Gulf War illness (GWI) as a neuroimmune disease
Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi: 10.1007/s00221-017-5010-8 , 2017 ). In a previous study (Georgopoulos et al., J Neural Eng 4:349–355, 2015 ), we identified six protective alleles...
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| creator | Georgopoulos, Apostolos P. James, Lisa M. Carpenter, Adam F. Engdahl, Brian E. Leuthold, Arthur C. Lewis, Scott M. |
| description | Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi:
10.1007/s00221-017-5010-8
,
2017
). In a previous study (Georgopoulos et al., J Neural Eng 4:349–355,
2015
), we identified six protective alleles from Class II human leukocyte antigen (HLA) genes, and more recently, we investigated the brain correlates of this protection (James et al., EBioMedicine 13:72–79,
2016
). Those and other studies (Israeli, Lupus, 21:190–194,
2012
) suggested an involvement of the immune system in GWI. In a recent study (Engdahl et al., EBioMedicine doi:
10.1016/j.ebiom.2016.08.030
,
2016
), we showed that the brain pattern of synchronous neural interactions (SNI; Georgopoulos et al., J Neural Eng 4:349–355,
2007
) in GWI is distinctly different from that in healthy controls. Here we focused on the SNI itself, as a basic measure of neural communication (irrespective of specific connections) and compared it between GWI and seven other diseases that cover a broad spectrum of etiology and pathophysiology. Specifically, we sought to determine which, if any, of those diseases might resemble GWI SNI, overall and within the HLA protective domain, and thus gain further knowledge regarding the nature of GWI brain abnormality. We studied a total of 962 participants from a healthy control population (
N
= 583) and eight different diseases, including GWI (
N
= 40), schizophrenia (SZ;
N
= 21), Alzheimer’s disease (AD;
N
= 66), posttraumatic stress disorder (PTSD;
N
= 159), major depressive disorder (MDD;
N
= 10), relapsing–remitting multiple sclerosis (RRMS;
N
= 43), Sjögren’s syndrome (SS;
N
= 32), and rheumatoid arthritis (RA;
N
= 8). They all underwent a resting-state magnetoencephalographic (MEG) scan to calculate SNIs. Data were analyzed using analysis of covariance (ANCOVA) with disease as fixed factor, and sex and age as covariates. We found that GWI SNIs differed significantly from control SZ, AD, PTSD and MDD but not from RRMS, SS and RA. In addition, we compared GWI to RRMS, SS and RA with respect to SNIs of MEG sensor pairs that were related to the HLA alleles protective for GWI (James et al., EBioMedicine 13:72–79,
2016
). We found that GWI SNIs did not differ significantly from any of these three diseases but they did so from control SZ, AD, PTSD and MDD. These findings indicate that (a) GWI brain synchronicity does not differ significantly from that of known immune-rel |
| doi_str_mv | 10.1007/s00221-017-5050-0 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1925280196</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A505367678</galeid><sourcerecordid>A505367678</sourcerecordid><originalsourceid>FETCH-LOGICAL-c439t-86bcfcca3b4daa692d8fb0ec0bedcc67a585fb489ab2774946cf7bb42a7101003</originalsourceid><addsrcrecordid>eNp1kUtLxTAQhYMoen38ADdScKOL3jtJ0yRdiuhVENwoLkOSTqTShya3C_-9Kdc3ShYhk28OZ-YQckhhTgHkIgIwRnOgMi-hhBw2yIzyguWUgtgkMwDKc65otUN2Y3yanoWEbbLDlBQMynJGFsux9dmDCVnTtj3GmJ0sH65PMxMzk_U4hqHpurHHrG4imoj7ZMubNuLB-71H7i8v7s6v8pvb5fX52U3ueFGtciWs886ZwvLaGFGxWnkL6MBi7ZyQplSlt1xVxjIpecWF89JazoykkGYr9sjJWvc5DC8jxpXumuiwbU2Pwxg1rVjJFNBKJPT4F_o0jKFP7hLF055kpeCLejQt6qb3wyoYN4nqs7S8QkghVaLmf1Dp1Ng1bujRN6n-o4GuG1wYYgzo9XNoOhNeNQU9haTXIekUkp5C0pOVo3fDo-2w_uz4SCUBbA3E9NU_Yvg20b-qb1p8mBs</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1940077980</pqid></control><display><type>article</type><title>Gulf War illness (GWI) as a neuroimmune disease</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Georgopoulos, Apostolos P. ; James, Lisa M. ; Carpenter, Adam F. ; Engdahl, Brian E. ; Leuthold, Arthur C. ; Lewis, Scott M.</creator><creatorcontrib>Georgopoulos, Apostolos P. ; James, Lisa M. ; Carpenter, Adam F. ; Engdahl, Brian E. ; Leuthold, Arthur C. ; Lewis, Scott M.</creatorcontrib><description>Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi:
10.1007/s00221-017-5010-8
,
2017
). In a previous study (Georgopoulos et al., J Neural Eng 4:349–355,
2015
), we identified six protective alleles from Class II human leukocyte antigen (HLA) genes, and more recently, we investigated the brain correlates of this protection (James et al., EBioMedicine 13:72–79,
2016
). Those and other studies (Israeli, Lupus, 21:190–194,
2012
) suggested an involvement of the immune system in GWI. In a recent study (Engdahl et al., EBioMedicine doi:
10.1016/j.ebiom.2016.08.030
,
2016
), we showed that the brain pattern of synchronous neural interactions (SNI; Georgopoulos et al., J Neural Eng 4:349–355,
2007
) in GWI is distinctly different from that in healthy controls. Here we focused on the SNI itself, as a basic measure of neural communication (irrespective of specific connections) and compared it between GWI and seven other diseases that cover a broad spectrum of etiology and pathophysiology. Specifically, we sought to determine which, if any, of those diseases might resemble GWI SNI, overall and within the HLA protective domain, and thus gain further knowledge regarding the nature of GWI brain abnormality. We studied a total of 962 participants from a healthy control population (
N
= 583) and eight different diseases, including GWI (
N
= 40), schizophrenia (SZ;
N
= 21), Alzheimer’s disease (AD;
N
= 66), posttraumatic stress disorder (PTSD;
N
= 159), major depressive disorder (MDD;
N
= 10), relapsing–remitting multiple sclerosis (RRMS;
N
= 43), Sjögren’s syndrome (SS;
N
= 32), and rheumatoid arthritis (RA;
N
= 8). They all underwent a resting-state magnetoencephalographic (MEG) scan to calculate SNIs. Data were analyzed using analysis of covariance (ANCOVA) with disease as fixed factor, and sex and age as covariates. We found that GWI SNIs differed significantly from control SZ, AD, PTSD and MDD but not from RRMS, SS and RA. In addition, we compared GWI to RRMS, SS and RA with respect to SNIs of MEG sensor pairs that were related to the HLA alleles protective for GWI (James et al., EBioMedicine 13:72–79,
2016
). We found that GWI SNIs did not differ significantly from any of these three diseases but they did so from control SZ, AD, PTSD and MDD. These findings indicate that (a) GWI brain synchronicity does not differ significantly from that of known immune-related diseases (RRMS, SS, RA), and (b) that this SNI similarity is present within the HLA-related SNIs. In contrast, GWI SNIs differed significantly from those of the other diseases. We conclude that altered brain communication in GWI likely reflects immune-related processes, as postulated previously (James et al., EBioMedicine 13:72–79,
2016
). By extension, these findings also indicate that functional brain abnormalities in RRMS, SS and RA might be, in part, due to lack of protective HLA alleles as documented for GWI (Georgopoulos et al., EBioMedicine 3:79–85,
2015
).</description><identifier>ISSN: 0014-4819</identifier><identifier>EISSN: 1432-1106</identifier><identifier>DOI: 10.1007/s00221-017-5050-0</identifier><identifier>PMID: 28762055</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease - genetics ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Analysis of covariance ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - physiopathology ; Autoimmune Diseases - genetics ; Autoimmune Diseases - physiopathology ; Biomedical and Life Sciences ; Biomedicine ; Brain - physiopathology ; Brain Diseases - genetics ; Brain Diseases - physiopathology ; Data processing ; Depressive Disorder, Major - genetics ; Depressive Disorder, Major - physiopathology ; Electroencephalography Phase Synchronization - physiology ; Etiology ; Female ; Gulf War ; Gulf War syndrome ; Histocompatibility antigen HLA ; Histocompatibility Antigens Class II - genetics ; Humans ; Immune system ; Magnetoencephalography ; Magnetoencephalography - methods ; Male ; Mental depression ; Mental disorders ; Mental Disorders - genetics ; Mental Disorders - physiopathology ; Middle Aged ; Multiple sclerosis ; Multiple Sclerosis, Relapsing-Remitting - genetics ; Multiple Sclerosis, Relapsing-Remitting - physiopathology ; Neurodegenerative diseases ; Neurology ; Neurosciences ; Organs ; Persian Gulf syndrome ; Persian Gulf Syndrome - classification ; Persian Gulf Syndrome - genetics ; Persian Gulf Syndrome - physiopathology ; Persian Gulf War ; Physiological aspects ; Post traumatic stress disorder ; Research Article ; Rheumatoid arthritis ; Schizophrenia ; Schizophrenia - genetics ; Schizophrenia - physiopathology ; Sjogren's syndrome ; Stress Disorders, Post-Traumatic - genetics ; Stress Disorders, Post-Traumatic - physiopathology ; War</subject><ispartof>Experimental brain research, 2017-10, Vol.235 (10), p.3217-3225</ispartof><rights>Springer-Verlag GmbH Germany (outside the USA) 2017</rights><rights>COPYRIGHT 2017 Springer</rights><rights>Experimental Brain Research is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-86bcfcca3b4daa692d8fb0ec0bedcc67a585fb489ab2774946cf7bb42a7101003</citedby><cites>FETCH-LOGICAL-c439t-86bcfcca3b4daa692d8fb0ec0bedcc67a585fb489ab2774946cf7bb42a7101003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00221-017-5050-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00221-017-5050-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28762055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Georgopoulos, Apostolos P.</creatorcontrib><creatorcontrib>James, Lisa M.</creatorcontrib><creatorcontrib>Carpenter, Adam F.</creatorcontrib><creatorcontrib>Engdahl, Brian E.</creatorcontrib><creatorcontrib>Leuthold, Arthur C.</creatorcontrib><creatorcontrib>Lewis, Scott M.</creatorcontrib><title>Gulf War illness (GWI) as a neuroimmune disease</title><title>Experimental brain research</title><addtitle>Exp Brain Res</addtitle><addtitle>Exp Brain Res</addtitle><description>Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi:
10.1007/s00221-017-5010-8
,
2017
). In a previous study (Georgopoulos et al., J Neural Eng 4:349–355,
2015
), we identified six protective alleles from Class II human leukocyte antigen (HLA) genes, and more recently, we investigated the brain correlates of this protection (James et al., EBioMedicine 13:72–79,
2016
). Those and other studies (Israeli, Lupus, 21:190–194,
2012
) suggested an involvement of the immune system in GWI. In a recent study (Engdahl et al., EBioMedicine doi:
10.1016/j.ebiom.2016.08.030
,
2016
), we showed that the brain pattern of synchronous neural interactions (SNI; Georgopoulos et al., J Neural Eng 4:349–355,
2007
) in GWI is distinctly different from that in healthy controls. Here we focused on the SNI itself, as a basic measure of neural communication (irrespective of specific connections) and compared it between GWI and seven other diseases that cover a broad spectrum of etiology and pathophysiology. Specifically, we sought to determine which, if any, of those diseases might resemble GWI SNI, overall and within the HLA protective domain, and thus gain further knowledge regarding the nature of GWI brain abnormality. We studied a total of 962 participants from a healthy control population (
N
= 583) and eight different diseases, including GWI (
N
= 40), schizophrenia (SZ;
N
= 21), Alzheimer’s disease (AD;
N
= 66), posttraumatic stress disorder (PTSD;
N
= 159), major depressive disorder (MDD;
N
= 10), relapsing–remitting multiple sclerosis (RRMS;
N
= 43), Sjögren’s syndrome (SS;
N
= 32), and rheumatoid arthritis (RA;
N
= 8). They all underwent a resting-state magnetoencephalographic (MEG) scan to calculate SNIs. Data were analyzed using analysis of covariance (ANCOVA) with disease as fixed factor, and sex and age as covariates. We found that GWI SNIs differed significantly from control SZ, AD, PTSD and MDD but not from RRMS, SS and RA. In addition, we compared GWI to RRMS, SS and RA with respect to SNIs of MEG sensor pairs that were related to the HLA alleles protective for GWI (James et al., EBioMedicine 13:72–79,
2016
). We found that GWI SNIs did not differ significantly from any of these three diseases but they did so from control SZ, AD, PTSD and MDD. These findings indicate that (a) GWI brain synchronicity does not differ significantly from that of known immune-related diseases (RRMS, SS, RA), and (b) that this SNI similarity is present within the HLA-related SNIs. In contrast, GWI SNIs differed significantly from those of the other diseases. We conclude that altered brain communication in GWI likely reflects immune-related processes, as postulated previously (James et al., EBioMedicine 13:72–79,
2016
). By extension, these findings also indicate that functional brain abnormalities in RRMS, SS and RA might be, in part, due to lack of protective HLA alleles as documented for GWI (Georgopoulos et al., EBioMedicine 3:79–85,
2015
).</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alleles</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Analysis of covariance</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - physiopathology</subject><subject>Autoimmune Diseases - genetics</subject><subject>Autoimmune Diseases - physiopathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - physiopathology</subject><subject>Brain Diseases - genetics</subject><subject>Brain Diseases - physiopathology</subject><subject>Data processing</subject><subject>Depressive Disorder, Major - genetics</subject><subject>Depressive Disorder, Major - physiopathology</subject><subject>Electroencephalography Phase Synchronization - physiology</subject><subject>Etiology</subject><subject>Female</subject><subject>Gulf War</subject><subject>Gulf War syndrome</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility Antigens Class II - genetics</subject><subject>Humans</subject><subject>Immune system</subject><subject>Magnetoencephalography</subject><subject>Magnetoencephalography - methods</subject><subject>Male</subject><subject>Mental depression</subject><subject>Mental disorders</subject><subject>Mental Disorders - genetics</subject><subject>Mental Disorders - physiopathology</subject><subject>Middle Aged</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis, Relapsing-Remitting - genetics</subject><subject>Multiple Sclerosis, Relapsing-Remitting - physiopathology</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Organs</subject><subject>Persian Gulf syndrome</subject><subject>Persian Gulf Syndrome - classification</subject><subject>Persian Gulf Syndrome - genetics</subject><subject>Persian Gulf Syndrome - physiopathology</subject><subject>Persian Gulf War</subject><subject>Physiological aspects</subject><subject>Post traumatic stress disorder</subject><subject>Research Article</subject><subject>Rheumatoid arthritis</subject><subject>Schizophrenia</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - physiopathology</subject><subject>Sjogren's syndrome</subject><subject>Stress Disorders, Post-Traumatic - genetics</subject><subject>Stress Disorders, Post-Traumatic - physiopathology</subject><subject>War</subject><issn>0014-4819</issn><issn>1432-1106</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kUtLxTAQhYMoen38ADdScKOL3jtJ0yRdiuhVENwoLkOSTqTShya3C_-9Kdc3ShYhk28OZ-YQckhhTgHkIgIwRnOgMi-hhBw2yIzyguWUgtgkMwDKc65otUN2Y3yanoWEbbLDlBQMynJGFsux9dmDCVnTtj3GmJ0sH65PMxMzk_U4hqHpurHHrG4imoj7ZMubNuLB-71H7i8v7s6v8pvb5fX52U3ueFGtciWs886ZwvLaGFGxWnkL6MBi7ZyQplSlt1xVxjIpecWF89JazoykkGYr9sjJWvc5DC8jxpXumuiwbU2Pwxg1rVjJFNBKJPT4F_o0jKFP7hLF055kpeCLejQt6qb3wyoYN4nqs7S8QkghVaLmf1Dp1Ng1bujRN6n-o4GuG1wYYgzo9XNoOhNeNQU9haTXIekUkp5C0pOVo3fDo-2w_uz4SCUBbA3E9NU_Yvg20b-qb1p8mBs</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Georgopoulos, Apostolos P.</creator><creator>James, Lisa M.</creator><creator>Carpenter, Adam F.</creator><creator>Engdahl, Brian E.</creator><creator>Leuthold, Arthur C.</creator><creator>Lewis, Scott M.</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88J</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2R</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20171001</creationdate><title>Gulf War illness (GWI) as a neuroimmune disease</title><author>Georgopoulos, Apostolos P. ; James, Lisa M. ; Carpenter, Adam F. ; Engdahl, Brian E. ; Leuthold, Arthur C. ; Lewis, Scott M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-86bcfcca3b4daa692d8fb0ec0bedcc67a585fb489ab2774946cf7bb42a7101003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alleles</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Analysis of covariance</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - physiopathology</topic><topic>Autoimmune Diseases - genetics</topic><topic>Autoimmune Diseases - physiopathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - physiopathology</topic><topic>Brain Diseases - genetics</topic><topic>Brain Diseases - physiopathology</topic><topic>Data processing</topic><topic>Depressive Disorder, Major - genetics</topic><topic>Depressive Disorder, Major - physiopathology</topic><topic>Electroencephalography Phase Synchronization - physiology</topic><topic>Etiology</topic><topic>Female</topic><topic>Gulf War</topic><topic>Gulf War syndrome</topic><topic>Histocompatibility antigen HLA</topic><topic>Histocompatibility Antigens Class II - genetics</topic><topic>Humans</topic><topic>Immune system</topic><topic>Magnetoencephalography</topic><topic>Magnetoencephalography - methods</topic><topic>Male</topic><topic>Mental depression</topic><topic>Mental disorders</topic><topic>Mental Disorders - genetics</topic><topic>Mental Disorders - physiopathology</topic><topic>Middle Aged</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis, Relapsing-Remitting - genetics</topic><topic>Multiple Sclerosis, Relapsing-Remitting - physiopathology</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Organs</topic><topic>Persian Gulf syndrome</topic><topic>Persian Gulf Syndrome - classification</topic><topic>Persian Gulf Syndrome - genetics</topic><topic>Persian Gulf Syndrome - physiopathology</topic><topic>Persian Gulf War</topic><topic>Physiological aspects</topic><topic>Post traumatic stress disorder</topic><topic>Research Article</topic><topic>Rheumatoid arthritis</topic><topic>Schizophrenia</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - physiopathology</topic><topic>Sjogren's syndrome</topic><topic>Stress Disorders, Post-Traumatic - genetics</topic><topic>Stress Disorders, Post-Traumatic - physiopathology</topic><topic>War</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Georgopoulos, Apostolos P.</creatorcontrib><creatorcontrib>James, Lisa M.</creatorcontrib><creatorcontrib>Carpenter, Adam F.</creatorcontrib><creatorcontrib>Engdahl, Brian E.</creatorcontrib><creatorcontrib>Leuthold, Arthur C.</creatorcontrib><creatorcontrib>Lewis, Scott M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Social Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Georgopoulos, Apostolos P.</au><au>James, Lisa M.</au><au>Carpenter, Adam F.</au><au>Engdahl, Brian E.</au><au>Leuthold, Arthur C.</au><au>Lewis, Scott M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gulf War illness (GWI) as a neuroimmune disease</atitle><jtitle>Experimental brain research</jtitle><stitle>Exp Brain Res</stitle><addtitle>Exp Brain Res</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>235</volume><issue>10</issue><spage>3217</spage><epage>3225</epage><pages>3217-3225</pages><issn>0014-4819</issn><eissn>1432-1106</eissn><abstract>Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi:
10.1007/s00221-017-5010-8
,
2017
). In a previous study (Georgopoulos et al., J Neural Eng 4:349–355,
2015
), we identified six protective alleles from Class II human leukocyte antigen (HLA) genes, and more recently, we investigated the brain correlates of this protection (James et al., EBioMedicine 13:72–79,
2016
). Those and other studies (Israeli, Lupus, 21:190–194,
2012
) suggested an involvement of the immune system in GWI. In a recent study (Engdahl et al., EBioMedicine doi:
10.1016/j.ebiom.2016.08.030
,
2016
), we showed that the brain pattern of synchronous neural interactions (SNI; Georgopoulos et al., J Neural Eng 4:349–355,
2007
) in GWI is distinctly different from that in healthy controls. Here we focused on the SNI itself, as a basic measure of neural communication (irrespective of specific connections) and compared it between GWI and seven other diseases that cover a broad spectrum of etiology and pathophysiology. Specifically, we sought to determine which, if any, of those diseases might resemble GWI SNI, overall and within the HLA protective domain, and thus gain further knowledge regarding the nature of GWI brain abnormality. We studied a total of 962 participants from a healthy control population (
N
= 583) and eight different diseases, including GWI (
N
= 40), schizophrenia (SZ;
N
= 21), Alzheimer’s disease (AD;
N
= 66), posttraumatic stress disorder (PTSD;
N
= 159), major depressive disorder (MDD;
N
= 10), relapsing–remitting multiple sclerosis (RRMS;
N
= 43), Sjögren’s syndrome (SS;
N
= 32), and rheumatoid arthritis (RA;
N
= 8). They all underwent a resting-state magnetoencephalographic (MEG) scan to calculate SNIs. Data were analyzed using analysis of covariance (ANCOVA) with disease as fixed factor, and sex and age as covariates. We found that GWI SNIs differed significantly from control SZ, AD, PTSD and MDD but not from RRMS, SS and RA. In addition, we compared GWI to RRMS, SS and RA with respect to SNIs of MEG sensor pairs that were related to the HLA alleles protective for GWI (James et al., EBioMedicine 13:72–79,
2016
). We found that GWI SNIs did not differ significantly from any of these three diseases but they did so from control SZ, AD, PTSD and MDD. These findings indicate that (a) GWI brain synchronicity does not differ significantly from that of known immune-related diseases (RRMS, SS, RA), and (b) that this SNI similarity is present within the HLA-related SNIs. In contrast, GWI SNIs differed significantly from those of the other diseases. We conclude that altered brain communication in GWI likely reflects immune-related processes, as postulated previously (James et al., EBioMedicine 13:72–79,
2016
). By extension, these findings also indicate that functional brain abnormalities in RRMS, SS and RA might be, in part, due to lack of protective HLA alleles as documented for GWI (Georgopoulos et al., EBioMedicine 3:79–85,
2015
).</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28762055</pmid><doi>10.1007/s00221-017-5050-0</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0014-4819 |
| ispartof | Experimental brain research, 2017-10, Vol.235 (10), p.3217-3225 |
| issn | 0014-4819 1432-1106 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1925280196 |
| source | MEDLINE; SpringerLink Journals |
| subjects | Adult Aged Aged, 80 and over Alleles Alzheimer Disease - genetics Alzheimer Disease - physiopathology Alzheimer's disease Analysis of covariance Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - physiopathology Autoimmune Diseases - genetics Autoimmune Diseases - physiopathology Biomedical and Life Sciences Biomedicine Brain - physiopathology Brain Diseases - genetics Brain Diseases - physiopathology Data processing Depressive Disorder, Major - genetics Depressive Disorder, Major - physiopathology Electroencephalography Phase Synchronization - physiology Etiology Female Gulf War Gulf War syndrome Histocompatibility antigen HLA Histocompatibility Antigens Class II - genetics Humans Immune system Magnetoencephalography Magnetoencephalography - methods Male Mental depression Mental disorders Mental Disorders - genetics Mental Disorders - physiopathology Middle Aged Multiple sclerosis Multiple Sclerosis, Relapsing-Remitting - genetics Multiple Sclerosis, Relapsing-Remitting - physiopathology Neurodegenerative diseases Neurology Neurosciences Organs Persian Gulf syndrome Persian Gulf Syndrome - classification Persian Gulf Syndrome - genetics Persian Gulf Syndrome - physiopathology Persian Gulf War Physiological aspects Post traumatic stress disorder Research Article Rheumatoid arthritis Schizophrenia Schizophrenia - genetics Schizophrenia - physiopathology Sjogren's syndrome Stress Disorders, Post-Traumatic - genetics Stress Disorders, Post-Traumatic - physiopathology War |
| title | Gulf War illness (GWI) as a neuroimmune disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T05%3A16%3A30IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Gulf%20War%20illness%20(GWI)%20as%20a%20neuroimmune%20disease&rft.jtitle=Experimental%20brain%20research&rft.au=Georgopoulos,%20Apostolos%20P.&rft.date=2017-10-01&rft.volume=235&rft.issue=10&rft.spage=3217&rft.epage=3225&rft.pages=3217-3225&rft.issn=0014-4819&rft.eissn=1432-1106&rft_id=info:doi/10.1007/s00221-017-5050-0&rft_dat=%3Cgale_proqu%3EA505367678%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1940077980&rft_id=info:pmid/28762055&rft_galeid=A505367678&rfr_iscdi=true |