Autism: Where Genetics Meets the Immune System / Antonio M. PERSICO in Autism Research and Treatment, (July 2012)  

Public ISBD [article]  inAutism Research and Treatment > (July 2012) . - 2 p. Titre : Autism: Where Genetics Meets the Immune System Type de document : texte imprimé Auteurs : Antonio M. PERSICO, Auteur ; Judy VAN DE WATER, Auteur ; Carlos A. PARDO, Auteur Année de publication : 2012 Article en page(s) : 2 p. Langues : Anglais (eng) Mots-clés : Immunologie Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1155/2012/486359 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=181 [article] Autism: Where Genetics Meets the Immune System [texte imprimé] / Antonio M. PERSICO, Auteur ; Judy VAN DE WATER, Auteur ; Carlos A. PARDO, Auteur . - 2012 . - 2 p. Langues : Anglais (eng) in Autism Research and Treatment > (July 2012) . - 2 p. Mots-clés : Immunologie Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1155/2012/486359 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=181

Candidate gene study of HOXB1 in autism spectrum disorder / Lucia A. MUSCARELLA in Molecular Autism, (May 2010)  

Public ISBD [article]  inMolecular Autism > (May 2010) . - 39 p. Titre : Candidate gene study of HOXB1 in autism spectrum disorder Type de document : texte imprimé Auteurs : Lucia A. MUSCARELLA, Auteur ; Carmela BRAVACCIO, Auteur ; Cindy SCHNEIDER, Auteur ; Monica SACCANI, Auteur ; Carlo LENTI, Auteur ; Roberto MILITERNI, Auteur ; Grazia GIANA, Auteur ; Riccardo ALESSANDRELLI, Auteur ; Barbara MANZI, Auteur ; Roberto SACCO, Auteur ; Vito GUARNIERI, Auteur ; Raun D. MELMED, Auteur ; Paolo CURATOLO, Auteur ; Antonio M. PERSICO, Auteur ; Leonardo D'AGRUMA, Auteur Année de publication : 2010 Article en page(s) : 39 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background HOXB1 plays a major role in brainstem morphogenesis and could partly determine the cranial circumference in conjunction with HOXA1. In our sample, HOXA1 alleles significantly influence head growth rates both in autistic patients and in population controls. An initial report, suggesting that HOXB1 could confer autism vulnerability in interaction with HOXA1, was not confirmed by five small association studies. Methods Our sample includes 269 autistic individuals, belonging to 219 simplex and 28 multiplex families. A mutational analysis of the two exons and flanking intronic sequences of the HOXB1 gene was carried out in 84 autistic patients by denaturing high performance liquid chromatography, followed by DNA sequencing. Identified rare variants were then searched by a restriction analysis in 236 autistic patients and 325-345 controls. Case-control and family-based association studies were performed on two common variants in 169 Italian patients versus 184 Italian controls and in 247 trios. Results We identified three common polymorphisms, rs72338773 [c.82insACAGCGCCC (INS/nINS)], rs12939811 [c.309A>T (Q103H)], and rs7207109 [c.450G>A (A150A)] and three rare variants, namely IVS1+63G>A, rs35115415 [c.702G>A (V234V)] and c.872_873delinsAA (S291N). SNPs rs72338773 and rs12939811 were not associated with autism, using either a case-control (alleles, exact P=0.13) or a family-based design [transmission/disequilibrium test (TDT)x2=1.774, P=0.183]. The rare variants, all inherited from one of the parents, were present in two Italian and in two Caucasian-American families. Autistic probands in two families surprisingly inherited a distinct rare variant from each parent. The IVS1+63A allele was present in 3/690 control chromosomes, whereas rare alleles at rs35115415 and c.872_873delinsAA (S291N) were not found in 662 and 650 control chromosomes, respectively. The INS-T309 allele influenced head size, but its effect appears more modest and shows no interaction with HOXA1 alleles. The INS-T309 allele is also associated with more severe stereotypic behaviours, according to ADI-R scores (N= 60 patients, P<0.01). Conclusions HOXB1 mutations do not represent a common cause of autism, nor do HOXB1 common variants play important roles in autism vulnerability. HOXB1 provides minor, albeit detectable contributions to head circumference in autistic patients, with HOXA1 displaying more prominent effects. HOXB1 variants may modulate the clinical phenotype, especially in the area of stereotypic behaviours. En ligne : http://dx.doi.org/10.1186/2040-2392-1-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=103 [article] Candidate gene study of HOXB1 in autism spectrum disorder [texte imprimé] / Lucia A. MUSCARELLA, Auteur ; Carmela BRAVACCIO, Auteur ; Cindy SCHNEIDER, Auteur ; Monica SACCANI, Auteur ; Carlo LENTI, Auteur ; Roberto MILITERNI, Auteur ; Grazia GIANA, Auteur ; Riccardo ALESSANDRELLI, Auteur ; Barbara MANZI, Auteur ; Roberto SACCO, Auteur ; Vito GUARNIERI, Auteur ; Raun D. MELMED, Auteur ; Paolo CURATOLO, Auteur ; Antonio M. PERSICO, Auteur ; Leonardo D'AGRUMA, Auteur . - 2010 . - 39 p. Langues : Anglais (eng) in Molecular Autism > (May 2010) . - 39 p. Index. décimale : PER Périodiques Résumé : Background HOXB1 plays a major role in brainstem morphogenesis and could partly determine the cranial circumference in conjunction with HOXA1. In our sample, HOXA1 alleles significantly influence head growth rates both in autistic patients and in population controls. An initial report, suggesting that HOXB1 could confer autism vulnerability in interaction with HOXA1, was not confirmed by five small association studies. Methods Our sample includes 269 autistic individuals, belonging to 219 simplex and 28 multiplex families. A mutational analysis of the two exons and flanking intronic sequences of the HOXB1 gene was carried out in 84 autistic patients by denaturing high performance liquid chromatography, followed by DNA sequencing. Identified rare variants were then searched by a restriction analysis in 236 autistic patients and 325-345 controls. Case-control and family-based association studies were performed on two common variants in 169 Italian patients versus 184 Italian controls and in 247 trios. Results We identified three common polymorphisms, rs72338773 [c.82insACAGCGCCC (INS/nINS)], rs12939811 [c.309A>T (Q103H)], and rs7207109 [c.450G>A (A150A)] and three rare variants, namely IVS1+63G>A, rs35115415 [c.702G>A (V234V)] and c.872_873delinsAA (S291N). SNPs rs72338773 and rs12939811 were not associated with autism, using either a case-control (alleles, exact P=0.13) or a family-based design [transmission/disequilibrium test (TDT)x2=1.774, P=0.183]. The rare variants, all inherited from one of the parents, were present in two Italian and in two Caucasian-American families. Autistic probands in two families surprisingly inherited a distinct rare variant from each parent. The IVS1+63A allele was present in 3/690 control chromosomes, whereas rare alleles at rs35115415 and c.872_873delinsAA (S291N) were not found in 662 and 650 control chromosomes, respectively. The INS-T309 allele influenced head size, but its effect appears more modest and shows no interaction with HOXA1 alleles. The INS-T309 allele is also associated with more severe stereotypic behaviours, according to ADI-R scores (N= 60 patients, P<0.01). Conclusions HOXB1 mutations do not represent a common cause of autism, nor do HOXB1 common variants play important roles in autism vulnerability. HOXB1 provides minor, albeit detectable contributions to head circumference in autistic patients, with HOXA1 displaying more prominent effects. HOXB1 variants may modulate the clinical phenotype, especially in the area of stereotypic behaviours. En ligne : http://dx.doi.org/10.1186/2040-2392-1-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=103

Clinical, developmental and serotonemia phenotyping of a sample of 70 Italian patients with Phelan-McDermid Syndrome / Lisa ASTA in Journal of Neurodevelopmental Disorders, 16 (2024)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 16 (2024) Titre : Clinical, developmental and serotonemia phenotyping of a sample of 70 Italian patients with Phelan-McDermid Syndrome Type de document : texte imprimé Auteurs : Lisa ASTA, Auteur ; Arianna RICCIARDELLO, Auteur ; Francesca CUCINOTTA, Auteur ; Laura TURRIZIANI, Auteur ; Maria BONCODDO, Auteur ; Fabiana BELLOMO, Auteur ; Jessica ANGELINI, Auteur ; Martina GNAZZO, Auteur ; Giulia SCANDOLO, Auteur ; Giulia PISANÒ, Auteur ; Francesco PELAGATTI, Auteur ; Fethia CHEHBANI, Auteur ; Michela CAMIA, Auteur ; Antonio M. PERSICO, Auteur Langues : Anglais (eng) Mots-clés : Humans  Male  Female  Italy  Phenotype  Child  Chromosome Deletion  Chromosomes, Human, Pair 22/genetics  Adolescent  Child, Preschool  Adult  Young Adult  Chromosome Disorders/physiopathology/complications/blood  Autism Spectrum Disorder/blood/physiopathology/complications  Nerve Tissue Proteins/blood/genetics  Intellectual Disability/etiology/blood  Shank3  22q13 deletion syndrome  Autism spectrum disorder  Hyperserotonemia  Intellectual disability  Macrocephaly  Neuroinflammation  Phelan-McDermid syndrome  Phenotype  Serotonin Index. décimale : PER Périodiques Résumé : BACKGROUND: Phelan-McDermid syndrome (PMS) is caused by monoallelic loss or inactivation at the SHANK3 gene, located in human chr 22q13.33, and is often associated with Autism Spectrum Disorder (ASD). OBJECTIVES: To assess the clinical and developmental phenotype in a novel sample of PMS patients, including for the first time auxometric trajectories and serotonin blood levels. METHODS: 70 Italian PMS patients were clinically characterized by parental report, direct medical observation, and a thorough medical and psychodiagnostic protocol. Serotonin levels were measured in platelet-rich plasma by HPLC. RESULTS: Our sample includes 59 (84.3%) cases with chr. 22q13 terminal deletion, 5 (7.1%) disruptive SHANK3 mutations, and 6 (8.6%) ring chromosome 22. Intellectual disability was present in 69 (98.6%) cases, motor coordination disorder in 65 (92.9%), ASD in 20 (28.6%), and lifetime bipolar disorder in 12 (17.1%). Prenatal and postnatal complications were frequent (22.9%-48.6%). Expressive and receptive language were absent in 49 (70.0%) and 19 (27.1%) cases, respectively. Decreased pain sensitivity was reported in 56 (80.0%), hyperactivity in 49 (80.3%), abnormal sleep in 45 (64.3%), congenital dysmorphisms in 35 (58.3%), chronic stool abnormalities and especially constipation in 29 (41.4%). Parents reported noticing behavioral abnormalities during early childhood immediately after an infective episode in 34 (48.6%) patients. Brain MRI anomalies were observed in 53 (79.1%), EEG abnormalities in 16 (23.5%), kidney and upper urinary tract malformations in 18 (28.1%). Two novel phenotypes emerged: (a) a subgroup of 12/44 (27.3%) PMS patients displays smaller head size at enrollment (mean age 11.8 yrs) compared to their first year of neonatal life, documenting a deceleration of head growth (p < 0.001); (b) serotonin blood levels are significantly lower in 21 PMS patients compared to their 21 unaffected siblings (P < 0.05), and to 432 idiopathic ASD cases (p < 0.001). CONCLUSIONS: We replicate and extend the description of many phenotypic characteristics present in PMS, and report two novel features: (1) growth trajectories are variable and head growth appears to slow down during childhood in some PMS patients; (2) serotonin blood levels are decreased in PMS, and not increased as frequently occurs in ASD. Further investigations of these novel features are under way. En ligne : https://dx.doi.org/10.1186/s11689-024-09572-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] Clinical, developmental and serotonemia phenotyping of a sample of 70 Italian patients with Phelan-McDermid Syndrome [texte imprimé] / Lisa ASTA, Auteur ; Arianna RICCIARDELLO, Auteur ; Francesca CUCINOTTA, Auteur ; Laura TURRIZIANI, Auteur ; Maria BONCODDO, Auteur ; Fabiana BELLOMO, Auteur ; Jessica ANGELINI, Auteur ; Martina GNAZZO, Auteur ; Giulia SCANDOLO, Auteur ; Giulia PISANÒ, Auteur ; Francesco PELAGATTI, Auteur ; Fethia CHEHBANI, Auteur ; Michela CAMIA, Auteur ; Antonio M. PERSICO, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 16 (2024) Mots-clés : Humans  Male  Female  Italy  Phenotype  Child  Chromosome Deletion  Chromosomes, Human, Pair 22/genetics  Adolescent  Child, Preschool  Adult  Young Adult  Chromosome Disorders/physiopathology/complications/blood  Autism Spectrum Disorder/blood/physiopathology/complications  Nerve Tissue Proteins/blood/genetics  Intellectual Disability/etiology/blood  Shank3  22q13 deletion syndrome  Autism spectrum disorder  Hyperserotonemia  Intellectual disability  Macrocephaly  Neuroinflammation  Phelan-McDermid syndrome  Phenotype  Serotonin Index. décimale : PER Périodiques Résumé : BACKGROUND: Phelan-McDermid syndrome (PMS) is caused by monoallelic loss or inactivation at the SHANK3 gene, located in human chr 22q13.33, and is often associated with Autism Spectrum Disorder (ASD). OBJECTIVES: To assess the clinical and developmental phenotype in a novel sample of PMS patients, including for the first time auxometric trajectories and serotonin blood levels. METHODS: 70 Italian PMS patients were clinically characterized by parental report, direct medical observation, and a thorough medical and psychodiagnostic protocol. Serotonin levels were measured in platelet-rich plasma by HPLC. RESULTS: Our sample includes 59 (84.3%) cases with chr. 22q13 terminal deletion, 5 (7.1%) disruptive SHANK3 mutations, and 6 (8.6%) ring chromosome 22. Intellectual disability was present in 69 (98.6%) cases, motor coordination disorder in 65 (92.9%), ASD in 20 (28.6%), and lifetime bipolar disorder in 12 (17.1%). Prenatal and postnatal complications were frequent (22.9%-48.6%). Expressive and receptive language were absent in 49 (70.0%) and 19 (27.1%) cases, respectively. Decreased pain sensitivity was reported in 56 (80.0%), hyperactivity in 49 (80.3%), abnormal sleep in 45 (64.3%), congenital dysmorphisms in 35 (58.3%), chronic stool abnormalities and especially constipation in 29 (41.4%). Parents reported noticing behavioral abnormalities during early childhood immediately after an infective episode in 34 (48.6%) patients. Brain MRI anomalies were observed in 53 (79.1%), EEG abnormalities in 16 (23.5%), kidney and upper urinary tract malformations in 18 (28.1%). Two novel phenotypes emerged: (a) a subgroup of 12/44 (27.3%) PMS patients displays smaller head size at enrollment (mean age 11.8 yrs) compared to their first year of neonatal life, documenting a deceleration of head growth (p < 0.001); (b) serotonin blood levels are significantly lower in 21 PMS patients compared to their 21 unaffected siblings (P < 0.05), and to 432 idiopathic ASD cases (p < 0.001). CONCLUSIONS: We replicate and extend the description of many phenotypic characteristics present in PMS, and report two novel features: (1) growth trajectories are variable and head growth appears to slow down during childhood in some PMS patients; (2) serotonin blood levels are decreased in PMS, and not increased as frequently occurs in ASD. Further investigations of these novel features are under way. En ligne : https://dx.doi.org/10.1186/s11689-024-09572-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

Cluster Analysis of Autistic Patients Based on Principal Pathogenetic Components / Roberto SACCO in Autism Research, 5-2 (April 2012)  

Public ISBD [article]  inAutism Research > 5-2 (April 2012) . - p.137-147 Titre : Cluster Analysis of Autistic Patients Based on Principal Pathogenetic Components Type de document : texte imprimé Auteurs : Roberto SACCO, Auteur ; Carlo LENTI, Auteur ; Monica SACCANI, Auteur ; Paolo CURATOLO, Auteur ; Barbara MANZI, Auteur ; Carmela BRAVACCIO, Auteur ; Antonio M. PERSICO, Auteur Année de publication : 2012 Article en page(s) : p.137-147 Langues : Anglais (eng) Mots-clés : pervasive developmental disorders  cluster analysis  immune system  neurodevelopment  principal component analysis Index. décimale : PER Périodiques Résumé : We have recently described four principal pathogenetic components in autism: (I) circadian and sensory dysfunction, (II) immune abnormalities, (III) neurodevelopmental delay, and (IV) stereotypic behaviors. Using hierarchical and k-means clustering, the same 245 patients assessed in our principal component analysis can be partitioned into four clusters: (a) 43 (17.6%) have prominent immune abnormalities accompanied by some circadian and sensory issues; (b) 44 (18.0%) display major circadian and sensory dysfunction, with little or no immune symptoms; (c) stereotypies predominate in 75 (31.0%); and (d) 83 (33.9%) show a mixture of all four components, with greater disruptive behaviors and mental retardation. The “immune” component provides the largest contributions to phenotypic variance (P = 2.7 x 10–45), followed by “stereotypic behaviors.” These patient clusters may likely differ in genetic and immune underpinnings, developmental trajectories, and response to treatment. En ligne : http://dx.doi.org/10.1002/aur.1226 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=155 [article] Cluster Analysis of Autistic Patients Based on Principal Pathogenetic Components [texte imprimé] / Roberto SACCO, Auteur ; Carlo LENTI, Auteur ; Monica SACCANI, Auteur ; Paolo CURATOLO, Auteur ; Barbara MANZI, Auteur ; Carmela BRAVACCIO, Auteur ; Antonio M. PERSICO, Auteur . - 2012 . - p.137-147. Langues : Anglais (eng) in Autism Research > 5-2 (April 2012) . - p.137-147 Mots-clés : pervasive developmental disorders  cluster analysis  immune system  neurodevelopment  principal component analysis Index. décimale : PER Périodiques Résumé : We have recently described four principal pathogenetic components in autism: (I) circadian and sensory dysfunction, (II) immune abnormalities, (III) neurodevelopmental delay, and (IV) stereotypic behaviors. Using hierarchical and k-means clustering, the same 245 patients assessed in our principal component analysis can be partitioned into four clusters: (a) 43 (17.6%) have prominent immune abnormalities accompanied by some circadian and sensory issues; (b) 44 (18.0%) display major circadian and sensory dysfunction, with little or no immune symptoms; (c) stereotypies predominate in 75 (31.0%); and (d) 83 (33.9%) show a mixture of all four components, with greater disruptive behaviors and mental retardation. The “immune” component provides the largest contributions to phenotypic variance (P = 2.7 x 10–45), followed by “stereotypic behaviors.” These patient clusters may likely differ in genetic and immune underpinnings, developmental trajectories, and response to treatment. En ligne : http://dx.doi.org/10.1002/aur.1226 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=155

Differential methylation at the RELN gene promoter in temporal cortex from autistic and typically developing post-puberal subjects / Carla LINTAS in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.18 Titre : Differential methylation at the RELN gene promoter in temporal cortex from autistic and typically developing post-puberal subjects Type de document : texte imprimé Auteurs : Carla LINTAS, Auteur ; Roberto SACCO, Auteur ; Antonio M. PERSICO, Auteur Article en page(s) : p.18 Langues : Anglais (eng) Mots-clés : Autism  DNA methylation  Epigenetics  Post-mortem brains  Reelin Index. décimale : PER Périodiques Résumé : BACKGROUND: Reelin plays a pivotal role in neurodevelopment and in post-natal synaptic plasticity and has been implicated in the pathogenesis of autism spectrum disorder (ASD). The reelin (RELN) gene expression is significantly decreased in ASD, both in the brain and peripherally. Methylation at the RELN gene promoter is largely triggered at puberty, and hypermethylation has been found in post-mortem brains of schizophrenic and bipolar patients. METHODS: In this study, we assessed RELN gene methylation status in post-mortem temporocortical tissue samples (BA41/42 or 22) of six pairs of post-puberal individuals with ASD and typically developing subjects, matched for sex (male:female, M:F = 5:1), age, and post-mortem interval. RESULTS: ASD patients display a significantly higher number of methylated CpG islands and heavier methylation in the 5' region of the RELN gene promoter, spanning from -458 to -223 bp, whereas controls have more methylated CpG positions and greater extent of methylation at the 3' promoter region, spanning from -222 to +1 bp. The most upstream promoter region (-458 to -364 bp) is methylated only in ASD brains, while the most downstream region (-131 to +1 bp) is methylated exclusively in control brains. Within this general framework, three different methylation patterns are discernible, each correlated with different extents of reduction in reelin gene expression among ASD individuals compared to controls. CONCLUSIONS: The methylation pattern is different in ASD and control post-mortem brains. ASD-specific CpG positions, located in the most upstream gene promoter region, may exert a functional role potentially conferring ASD risk by blunting RELN gene expression. En ligne : http://dx.doi.org/10.1186/s11689-016-9151-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348 [article] Differential methylation at the RELN gene promoter in temporal cortex from autistic and typically developing post-puberal subjects [texte imprimé] / Carla LINTAS, Auteur ; Roberto SACCO, Auteur ; Antonio M. PERSICO, Auteur . - p.18. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.18 Mots-clés : Autism  DNA methylation  Epigenetics  Post-mortem brains  Reelin Index. décimale : PER Périodiques Résumé : BACKGROUND: Reelin plays a pivotal role in neurodevelopment and in post-natal synaptic plasticity and has been implicated in the pathogenesis of autism spectrum disorder (ASD). The reelin (RELN) gene expression is significantly decreased in ASD, both in the brain and peripherally. Methylation at the RELN gene promoter is largely triggered at puberty, and hypermethylation has been found in post-mortem brains of schizophrenic and bipolar patients. METHODS: In this study, we assessed RELN gene methylation status in post-mortem temporocortical tissue samples (BA41/42 or 22) of six pairs of post-puberal individuals with ASD and typically developing subjects, matched for sex (male:female, M:F = 5:1), age, and post-mortem interval. RESULTS: ASD patients display a significantly higher number of methylated CpG islands and heavier methylation in the 5' region of the RELN gene promoter, spanning from -458 to -223 bp, whereas controls have more methylated CpG positions and greater extent of methylation at the 3' promoter region, spanning from -222 to +1 bp. The most upstream promoter region (-458 to -364 bp) is methylated only in ASD brains, while the most downstream region (-131 to +1 bp) is methylated exclusively in control brains. Within this general framework, three different methylation patterns are discernible, each correlated with different extents of reduction in reelin gene expression among ASD individuals compared to controls. CONCLUSIONS: The methylation pattern is different in ASD and control post-mortem brains. ASD-specific CpG positions, located in the most upstream gene promoter region, may exert a functional role potentially conferring ASD risk by blunting RELN gene expression. En ligne : http://dx.doi.org/10.1186/s11689-016-9151-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348

Environmental Factors and Autism Spectrum Disorder / Antonio M. PERSICO in Key Issues in Mental Health, 180 (2015)

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Evaluating Sex and Age Differences in ADI-R and ADOS Scores in a Large European Multi-site Sample of Individuals with Autism Spectrum Disorder / Julian TILLMANN in Journal of Autism and Developmental Disorders, 48-7 (July 2018)  

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Gene–environment interactions in autism spectrum disorder / Antonio M. PERSICO

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Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder / Daniel B. CAMPBELL in Autism Research, 1-3 (June 2008)  

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Gut mobilization improves behavioral symptoms and modulates urinary p-cresol in chronically constipated autistic children: A prospective study / Laura TURRIZIANI in Autism Research, 15-1 (January 2022)  

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Interactions gènes-environnement dans la pathogénie / Marcello D’AMELIO

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Preference for biological motion is reduced in ASD: implications for clinical trials and the search for biomarkers / Luke MASON in Molecular Autism, 12 (2021)  

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Principal pathogenetic components and biological endophenotypes in autism spectrum disorders / Roberto SACCO in Autism Research, 3-5 (October 2010)  

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Resting state EEG power spectrum and functional connectivity in autism: a cross-sectional analysis / Pilar GARCES in Molecular Autism, 13 (2022)  

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Slow intestinal transit contributes to elevate urinary p-cresol level in Italian autistic children / Stefano GABRIELE in Autism Research, 9-7 (July 2016)  

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