremy A aut Schaafsma, Wandert aut Yin, Zhuoran aut Brouwer, Nieske aut Wes, Paul D aut Möller, Thomas aut Orre, Marie aut Kamphuis, Willem aut Hol, Elly M aut Boddeke, Erik W G M aut Eggen, Bart J L aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Mai (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:05 https://dx.doi.org/10.1186/s40478-015-0203-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 05
spelling	10.1186/s40478-015-0203-5 doi (DE-627)SPR036509515 (SPR)s40478-015-0203-5-e DE-627 ger DE-627 rakwb eng Holtman, Inge R verfasserin aut Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213 Raj, Divya D aut Miller, Jeremy A aut Schaafsma, Wandert aut Yin, Zhuoran aut Brouwer, Nieske aut Wes, Paul D aut Möller, Thomas aut Orre, Marie aut Kamphuis, Willem aut Hol, Elly M aut Boddeke, Erik W G M aut Eggen, Bart J L aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Mai (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:05 https://dx.doi.org/10.1186/s40478-015-0203-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 05
allfields_unstemmed	10.1186/s40478-015-0203-5 doi (DE-627)SPR036509515 (SPR)s40478-015-0203-5-e DE-627 ger DE-627 rakwb eng Holtman, Inge R verfasserin aut Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213 Raj, Divya D aut Miller, Jeremy A aut Schaafsma, Wandert aut Yin, Zhuoran aut Brouwer, Nieske aut Wes, Paul D aut Möller, Thomas aut Orre, Marie aut Kamphuis, Willem aut Hol, Elly M aut Boddeke, Erik W G M aut Eggen, Bart J L aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Mai (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:05 https://dx.doi.org/10.1186/s40478-015-0203-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 05
allfieldsGer	10.1186/s40478-015-0203-5 doi (DE-627)SPR036509515 (SPR)s40478-015-0203-5-e DE-627 ger DE-627 rakwb eng Holtman, Inge R verfasserin aut Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213 Raj, Divya D aut Miller, Jeremy A aut Schaafsma, Wandert aut Yin, Zhuoran aut Brouwer, Nieske aut Wes, Paul D aut Möller, Thomas aut Orre, Marie aut Kamphuis, Willem aut Hol, Elly M aut Boddeke, Erik W G M aut Eggen, Bart J L aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Mai (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:05 https://dx.doi.org/10.1186/s40478-015-0203-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 05
allfieldsSound	10.1186/s40478-015-0203-5 doi (DE-627)SPR036509515 (SPR)s40478-015-0203-5-e DE-627 ger DE-627 rakwb eng Holtman, Inge R verfasserin aut Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213 Raj, Divya D aut Miller, Jeremy A aut Schaafsma, Wandert aut Yin, Zhuoran aut Brouwer, Nieske aut Wes, Paul D aut Möller, Thomas aut Orre, Marie aut Kamphuis, Willem aut Hol, Elly M aut Boddeke, Erik W G M aut Eggen, Bart J L aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 3(2015), 1 vom: 23. Mai (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:3 year:2015 number:1 day:23 month:05 https://dx.doi.org/10.1186/s40478-015-0203-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 3 2015 1 23 05
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source	Enthalten in Acta Neuropathologica Communications 3(2015), 1 vom: 23. Mai volume:3 year:2015 number:1 day:23 month:05
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. 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author	Holtman, Inge R
spellingShingle	Holtman, Inge R misc Amyotrophic Lateral Sclerosis misc Primed Microglia misc Module Membership misc rTg4510 Mouse misc Consensus Network Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
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topic_title	Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Primed Microglia (dpeaa)DE-He213 Module Membership (dpeaa)DE-He213 rTg4510 Mouse (dpeaa)DE-He213 Consensus Network (dpeaa)DE-He213
topic	misc Amyotrophic Lateral Sclerosis misc Primed Microglia misc Module Membership misc rTg4510 Mouse misc Consensus Network
topic_unstemmed	misc Amyotrophic Lateral Sclerosis misc Primed Microglia misc Module Membership misc rTg4510 Mouse misc Consensus Network
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title	Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
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title_full	Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
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author_browse	Holtman, Inge R Raj, Divya D Miller, Jeremy A Schaafsma, Wandert Yin, Zhuoran Brouwer, Nieske Wes, Paul D Möller, Thomas Orre, Marie Kamphuis, Willem Hol, Elly M Boddeke, Erik W G M Eggen, Bart J L
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title_sort	induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
title_auth	Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
abstract	Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects. © Holtman et al.; licensee BioMed Central. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis
url	https://dx.doi.org/10.1186/s40478-015-0203-5
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author2	Raj, Divya D Miller, Jeremy A Schaafsma, Wandert Yin, Zhuoran Brouwer, Nieske Wes, Paul D Möller, Thomas Orre, Marie Kamphuis, Willem Hol, Elly M Boddeke, Erik W G M Eggen, Bart J L
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up_date	2024-07-03T18:03:28.596Z
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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction Microglia are tissue macrophages of the central nervous system that monitor brain homeostasis and react upon neuronal damage and stress. Aging and neurodegeneration induce a hypersensitive, pro-inflammatory phenotype, referred to as primed microglia. To determine the gene expression signature of priming, the transcriptomes of microglia in aging, Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) mouse models were compared using Weighted Gene Co-expression Network Analysis (WGCNA). Results A highly consistent consensus transcriptional profile of up-regulated genes was identified, which prominently differed from the acute inflammatory gene network induced by lipopolysaccharide (LPS). Where the acute inflammatory network was significantly enriched for NF-κB signaling, the primed microglia profile contained key features related to phagosome, lysosome, antigen presentation, and AD signaling. In addition, specific signatures for aging, AD, and ALS were identified. Conclusion Microglia priming induces a highly conserved transcriptional signature with aging- and disease-specific aspects.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Amyotrophic Lateral Sclerosis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Primed Microglia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Module Membership</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">rTg4510 Mouse</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Consensus Network</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Raj, Divya D</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Miller, Jeremy A</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schaafsma, Wandert</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yin, Zhuoran</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brouwer, Nieske</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wes, Paul D</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Möller, Thomas</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Orre, Marie</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kamphuis, Willem</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hol, Elly M</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Boddeke, Erik W G M</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Eggen, Bart J L</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Acta Neuropathologica Communications</subfield><subfield code="d">London : Biomed Central, 2013</subfield><subfield code="g">3(2015), 1 vom: 23. 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Induction of a common microglia gene expression signature by aging and neurodegenerative conditions: a co-expression meta-analysis

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