GABAergic/glutamatergic imbalance relative to excessive neuroinflammation in autism spectrum disorders
Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflamma...
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| Published in | Journal of neuroinflammation Vol. 11; no. 1; p. 189 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
England
BioMed Central Ltd
19.11.2014
BioMed Central |
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| Online Access | Get full text |
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| Abstract | Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms.
Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-α, IL-6, IFN-γ and IFI16 as markers of neuroinflammation were determined in both groups.
Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-α and IL-6 were significantly lower, whereas IFN-γ and IFI16 were remarkably higher in the autistic patients than in the control subjects.
Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. |
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| AbstractList | Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms.
Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-α, IL-6, IFN-γ and IFI16 as markers of neuroinflammation were determined in both groups.
Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-α and IL-6 were significantly lower, whereas IFN-γ and IFI16 were remarkably higher in the autistic patients than in the control subjects.
Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. Doc number: 189 Abstract Background: Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms. Methods: Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-α, IL-6, IFN-γ and IFI16 as markers of neuroinflammation were determined in both groups. Results: Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-α and IL-6 were significantly lower, whereas IFN-γ and IFI16 were remarkably higher in the autistic patients than in the control subjects. Conclusion: Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms.BACKGROUNDAutism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms.Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-α, IL-6, IFN-γ and IFI16 as markers of neuroinflammation were determined in both groups.METHODSTwenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-α, IL-6, IFN-γ and IFI16 as markers of neuroinflammation were determined in both groups.Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-α and IL-6 were significantly lower, whereas IFN-γ and IFI16 were remarkably higher in the autistic patients than in the control subjects.RESULTSAutistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-α and IL-6 were significantly lower, whereas IFN-γ and IFI16 were remarkably higher in the autistic patients than in the control subjects.Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation.CONCLUSIONMultiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. Background Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms. Methods Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-[alpha], IL-6, IFN-[gamma] and IFI16 as markers of neuroinflammation were determined in both groups. Results Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-[alpha] and IL-6 were significantly lower, whereas IFN-[gamma] and IFI16 were remarkably higher in the autistic patients than in the control subjects. Conclusion Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. Keywords: Autism, Glutamate excitotoxicity, Gamma aminobutyric acid (GABA), Glutamate/GABA, Tumor necrosis factor-[alpha], Interleukin-6, Interferon-gamma, Interferon-gamma-inducible protein 16 Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms. Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-[alpha], IL-6, IFN-[gamma] and IFI16 as markers of neuroinflammation were determined in both groups. Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-[alpha] and IL-6 were significantly lower, whereas IFN-[gamma] and IFI16 were remarkably higher in the autistic patients than in the control subjects. Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. Background: Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors. Glutamatergic/GABAergic imbalance has been found in various preclinical models of ASD. Additionally, autoimmunity immune dysfunction, and neuroinflammation are also considered as etiological mechanisms of this disorder. This study aimed to elucidate the relationship between glutamatergic/ GABAergic imbalance and neuroinflammation as two recently-discovered autism-related etiological mechanisms. Methods: Twenty autistic patients aged 3 to 15 years and 19 age- and gender-matched healthy controls were included in this study. The plasma levels of glutamate, GABA and glutamate/GABA ratio as markers of excitotoxicity together with TNF-[alpha], IL-6, IFN-[gamma] and IFI16 as markers of neuroinflammation were determined in both groups. Results: Autistic patients exhibited glutamate excitotoxicity based on a much higher glutamate concentration in the autistic patients than in the control subjects. Unexpectedly higher GABA and lower glutamate/GABA levels were recorded in autistic patients compared to control subjects. TNF-[alpha] and IL-6 were significantly lower, whereas IFN-[gamma] and IFI16 were remarkably higher in the autistic patients than in the control subjects. Conclusion: Multiple regression analysis revealed associations between reduced GABA level, neuroinflammation and glutamate excitotoxicity. This study indicates that autism is a developmental synaptic disorder showing imbalance in GABAergic and glutamatergic synapses as a consequence of neuroinflammation. |
| ArticleNumber | 189 |
| Audience | Academic |
| Author | El-Ansary, Afaf Al-Ayadhi, Laila |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25407263$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1126/science.1157657 10.1523/JNEUROSCI.0302-11.2011 10.1016/0003-2697(76)90527-3 10.1186/1742-2094-8-52 10.1007/s10803-006-0226-7 10.1080/13550280290100969 10.1016/j.neuron.2014.01.016 10.1016/j.pnpbp.2006.06.013 10.1096/fj.07-099499 10.1007/BF02867967 10.1016/S0306-4522(00)00036-1 10.1186/1866-1955-4-4 10.1038/nrn919 10.1038/ng1933 10.1523/JNEUROSCI.0530-13.2013 10.1113/expphysiol.2005.030734 10.1038/nrg2346 10.1016/S0006-3223(02)01430-0 10.1016/S0896-6273(00)80983-6 10.1111/j.1469-7793.1998.867bj.x 10.1007/s12311-008-0075-3 10.1002/ana.20315 10.1007/s10803-008-0646-7 10.1007/s10803-010-1065-0 10.1016/j.jneuroim.2008.12.002 10.1007/s00787-006-0563-2 10.1056/NEJM199205283262204 10.1016/S1474-4422(02)00160-6 10.1155/2014/861231 10.1016/j.semcdb.2003.12.018 10.3389/fncel.2014.00119 |
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| Copyright | COPYRIGHT 2014 BioMed Central Ltd. 2014 El-Ansary and Al-Ayadhi; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. El-Ansary and Al-Ayadhi; licensee BioMed Central Ltd. 2014 |
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| References | H Pribiag (189_CR29) 2013; 33 R Dingledine (189_CR3) 1999; 51 L Fagni (189_CR4) 2004; 15 C Levenes (189_CR22) 1998; 510 B Szabo (189_CR23) 2000; 97 JD Rothstein (189_CR26) 1992; 326 M Harada (189_CR10) 2011; 41 GJ Blatt (189_CR31) 2007; 6 189_CR25 E Neher (189_CR24) 1998; 20 GA Abu Shmais (189_CR9) 2012; 4 M Pickering (189_CR28) 2005; 90 M Ghosh (189_CR27) 2011; 31 VS Suresh Babu (189_CR11) 2002; 17 R Canitano (189_CR18) 2007; 16 JT Guptill (189_CR32) 2007; 37 S Han (189_CR15) 2014; 81 R Tuchman (189_CR5) 2002; 6 G Deidda (189_CR14) 2014; 8 SH Fatemi (189_CR35) 2009; 39 DF Owens (189_CR7) 2002; 9 RL Blaylock (189_CR1) 2004; 9 T Mizuno (189_CR30) 2008; 22 EM Morrow (189_CR21) 2008; 321 PL McGeer (189_CR2) 2002; 8 M Bradford (189_CR12) 1976; 76 DL Vargas (189_CR16) 2005; 57 189_CR8 CM Durand (189_CR19) 2007; 39 BS Abrahams (189_CR20) 2008; 9 H Wei (189_CR13) 2011; 8 SH Fatemi (189_CR33) 2009; 8 A Shinohe (189_CR6) 2006; 30 SH Fatemi (189_CR34) 2002; 52 X Li (189_CR17) 2009; 207 9539117 - Neuron. 1998 Mar;20(3):389-99 15944202 - Exp Physiol. 2005 Sep;90(5):663-70 24904277 - Front Cell Neurosci. 2014 May 22;8:119 15125892 - Semin Cell Dev Biol. 2004 Jun;15(3):289-98 22958401 - J Neurodev Disord. 2012 Feb 13;4(1):4 17173049 - Nat Genet. 2007 Jan;39(1):25-7 12849396 - Lancet Neurol. 2002 Oct;1(6):352-8 17019626 - J Autism Dev Disord. 2007 May;37(5):911-20 19002745 - Cerebellum. 2009 Mar;8(1):64-9 21697367 - J Neurosci. 2011 Jun 22;31(25):9159-69 12209120 - Nat Rev Neurosci. 2002 Sep;3(9):715-27 20652388 - J Autism Dev Disord. 2011 Apr;41(4):447-54 16863675 - Prog Neuropsychopharmacol Biol Psychiatry. 2006 Dec 30;30(8):1472-7 21766041 - Neural Plast. 2011;2011:297153 942051 - Anal Biochem. 1976 May 7;72:248-54 9660899 - J Physiol. 1998 Aug 1;510 ( Pt 3):867-79 24656250 - Neuron. 2014 Mar 19;81(6):1282-9 23105346 - Indian J Clin Biochem. 2002 Jul;17(2):7-26 18414403 - Nat Rev Genet. 2008 May;9(5):341-55 12372652 - Biol Psychiatry. 2002 Oct 15;52(8):805-10 24089494 - J Neurosci. 2013 Oct 2;33(40):15879-93 24966471 - Mediators Inflamm. 2014;2014:861231 18821008 - J Autism Dev Disord. 2009 Feb;39(2):223-30 12476347 - J Neurovirol. 2002 Dec;8(6):529-38 21595886 - J Neuroinflammation. 2011;8:52 19157572 - J Neuroimmunol. 2009 Feb 15;207(1-2):111-6 10049997 - Pharmacol Rev. 1999 Mar;51(1):7-61 16932856 - Eur Child Adolesc Psychiatry. 2007 Feb;16(1):61-6 1349424 - N Engl J Med. 1992 May 28;326(22):1464-8 15546155 - Ann Neurol. 2005 Jan;57(1):67-81 18198214 - FASEB J. 2008 Jun;22(6):1797-806 10771342 - Neuroscience. 2000;97(1):89-97 18621663 - Science. 2008 Jul 11;321(5886):218-23 |
| References_xml | – volume: 51 start-page: 7 issue: 1 year: 1999 ident: 189_CR3 publication-title: Pharmacol – volume: 321 start-page: 218 year: 2008 ident: 189_CR21 publication-title: Science doi: 10.1126/science.1157657 – volume: 31 start-page: 9159 issue: 25 year: 2011 ident: 189_CR27 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0302-11.2011 – volume: 76 start-page: 248 year: 1976 ident: 189_CR12 publication-title: Anal Biochem doi: 10.1016/0003-2697(76)90527-3 – volume: 8 start-page: 52 year: 2011 ident: 189_CR13 publication-title: J Neuroinflammation doi: 10.1186/1742-2094-8-52 – volume: 37 start-page: 911 year: 2007 ident: 189_CR32 publication-title: J Autism Dev Disord doi: 10.1007/s10803-006-0226-7 – volume: 8 start-page: 529 year: 2002 ident: 189_CR2 publication-title: J Neurovirol doi: 10.1080/13550280290100969 – volume: 81 start-page: 1282 issue: 6 year: 2014 ident: 189_CR15 publication-title: Neuron doi: 10.1016/j.neuron.2014.01.016 – volume: 30 start-page: 1472 issue: 8 year: 2006 ident: 189_CR6 publication-title: Prog Neuropsychopharmacol Biol Psychiatry doi: 10.1016/j.pnpbp.2006.06.013 – volume: 22 start-page: 1797 issue: 6 year: 2008 ident: 189_CR30 publication-title: FASEB J doi: 10.1096/fj.07-099499 – volume: 17 start-page: 7 issue: 2 year: 2002 ident: 189_CR11 publication-title: Indian J Clin Biochem doi: 10.1007/BF02867967 – volume: 97 start-page: 89 year: 2000 ident: 189_CR23 publication-title: Neuroscience doi: 10.1016/S0306-4522(00)00036-1 – volume: 4 start-page: 4 issue: 1 year: 2012 ident: 189_CR9 publication-title: J Neurodev Disord doi: 10.1186/1866-1955-4-4 – volume: 9 start-page: 715 year: 2002 ident: 189_CR7 publication-title: Nat Rev Neurosci doi: 10.1038/nrn919 – volume: 39 start-page: 25 year: 2007 ident: 189_CR19 publication-title: Nat Genet doi: 10.1038/ng1933 – volume: 33 start-page: 15879 issue: 40 year: 2013 ident: 189_CR29 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0530-13.2013 – volume: 90 start-page: 663 issue: 5 year: 2005 ident: 189_CR28 publication-title: Exp Physiol doi: 10.1113/expphysiol.2005.030734 – volume: 9 start-page: 341 year: 2008 ident: 189_CR20 publication-title: Nat Rev Genet doi: 10.1038/nrg2346 – volume: 52 start-page: 805 year: 2002 ident: 189_CR34 publication-title: Biol Psych doi: 10.1016/S0006-3223(02)01430-0 – volume: 20 start-page: 389 year: 1998 ident: 189_CR24 publication-title: Neuron doi: 10.1016/S0896-6273(00)80983-6 – ident: 189_CR8 – volume: 510 start-page: 867 issue: 3 year: 1998 ident: 189_CR22 publication-title: J Physiol doi: 10.1111/j.1469-7793.1998.867bj.x – volume: 8 start-page: 64 year: 2009 ident: 189_CR33 publication-title: Cerebellum doi: 10.1007/s12311-008-0075-3 – volume: 57 start-page: 67 year: 2005 ident: 189_CR16 publication-title: Ann Neurol doi: 10.1002/ana.20315 – volume: 39 start-page: 223 year: 2009 ident: 189_CR35 publication-title: J Autism Dev Disord doi: 10.1007/s10803-008-0646-7 – volume: 9 start-page: 46 issue: 2 year: 2004 ident: 189_CR1 publication-title: J Am Physicians Surg – volume: 41 start-page: 447 issue: 4 year: 2011 ident: 189_CR10 publication-title: J Autism Dev Disord doi: 10.1007/s10803-010-1065-0 – volume: 207 start-page: 111 year: 2009 ident: 189_CR17 publication-title: J Neuroimmunol doi: 10.1016/j.jneuroim.2008.12.002 – volume: 16 start-page: 61 year: 2007 ident: 189_CR18 publication-title: Eur Child Adolesc Psychiatry doi: 10.1007/s00787-006-0563-2 – volume: 6 start-page: 144 year: 2007 ident: 189_CR31 publication-title: Int Meet Autism Res – volume: 326 start-page: 1464 year: 1992 ident: 189_CR26 publication-title: N Engl J Med doi: 10.1056/NEJM199205283262204 – volume: 6 start-page: 352 issue: 1 year: 2002 ident: 189_CR5 publication-title: Lancet Neurol doi: 10.1016/S1474-4422(02)00160-6 – ident: 189_CR25 doi: 10.1155/2014/861231 – volume: 15 start-page: 289 issue: 3 year: 2004 ident: 189_CR4 publication-title: Semin Cell Dev Biol doi: 10.1016/j.semcdb.2003.12.018 – volume: 8 start-page: 119 year: 2014 ident: 189_CR14 publication-title: Front Cell Neurosci doi: 10.3389/fncel.2014.00119 – reference: 16863675 - Prog Neuropsychopharmacol Biol Psychiatry. 2006 Dec 30;30(8):1472-7 – reference: 18414403 - Nat Rev Genet. 2008 May;9(5):341-55 – reference: 21697367 - J Neurosci. 2011 Jun 22;31(25):9159-69 – reference: 19002745 - Cerebellum. 2009 Mar;8(1):64-9 – reference: 17173049 - Nat Genet. 2007 Jan;39(1):25-7 – reference: 20652388 - J Autism Dev Disord. 2011 Apr;41(4):447-54 – reference: 17019626 - J Autism Dev Disord. 2007 May;37(5):911-20 – reference: 942051 - Anal Biochem. 1976 May 7;72:248-54 – reference: 12372652 - Biol Psychiatry. 2002 Oct 15;52(8):805-10 – reference: 12476347 - J Neurovirol. 2002 Dec;8(6):529-38 – reference: 23105346 - Indian J Clin Biochem. 2002 Jul;17(2):7-26 – reference: 16932856 - Eur Child Adolesc Psychiatry. 2007 Feb;16(1):61-6 – reference: 19157572 - J Neuroimmunol. 2009 Feb 15;207(1-2):111-6 – reference: 21766041 - Neural Plast. 2011;2011:297153 – reference: 22958401 - J Neurodev Disord. 2012 Feb 13;4(1):4 – reference: 21595886 - J Neuroinflammation. 2011;8:52 – reference: 9660899 - J Physiol. 1998 Aug 1;510 ( Pt 3):867-79 – reference: 15125892 - Semin Cell Dev Biol. 2004 Jun;15(3):289-98 – reference: 10049997 - Pharmacol Rev. 1999 Mar;51(1):7-61 – reference: 9539117 - Neuron. 1998 Mar;20(3):389-99 – reference: 1349424 - N Engl J Med. 1992 May 28;326(22):1464-8 – reference: 12849396 - Lancet Neurol. 2002 Oct;1(6):352-8 – reference: 15546155 - Ann Neurol. 2005 Jan;57(1):67-81 – reference: 18621663 - Science. 2008 Jul 11;321(5886):218-23 – reference: 24656250 - Neuron. 2014 Mar 19;81(6):1282-9 – reference: 18821008 - J Autism Dev Disord. 2009 Feb;39(2):223-30 – reference: 24966471 - Mediators Inflamm. 2014;2014:861231 – reference: 12209120 - Nat Rev Neurosci. 2002 Sep;3(9):715-27 – reference: 18198214 - FASEB J. 2008 Jun;22(6):1797-806 – reference: 15944202 - Exp Physiol. 2005 Sep;90(5):663-70 – reference: 10771342 - Neuroscience. 2000;97(1):89-97 – reference: 24089494 - J Neurosci. 2013 Oct 2;33(40):15879-93 – reference: 24904277 - Front Cell Neurosci. 2014 May 22;8:119 |
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| Snippet | Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors.... Background Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive behaviors.... Doc number: 189 Abstract Background: Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication,... Background: Autism spectrum disorder (ASD) is characterized by three core behavioral domains: social deficits, impaired communication, and repetitive... |
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| SubjectTerms | Acids Adolescent Analysis Animals Autism Autism Spectrum Disorder - blood Autism Spectrum Disorder - diagnosis Autoimmunity Biomarkers - blood Brain research Child Child, Preschool Consent Cytokines Data analysis Female GABA gamma-Aminobutyric Acid - blood Glutamate Glutamic Acid - blood Hospitals Humans Immune system Inflammation - blood Inflammation - diagnosis Interleukin-6 - blood Male Medical research Medicine, Experimental Methods Mice Physiological aspects Plasma Proteins Rats Tumor Necrosis Factor-alpha - blood |
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| Title | GABAergic/glutamatergic imbalance relative to excessive neuroinflammation in autism spectrum disorders |
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