The GLO1 C332 (Ala111) allele confers autism vulnerability: Family-based genetic association and functional correlates

Abstract Glyoxalase I (GLO1) is a homodimeric Zn2+ -dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associ...

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Published inJournal of psychiatric research Vol. 59; pp. 108 - 116
Main Authors Gabriele, Stefano, Lombardi, Federica, Sacco, Roberto, Napolioni, Valerio, Altieri, Laura, Tirindelli, Maria Cristina, Gregorj, Chiara, Bravaccio, Carmela, Rousseau, Francis, Persico, Antonio M
Format Journal Article
LanguageEnglish
Published Kidlington Elsevier Ltd 01.12.2014
Elsevier
Subjects
Adolescent
Adult
Advanced glycation end-products
Alanine - genetics
Autism
Autism spectrum disorder
Biological and medical sciences
Brain - pathology
Child
Child clinical studies
Child Development Disorders, Pervasive - genetics
Child Development Disorders, Pervasive - pathology
Child, Preschool
Developmental disorders
Family Health
Female
Genetic Association Studies
Genotype
Glycation End Products, Advanced
Glyoxalase
Humans
Infantile autism
Lactoylglutathione Lyase - genetics
Lactoylglutathione Lyase - metabolism
Linkage Disequilibrium
Male
Medical sciences
Methylglyoxal
Middle Aged
Pervasive developmental disorders
Polymorphism, Single Nucleotide - genetics
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Serotonin - blood
Serotonin - urine
Statistics as Topic
Young Adult
Autism
Methylglyoxal
Advanced glycation end-products
Glyoxalase
Autism spectrum disorder
Pervasive developmental disorders
Social environment
Reaction product
Developmental disorder
Vulnerability
Glycation
Pervasive developmental disorder
Family environment
Genetics
Online AccessGet full text

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Abstract Abstract Glyoxalase I (GLO1) is a homodimeric Zn2+ -dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with “unaffected sibling” status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon–intron junctions, detecting two additional SNPs ( rs1049346 , rs1130534 ) in linkage disequilibrium with rs4746 . A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself ( P  < 0.05 and P  < 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue ( N  = 38 and 13, respectively) of typically developing C332 allele carriers ( P  < 0.05 and <0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains ( P  = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels ( τ  = −0.588, P  < 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis ( τ  = −0.209, P  = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls ( P  < 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects.
AbstractList Glyoxalase I (GLO1) is a homodimeric Zn2+-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with “unaffected sibling” status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon–intron junctions, detecting two additional SNPs (rs1049346, rs1130534) in linkage disequilibrium with rs4746. A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself (P < 0.05 and P < 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue (N = 38 and 13, respectively) of typically developing C332 allele carriers (P < 0.05 and <0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains (P = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels (τ = −0.588, P < 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis (τ = −0.209, P = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls (P < 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects. •Autism risk is increased by the C332 (Ala111) allele at rs4942, and by no other common variant located in the GLO1 locus.•In typically developing individuals, the C332 allele reduces brain GLO1 enzymatic activity.•Reduction in GLO1 activity translates into higher AGE levels in post-mortem C332 control brains.•AGE levels are lower in autistic compared to control brains.•Autistic and control brains differ in AGE levels only among C332 allele carriers.
Glyoxalase I (GLO1) is a homodimeric Zn(2+)-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with "unaffected sibling" status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon-intron junctions, detecting two additional SNPs (rs1049346, rs1130534) in linkage disequilibrium with rs4746. A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself (P < 0.05 and P < 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue (N = 38 and 13, respectively) of typically developing C332 allele carriers (P < 0.05 and <0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains (P = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels (τ = -0.588, P < 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis (τ = -0.209, P = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls (P < 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects.
Glyoxalase I (GLO1) is a homodimeric Zn(2+)-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with "unaffected sibling" status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon-intron junctions, detecting two additional SNPs (rs1049346, rs1130534) in linkage disequilibrium with rs4746. A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself (P &lt; 0.05 and P &lt; 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue (N = 38 and 13, respectively) of typically developing C332 allele carriers (P &lt; 0.05 and &lt;0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains (P = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels (τ = -0.588, P &lt; 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis (τ = -0.209, P = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls (P &lt; 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects.
Abstract Glyoxalase I (GLO1) is a homodimeric Zn2+ -dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with “unaffected sibling” status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon–intron junctions, detecting two additional SNPs ( rs1049346 , rs1130534 ) in linkage disequilibrium with rs4746 . A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself ( P  < 0.05 and P  < 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue ( N  = 38 and 13, respectively) of typically developing C332 allele carriers ( P  < 0.05 and <0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains ( P  = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels ( τ  = −0.588, P  < 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis ( τ  = −0.209, P  = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls ( P  < 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects.
Glyoxalase I (GLO1) is a homodimeric Zn super(2+)-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced glycation end-products (AGE). We previously found the rs4746 A332 (Glu111) allele of the GLO1 gene, which encodes for glyoxalase I, associated with "unaffected sibling" status in families with one or more children affected by Autism Spectrum Disorder (ASD). To identify and characterize this protective allele, we sequenced GLO1 exons and exon-intron junctions, detecting two additional SNPs (rs1049346, rs1130534) in linkage disequilibrium with rs4746. A family-based association study involving 385 simplex and 20 multiplex Italian families yielded a significant association with autism driven only by the rs4746 C332 (Ala111) allele itself (P < 0.05 and P < 0.001 under additive and dominant/recessive models, respectively). Glyoxalase enzymatic activity was significantly reduced both in leukocytes and in post-mortem temporocortical tissue (N = 38 and 13, respectively) of typically developing C332 allele carriers (P < 0.05 and <0.01), with no difference in Glo1 protein levels. Conversely, AGE amounts were significantly higher in the same C332 post-mortem brains (P = 0.001), with a strong negative correlation between glyoxalase activity and AGE levels ( tau = -0.588, P < 0.01). Instead, 19 autistic brains show a dysregulation of the glyoxalase-AGE axis ( tau = -0.209, P = 0.260), with significant blunting of glyoxalase activity and AGE amounts compared to controls (P < 0.05), and loss of rs4746 genotype effects. In summary, the GLO1 C332 (Ala111) allele confers autism vulnerability by reducing brain glyoxalase activity and enhancing AGE formation, but years after an autism diagnosis the glyoxalase-AGE axis appears profoundly disrupted, with loss of C332 allelic effects.
Author Gabriele, Stefano
Napolioni, Valerio
Persico, Antonio M
Lombardi, Federica
Altieri, Laura
Rousseau, Francis
Tirindelli, Maria Cristina
Sacco, Roberto
Bravaccio, Carmela
Gregorj, Chiara
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Keywords Autism
Methylglyoxal
Advanced glycation end-products
Glyoxalase
Autism spectrum disorder
Pervasive developmental disorders
Social environment
Reaction product
Developmental disorder
Vulnerability
Glycation
Pervasive developmental disorder
Family environment
Genetics
Language English
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Copyright © 2014 Elsevier Ltd. All rights reserved.
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Snippet Abstract Glyoxalase I (GLO1) is a homodimeric Zn2+ -dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of...
Glyoxalase I (GLO1) is a homodimeric Zn2+-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced...
Glyoxalase I (GLO1) is a homodimeric Zn(2+)-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced...
Glyoxalase I (GLO1) is a homodimeric Zn super(2+)-dependent isomerase involved in the detoxification of methylglyoxal and in limiting the formation of advanced...
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SubjectTerms Adolescent
Adult
Advanced glycation end-products
Alanine - genetics
Autism
Autism spectrum disorder
Biological and medical sciences
Brain - pathology
Child
Child clinical studies
Child Development Disorders, Pervasive - genetics
Child Development Disorders, Pervasive - pathology
Child, Preschool
Developmental disorders
Family Health
Female
Genetic Association Studies
Genotype
Glycation End Products, Advanced
Glyoxalase
Humans
Infantile autism
Lactoylglutathione Lyase - genetics
Lactoylglutathione Lyase - metabolism
Linkage Disequilibrium
Male
Medical sciences
Methylglyoxal
Middle Aged
Pervasive developmental disorders
Polymorphism, Single Nucleotide - genetics
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Serotonin - blood
Serotonin - urine
Statistics as Topic
Young Adult
Title The GLO1 C332 (Ala111) allele confers autism vulnerability: Family-based genetic association and functional correlates
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https://dx.doi.org/10.1016/j.jpsychires.2014.07.021
https://www.ncbi.nlm.nih.gov/pubmed/25201284
https://search.proquest.com/docview/1629960561
https://search.proquest.com/docview/1635042460
Volume 59
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