Downregulation of GABAA Receptor Protein Subunits ?6, ?2, ?, ?, ?2, ?, and ?2 in Superior Frontal Cortex of Subjects with Autism / S. Hossein FATEMI in Journal of Autism and Developmental Disorders, 44-8 (August 2014)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 44-8 (August 2014) . - p.1833-1845 Titre : Downregulation of GABAA Receptor Protein Subunits ?6, ?2, ?, ?, ?2, ?, and ?2 in Superior Frontal Cortex of Subjects with Autism Type de document : Texte imprimé et/ou numérique Auteurs : S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Oyvind G. RUSTAN, Auteur ; Robert J. ROONEY, Auteur ; Paul D. THURAS, Auteur Article en page(s) : p.1833-1845 Langues : Anglais (eng) Mots-clés : Autism  GABA  Brain  GABR?6  Frontal cortex  GABR?2 Index. décimale : PER Périodiques Résumé : We measured protein and mRNA levels for nine gamma-aminobutyric acid A (GABAA) receptor subunits in three brain regions (cerebellum, superior frontal cortex, and parietal cortex) in subjects with autism versus matched controls. We observed changes in mRNA for a number of GABAA and GABAB subunits and overall reduced protein expression for GABAA receptor alpha 6 (GABR?6), GABAA receptor beta 2 (GABR?2), GABAA receptor delta (GABR?), GABAA receptor epsilon (GABR?), GABAA receptor gamma 2 (GABR?2), GABAA receptor theta (GABR?), and GABAA receptor rho 2 (GABR?2) in superior frontal cortex from subjects with autism. Our data demonstrate systematic changes in GABAAB subunit expression in brains of subjects with autism, which may help explain the presence of cognitive abnormalities in subjects with autism. En ligne : http://dx.doi.org/10.1007/s10803-014-2078-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=236 [article] Downregulation of GABAA Receptor Protein Subunits ?6, ?2, ?, ?, ?2, ?, and ?2 in Superior Frontal Cortex of Subjects with Autism [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Oyvind G. RUSTAN, Auteur ; Robert J. ROONEY, Auteur ; Paul D. THURAS, Auteur . - p.1833-1845. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 44-8 (August 2014) . - p.1833-1845 Mots-clés : Autism  GABA  Brain  GABR?6  Frontal cortex  GABR?2 Index. décimale : PER Périodiques Résumé : We measured protein and mRNA levels for nine gamma-aminobutyric acid A (GABAA) receptor subunits in three brain regions (cerebellum, superior frontal cortex, and parietal cortex) in subjects with autism versus matched controls. We observed changes in mRNA for a number of GABAA and GABAB subunits and overall reduced protein expression for GABAA receptor alpha 6 (GABR?6), GABAA receptor beta 2 (GABR?2), GABAA receptor delta (GABR?), GABAA receptor epsilon (GABR?), GABAA receptor gamma 2 (GABR?2), GABAA receptor theta (GABR?), and GABAA receptor rho 2 (GABR?2) in superior frontal cortex from subjects with autism. Our data demonstrate systematic changes in GABAAB subunit expression in brains of subjects with autism, which may help explain the presence of cognitive abnormalities in subjects with autism. En ligne : http://dx.doi.org/10.1007/s10803-014-2078-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=236

Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study / S. Hossein FATEMI in Molecular Autism, (May 2011)  

Public ISBD [article]  inMolecular Autism > (May 2011) . - 11 p. Titre : Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study Type de document : Texte imprimé et/ou numérique Auteurs : S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur Année de publication : 2011 Article en page(s) : 11 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background Fragile × syndrome is caused by loss of function of the fragile × mental retardation 1 (FMR1) gene and shares multiple phenotypes with autism. We have previously found reduced expression of the protein product of FMR1 (FMRP) in vermis of adults with autism. Methods In the current study, we have investigated levels of FMRP in the superior frontal cortex of people with autism and matched controls using Western blot analysis. Because FMRP regulates the translation of multiple genes, we also measured protein levels for downstream molecules metabotropic glutamate receptor 5 (mGluR5) and γ-aminobutyric acid (GABA) A receptor β3 (GABRβ3), as well as glial fibrillary acidic protein (GFAP). Results We observed significantly reduced levels of protein for FMRP in adults with autism, significantly increased levels of protein for mGluR5 in children with autism and significantly increased levels of GFAP in adults and children with autism. We found no change in expression of GABRβ3. Our results for FMRP, mGluR5 and GFAP confirm our previous work in the cerebellar vermis of people with autism. Conclusion These changes may be responsible for cognitive deficits and seizure disorder in people with autism. En ligne : http://dx.doi.org/10.1186/2040-2392-2-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131 [article] Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur . - 2011 . - 11 p. Langues : Anglais (eng) in Molecular Autism > (May 2011) . - 11 p. Index. décimale : PER Périodiques Résumé : Background Fragile × syndrome is caused by loss of function of the fragile × mental retardation 1 (FMR1) gene and shares multiple phenotypes with autism. We have previously found reduced expression of the protein product of FMR1 (FMRP) in vermis of adults with autism. Methods In the current study, we have investigated levels of FMRP in the superior frontal cortex of people with autism and matched controls using Western blot analysis. Because FMRP regulates the translation of multiple genes, we also measured protein levels for downstream molecules metabotropic glutamate receptor 5 (mGluR5) and γ-aminobutyric acid (GABA) A receptor β3 (GABRβ3), as well as glial fibrillary acidic protein (GFAP). Results We observed significantly reduced levels of protein for FMRP in adults with autism, significantly increased levels of protein for mGluR5 in children with autism and significantly increased levels of GFAP in adults and children with autism. We found no change in expression of GABRβ3. Our results for FMRP, mGluR5 and GFAP confirm our previous work in the cerebellar vermis of people with autism. Conclusion These changes may be responsible for cognitive deficits and seizure disorder in people with autism. En ligne : http://dx.doi.org/10.1186/2040-2392-2-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131

GABAa Receptor Downregulation in Brains of Subjects with Autism / S. Hossein FATEMI in Journal of Autism and Developmental Disorders, 39-2 (February 2009)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 39-2 (February 2009) . - p.223-230 Titre : GABAa Receptor Downregulation in Brains of Subjects with Autism Type de document : Texte imprimé et/ou numérique Auteurs : S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Paul D. THURAS, Auteur Année de publication : 2009 Article en page(s) : p.223-230 Langues : Anglais (eng) Mots-clés : GABRA1 GABRA2 GABRA3 GABRB3 Autism Brain Index. décimale : PER Périodiques Résumé : Gamma-aminobutyric acid A (GABAA) receptors are ligand-gated ion channels responsible for mediation of fast inhibitory action of GABA in the brain. Preliminary reports have demonstrated altered expression of GABA receptors in the brains of subjects with autism suggesting GABA/glutamate system dysregulation. We investigated the expression of four GABAA receptor subunits and observed significant reductions in GABRA1, GABRA2, GABRA3, and GABRB3 in parietal cortex (Brodmann’s Area 40 (BA40)), while GABRA1 and GABRB3 were significantly altered in cerebellum, and GABRA1 was significantly altered in superior frontal cortex (BA9). The presence of seizure disorder did not have a significant impact on GABAA receptor subunit expression in the three brain areas. Our results demonstrate that GABAA receptors are reduced in three brain regions that have previously been implicated in the pathogenesis of autism, suggesting widespread GABAergic dysfunction in the brains of subjects with autism. En ligne : http://dx.doi.org/10.1007/s10803-008-0646-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=683 [article] GABAa Receptor Downregulation in Brains of Subjects with Autism [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Paul D. THURAS, Auteur . - 2009 . - p.223-230. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 39-2 (February 2009) . - p.223-230 Mots-clés : GABRA1 GABRA2 GABRA3 GABRB3 Autism Brain Index. décimale : PER Périodiques Résumé : Gamma-aminobutyric acid A (GABAA) receptors are ligand-gated ion channels responsible for mediation of fast inhibitory action of GABA in the brain. Preliminary reports have demonstrated altered expression of GABA receptors in the brains of subjects with autism suggesting GABA/glutamate system dysregulation. We investigated the expression of four GABAA receptor subunits and observed significant reductions in GABRA1, GABRA2, GABRA3, and GABRB3 in parietal cortex (Brodmann’s Area 40 (BA40)), while GABRA1 and GABRB3 were significantly altered in cerebellum, and GABRA1 was significantly altered in superior frontal cortex (BA9). The presence of seizure disorder did not have a significant impact on GABAA receptor subunit expression in the three brain areas. Our results demonstrate that GABAA receptors are reduced in three brain regions that have previously been implicated in the pathogenesis of autism, suggesting widespread GABAergic dysfunction in the brains of subjects with autism. En ligne : http://dx.doi.org/10.1007/s10803-008-0646-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=683

Impairment of fragile X mental retardation protein-metabotropic glutamate receptor 5 signaling and its downstream cognates ras-related C3 botulinum toxin substrate 1, amyloid beta A4 precursor protein, striatal-enriched protein tyrosine phosphatase, and homer 1, in autism: a postmortem study in cerebellar vermis and superior frontal cortex / S. Hossein FATEMI in Molecular Autism, (June 2013)  

Public ISBD [article]  inMolecular Autism > (June 2013) . - 19 p. Titre : Impairment of fragile X mental retardation protein-metabotropic glutamate receptor 5 signaling and its downstream cognates ras-related C3 botulinum toxin substrate 1, amyloid beta A4 precursor protein, striatal-enriched protein tyrosine phosphatase, and homer 1, in autism: a postmortem study in cerebellar vermis and superior frontal cortex Type de document : Texte imprimé et/ou numérique Auteurs : S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur ; Rachel E. KNEELAND, Auteur ; Mahtab K. YOUSEFI, Auteur ; Stephanie B. LIESCH, Auteur ; Paul D. THURAS, Auteur Année de publication : 2013 Article en page(s) : 19 p. Langues : Anglais (eng) Mots-clés : Autism  RAC1  Homer 1  APP  STEP  BA9  Cerebellar vermis  Children  Adults Index. décimale : PER Périodiques Résumé : Background Candidate genes associated with idiopathic forms of autism overlap with other disorders including fragile X syndrome. Our laboratory has previously shown reduction in fragile X mental retardation protein (FMRP) and increase in metabotropic glutamate receptor 5 (mGluR5) in cerebellar vermis and superior frontal cortex (BA9) of individuals with autism. Methods In the current study we have investigated expression of four targets of FMRP and mGluR5 signaling - homer 1, amyloid beta A4 precursor protein (APP), ras-related C3 botulinum toxin substrate 1 (RAC1), and striatal-enriched protein tyrosine phosphatase (STEP) - in the cerebellar vermis and superior frontal cortex (BA9) via SDS-PAGE and western blotting. Data were analyzed based on stratification with respect to age (children and adolescents vs. adults), anatomic region of the brain (BA9 vs. cerebellar vermis), and impact of medications (children and adolescents on medications (n = 4) vs. total children and adolescents (n = 12); adults on medications (n = 6) vs. total adults (n = 12)). Results There were significant increases in RAC1, APP 120 kDa and APP 80 kDa proteins in BA9 of children with autism vs. healthy controls. None of the same proteins were significantly affected in cerebellar vermis of children with autism. In BA9 of adults with autism there were significant increases in RAC1 and STEP 46 kDa and a significant decrease in homer 1 vs. controls. In the vermis of adult subjects with autism, RAC1 was significantly increased while APP 120, STEP 66 kDa, STEP 27 kDa, and homer 1 were significantly decreased when compared with healthy controls. No changes were observed in vermis of children with autism. There was a significant effect of anticonvulsant use on STEP 46 kDa/?-actin and a potential effect on homer 1/NSE, in BA9 of adults with autism. However, no other significant confound effects were observed in this study. Conclusions Our findings provide further evidence of abnormalities in FMRP and mGluR5 signaling partners in brains of individuals with autism and open the door to potential targeted treatments which could help ameliorate the symptoms of autism. En ligne : http://dx.doi.org/10.1186/2040-2392-4-21 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=211 [article] Impairment of fragile X mental retardation protein-metabotropic glutamate receptor 5 signaling and its downstream cognates ras-related C3 botulinum toxin substrate 1, amyloid beta A4 precursor protein, striatal-enriched protein tyrosine phosphatase, and homer 1, in autism: a postmortem study in cerebellar vermis and superior frontal cortex [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur ; Rachel E. KNEELAND, Auteur ; Mahtab K. YOUSEFI, Auteur ; Stephanie B. LIESCH, Auteur ; Paul D. THURAS, Auteur . - 2013 . - 19 p. Langues : Anglais (eng) in Molecular Autism > (June 2013) . - 19 p. Mots-clés : Autism  RAC1  Homer 1  APP  STEP  BA9  Cerebellar vermis  Children  Adults Index. décimale : PER Périodiques Résumé : Background Candidate genes associated with idiopathic forms of autism overlap with other disorders including fragile X syndrome. Our laboratory has previously shown reduction in fragile X mental retardation protein (FMRP) and increase in metabotropic glutamate receptor 5 (mGluR5) in cerebellar vermis and superior frontal cortex (BA9) of individuals with autism. Methods In the current study we have investigated expression of four targets of FMRP and mGluR5 signaling - homer 1, amyloid beta A4 precursor protein (APP), ras-related C3 botulinum toxin substrate 1 (RAC1), and striatal-enriched protein tyrosine phosphatase (STEP) - in the cerebellar vermis and superior frontal cortex (BA9) via SDS-PAGE and western blotting. Data were analyzed based on stratification with respect to age (children and adolescents vs. adults), anatomic region of the brain (BA9 vs. cerebellar vermis), and impact of medications (children and adolescents on medications (n = 4) vs. total children and adolescents (n = 12); adults on medications (n = 6) vs. total adults (n = 12)). Results There were significant increases in RAC1, APP 120 kDa and APP 80 kDa proteins in BA9 of children with autism vs. healthy controls. None of the same proteins were significantly affected in cerebellar vermis of children with autism. In BA9 of adults with autism there were significant increases in RAC1 and STEP 46 kDa and a significant decrease in homer 1 vs. controls. In the vermis of adult subjects with autism, RAC1 was significantly increased while APP 120, STEP 66 kDa, STEP 27 kDa, and homer 1 were significantly decreased when compared with healthy controls. No changes were observed in vermis of children with autism. There was a significant effect of anticonvulsant use on STEP 46 kDa/?-actin and a potential effect on homer 1/NSE, in BA9 of adults with autism. However, no other significant confound effects were observed in this study. Conclusions Our findings provide further evidence of abnormalities in FMRP and mGluR5 signaling partners in brains of individuals with autism and open the door to potential targeted treatments which could help ameliorate the symptoms of autism. En ligne : http://dx.doi.org/10.1186/2040-2392-4-21 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=211

mRNA and Protein Levels for GABAAα4, α5, β1 and GABABR1 Receptors are Altered in Brains from Subjects with Autism / S. Hossein FATEMI in Journal of Autism and Developmental Disorders, 40-6 (June 2010)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 40-6 (June 2010) . - p.743-750 Titre : mRNA and Protein Levels for GABAAα4, α5, β1 and GABABR1 Receptors are Altered in Brains from Subjects with Autism Type de document : Texte imprimé et/ou numérique Auteurs : S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Paul D. THURAS, Auteur ; Robert J. ROONEY, Auteur ; Diven H. PATEL, Auteur Année de publication : 2010 Article en page(s) : p.743-750 Langues : Anglais (eng) Mots-clés : GABBR1 GABRα4 GABRα5 GABRβ1 Autism Brain Index. décimale : PER Périodiques Résumé : We have shown altered expression of gamma-aminobutyric acid A (GABAA) and gamma-aminobutyric acid B (GABAB) receptors in the brains of subjects with autism. In the current study, we sought to verify our western blotting data for GABBR1 via qRT-PCR and to expand our previous work to measure mRNA and protein levels of 3 GABAA subunits previously associated with autism (GABRα4; GABRα5; GABRβ1). Three GABA receptor subunits demonstrated mRNA and protein level concordance in superior frontal cortex (GABRα4, GABRα5, GABRβ1) and one demonstrated concordance in cerebellum (GABΒR1). These results provide further evidence of impairment of GABAergic signaling in autism. En ligne : http://dx.doi.org/10.1007/s10803-009-0924-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102 [article] mRNA and Protein Levels for GABAAα4, α5, β1 and GABABR1 Receptors are Altered in Brains from Subjects with Autism [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Teri J. REUTIMAN, Auteur ; Timothy D. FOLSOM, Auteur ; Paul D. THURAS, Auteur ; Robert J. ROONEY, Auteur ; Diven H. PATEL, Auteur . - 2010 . - p.743-750. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 40-6 (June 2010) . - p.743-750 Mots-clés : GABBR1 GABRα4 GABRα5 GABRβ1 Autism Brain Index. décimale : PER Périodiques Résumé : We have shown altered expression of gamma-aminobutyric acid A (GABAA) and gamma-aminobutyric acid B (GABAB) receptors in the brains of subjects with autism. In the current study, we sought to verify our western blotting data for GABBR1 via qRT-PCR and to expand our previous work to measure mRNA and protein levels of 3 GABAA subunits previously associated with autism (GABRα4; GABRα5; GABRβ1). Three GABA receptor subunits demonstrated mRNA and protein level concordance in superior frontal cortex (GABRα4, GABRα5, GABRβ1) and one demonstrated concordance in cerebellum (GABΒR1). These results provide further evidence of impairment of GABAergic signaling in autism. En ligne : http://dx.doi.org/10.1007/s10803-009-0924-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102

Phosphorylated fragile X mental retardation protein at serine 499, is reduced in cerebellar vermis and superior frontal cortex of subjects with autism: implications for fragile X mental retardation protein-metabotropic glutamate receptor 5 signaling UR - http://dx.doi.org/10.1186/2040-2392-4-41 / Oyvind RUSTAN in Molecular Autism, (November 2013)

Permalink

Reelin glycoprotein in autism and schizophrenia / S. Hossein FATEMI

Permalink

The role of reelin in autism / S. Hossein FATEMI

Permalink

---

1 (1 - 8 / 8)