Familial aggregation of attention-deficit/hyperactivity disorder / Qi CHEN in Journal of Child Psychology and Psychiatry, 58-3 (March 2017)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 58-3 (March 2017) . - p.231-239 Titre : Familial aggregation of attention-deficit/hyperactivity disorder Type de document : texte imprimé Auteurs : Qi CHEN, Auteur ; Isabell BRIKELL, Auteur ; Paul LICHTENSTEIN, Auteur ; Eva SERLACHIUS, Auteur ; Ralf KUJA-HALKOLA, Auteur ; Sven SANDIN, Auteur ; Henrik LARSSON, Auteur Article en page(s) : p.231-239 Langues : Anglais (eng) Mots-clés : Attention-deficit/hyperactivity disorder  diagnosis  family factor  sex differences  adulthood Index. décimale : PER Périodiques Résumé : Background Attention-deficit/hyperactivity disorder (ADHD) aggregates in families. To date, the strength, pattern, and characteristics of the familial aggregation have not been thoroughly assessed in a population-based family sample. Methods In this cohort study, we identified relative pairs of twins, full and half-siblings, and full and half cousins from 1,656,943 unique individuals born in Sweden between 1985 and 2006. The relatives of index persons were followed from their third birthday to 31 December 2009 for ADHD diagnosis. Birth year adjusted hazard ratio (HR), that is, the rate of ADHD in relatives of ADHD-affected index persons compared with the rate of ADHD in relatives of unaffected index persons, was estimated in the different types of relatives using Cox proportional hazards model. Results During the follow-up, 31,865 individuals were diagnosed with ADHD (male to female ratio was 3.7). The birth year adjusted HRs were as follows: 70.45 for monozygotic twins; 8.44 for dizygotic twins; 8.27 for full siblings; 2.86 for maternal half-siblings; 2.31 for paternal half-siblings; 2.24 for full cousins; 1.47 for half cousins. Maternal half-siblings had significantly higher HR than in paternal half-siblings. The HR did not seem to be affected by index person's sex. Full siblings of index persons with ADHD diagnosis present at age 18 or older had a higher rate of ADHD (HR: 11.49) than full siblings of index persons with ADHD diagnosis only before age 18 (HR: 4.68). Conclusions Familial aggregation of ADHD increases with increasing genetic relatedness. The familial aggregation is driven by not only genetic factors but also a small amount of shared environmental factors. Persistence of ADHD into adulthood indexes stronger familial aggregation of ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12616 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303 [article] Familial aggregation of attention-deficit/hyperactivity disorder [texte imprimé] / Qi CHEN, Auteur ; Isabell BRIKELL, Auteur ; Paul LICHTENSTEIN, Auteur ; Eva SERLACHIUS, Auteur ; Ralf KUJA-HALKOLA, Auteur ; Sven SANDIN, Auteur ; Henrik LARSSON, Auteur . - p.231-239. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 58-3 (March 2017) . - p.231-239 Mots-clés : Attention-deficit/hyperactivity disorder  diagnosis  family factor  sex differences  adulthood Index. décimale : PER Périodiques Résumé : Background Attention-deficit/hyperactivity disorder (ADHD) aggregates in families. To date, the strength, pattern, and characteristics of the familial aggregation have not been thoroughly assessed in a population-based family sample. Methods In this cohort study, we identified relative pairs of twins, full and half-siblings, and full and half cousins from 1,656,943 unique individuals born in Sweden between 1985 and 2006. The relatives of index persons were followed from their third birthday to 31 December 2009 for ADHD diagnosis. Birth year adjusted hazard ratio (HR), that is, the rate of ADHD in relatives of ADHD-affected index persons compared with the rate of ADHD in relatives of unaffected index persons, was estimated in the different types of relatives using Cox proportional hazards model. Results During the follow-up, 31,865 individuals were diagnosed with ADHD (male to female ratio was 3.7). The birth year adjusted HRs were as follows: 70.45 for monozygotic twins; 8.44 for dizygotic twins; 8.27 for full siblings; 2.86 for maternal half-siblings; 2.31 for paternal half-siblings; 2.24 for full cousins; 1.47 for half cousins. Maternal half-siblings had significantly higher HR than in paternal half-siblings. The HR did not seem to be affected by index person's sex. Full siblings of index persons with ADHD diagnosis present at age 18 or older had a higher rate of ADHD (HR: 11.49) than full siblings of index persons with ADHD diagnosis only before age 18 (HR: 4.68). Conclusions Familial aggregation of ADHD increases with increasing genetic relatedness. The familial aggregation is driven by not only genetic factors but also a small amount of shared environmental factors. Persistence of ADHD into adulthood indexes stronger familial aggregation of ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12616 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303

How rare and common risk variation jointly affect liability for autism spectrum disorder / Lambertus KLEI in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 66 p. Titre : How rare and common risk variation jointly affect liability for autism spectrum disorder Type de document : texte imprimé Auteurs : Lambertus KLEI, Auteur ; Lora Lee MCCLAIN, Auteur ; Behrang MAHJANI, Auteur ; Klea PANAYIDOU, Auteur ; Silvia DE RUBEIS, Auteur ; Anna-Carin Säll GRAHNAT, Auteur ; Gun KARLSSON, Auteur ; Yanchun LU, Auteur ; Nadine MELHEM, Auteur ; Xiu XU, Auteur ; Abraham REICHENBERG, Auteur ; Sven SANDIN, Auteur ; Christina M. HULTMAN, Auteur ; Joseph D. BUXBAUM, Auteur ; Kathryn ROEDER, Auteur ; Bernie DEVLIN, Auteur Article en page(s) : 66 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  De novo mutation  Genomic-Best Linear Unbiased Prediction (G-BLUP)  Liability  Polygenic risk score Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic studies have implicated rare and common variations in liability for autism spectrum disorder (ASD). Of the discovered risk variants, those rare in the population invariably have large impact on liability, while common variants have small effects. Yet, collectively, common risk variants account for the majority of population-level variability. How these rare and common risk variants jointly affect liability for individuals requires further study. METHODS: To explore how common and rare variants jointly affect liability, we assessed two cohorts of ASD families characterized for rare and common genetic variations (Simons Simplex Collection and Population-Based Autism Genetics and Environment Study). We analyzed data from 3011 affected subjects, as well as two cohorts of unaffected individuals characterized for common genetic variation: 3011 subjects matched for ancestry to ASD subjects and 11,950 subjects for estimating allele frequencies. We used genetic scores, which assessed the relative burden of common genetic variation affecting risk of ASD (henceforth "burden"), and determined how this burden was distributed among three subpopulations: ASD subjects who carry a potentially damaging variant implicated in risk of ASD ("PDV carriers"); ASD subjects who do not ("non-carriers"); and unaffected subjects who are assumed to be non-carriers. RESULTS: Burden harbored by ASD subjects is stochastically greater than that harbored by control subjects. For PDV carriers, their average burden is intermediate between non-carrier ASD and control subjects. Both carrier and non-carrier ASD subjects have greater burden, on average, than control subjects. The effects of common and rare variants likely combine additively to determine individual-level liability. LIMITATIONS: Only 305 ASD subjects were known PDV carriers. This relatively small subpopulation limits this study to characterizing general patterns of burden, as opposed to effects of specific PDVs or genes. Also, a small fraction of subjects that are categorized as non-carriers could be PDV carriers. CONCLUSIONS: Liability arising from common and rare risk variations likely combines additively to determine risk of any individual diagnosed with ASD. On average, ASD subjects carry a substantial burden of common risk variation, even if they also carry a rare PDV affecting risk. En ligne : http://dx.doi.org/10.1186/s13229-021-00466-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 [article] How rare and common risk variation jointly affect liability for autism spectrum disorder [texte imprimé] / Lambertus KLEI, Auteur ; Lora Lee MCCLAIN, Auteur ; Behrang MAHJANI, Auteur ; Klea PANAYIDOU, Auteur ; Silvia DE RUBEIS, Auteur ; Anna-Carin Säll GRAHNAT, Auteur ; Gun KARLSSON, Auteur ; Yanchun LU, Auteur ; Nadine MELHEM, Auteur ; Xiu XU, Auteur ; Abraham REICHENBERG, Auteur ; Sven SANDIN, Auteur ; Christina M. HULTMAN, Auteur ; Joseph D. BUXBAUM, Auteur ; Kathryn ROEDER, Auteur ; Bernie DEVLIN, Auteur . - 66 p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 66 p. Mots-clés : Autism spectrum disorder  De novo mutation  Genomic-Best Linear Unbiased Prediction (G-BLUP)  Liability  Polygenic risk score Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic studies have implicated rare and common variations in liability for autism spectrum disorder (ASD). Of the discovered risk variants, those rare in the population invariably have large impact on liability, while common variants have small effects. Yet, collectively, common risk variants account for the majority of population-level variability. How these rare and common risk variants jointly affect liability for individuals requires further study. METHODS: To explore how common and rare variants jointly affect liability, we assessed two cohorts of ASD families characterized for rare and common genetic variations (Simons Simplex Collection and Population-Based Autism Genetics and Environment Study). We analyzed data from 3011 affected subjects, as well as two cohorts of unaffected individuals characterized for common genetic variation: 3011 subjects matched for ancestry to ASD subjects and 11,950 subjects for estimating allele frequencies. We used genetic scores, which assessed the relative burden of common genetic variation affecting risk of ASD (henceforth "burden"), and determined how this burden was distributed among three subpopulations: ASD subjects who carry a potentially damaging variant implicated in risk of ASD ("PDV carriers"); ASD subjects who do not ("non-carriers"); and unaffected subjects who are assumed to be non-carriers. RESULTS: Burden harbored by ASD subjects is stochastically greater than that harbored by control subjects. For PDV carriers, their average burden is intermediate between non-carrier ASD and control subjects. Both carrier and non-carrier ASD subjects have greater burden, on average, than control subjects. The effects of common and rare variants likely combine additively to determine individual-level liability. LIMITATIONS: Only 305 ASD subjects were known PDV carriers. This relatively small subpopulation limits this study to characterizing general patterns of burden, as opposed to effects of specific PDVs or genes. Also, a small fraction of subjects that are categorized as non-carriers could be PDV carriers. CONCLUSIONS: Liability arising from common and rare risk variations likely combines additively to determine risk of any individual diagnosed with ASD. On average, ASD subjects carry a substantial burden of common risk variation, even if they also carry a rare PDV affecting risk. En ligne : http://dx.doi.org/10.1186/s13229-021-00466-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459

Medications for attention-deficit/hyperactivity disorder in individuals with or without coexisting autism spectrum disorder: analysis of data from the Swedish prescribed drug register / Viktoria JOHANSSON in Journal of Neurodevelopmental Disorders, 12 (2020)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 12 (2020) Titre : Medications for attention-deficit/hyperactivity disorder in individuals with or without coexisting autism spectrum disorder: analysis of data from the Swedish prescribed drug register Type de document : texte imprimé Auteurs : Viktoria JOHANSSON, Auteur ; Sven SANDIN, Auteur ; Zheng CHANG, Auteur ; Mark J. TAYLOR, Auteur ; Paul LICHTENSTEIN, Auteur ; Brian M. D'ONOFRIO, Auteur ; Henrik LARSSON, Auteur ; Clara HELLNER, Auteur ; Linda HALLDNER, Auteur Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Aged  Aged, 80 and over  Attention Deficit Disorder with Hyperactivity/complications/drug  therapy/epidemiology  Autism Spectrum Disorder/complications/drug therapy/epidemiology  Child  Child, Preschool  Humans  Methylphenidate/therapeutic use  Middle Aged  Pharmaceutical Preparations  Sweden/epidemiology  Young Adult Index. décimale : PER Périodiques Résumé : BACKGROUND: Clinical studies found that medication for attention-deficit/hyperactivity disorder (ADHD) is effective in coexisting autism spectrum disorder (ASD), but current research is based on small clinical studies mainly performed on children or adolescents. We here use register data to examine if individuals with ADHD and coexisting ASD present differences in the prescribing patterns of ADHD medication when compared to individuals with pure ADHD. METHODS: Data with information on filled prescriptions and diagnoses was retrieved from the Swedish Prescribed Drug Register and the National Patient Register. We identified 34,374 individuals with pure ADHD and 5012 individuals with ADHD and coexisting ASD, aged between 3 and 80 years. The first treatment episode with ADHD medications (≥ 2 filled prescriptions within 90 days) and daily doses of methylphenidate during a 3-year period was measured. Odds ratios (ORs) were calculated for the likelihood of being prescribed ADHD medication in individuals with and without ASD and Wilcoxon rank-sum test was used to compare group differences in dose per day. RESULTS: Individuals with ADHD and coexisting ASD were less likely to start continuous treatment with ADHD medication (ADHD 80.5%; ADHD with ASD 76.2%; OR, 0.80; 95% confidence interval, 0.75-0.86), were less likely to be prescribed methylphenidate, and were more commonly prescribed second line treatments such as dexamphetamine, amphetamine, or modafinil. No group difference was observed for atomoxetine. In adults with ADHD and coexisting ASD, methylphenidate was prescribed in lower daily doses over three years as compared to individuals with pure ADHD. CONCLUSIONS: The findings indicate that there are differences in the medical treatment of individuals with or without ASD. If these differences are due to different medication responses in ASD or due to other factors such as clinicians' perceptions of medication effects in patients with ASD, needs to be further studied. En ligne : https://dx.doi.org/10.1186/s11689-020-09352-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 [article] Medications for attention-deficit/hyperactivity disorder in individuals with or without coexisting autism spectrum disorder: analysis of data from the Swedish prescribed drug register [texte imprimé] / Viktoria JOHANSSON, Auteur ; Sven SANDIN, Auteur ; Zheng CHANG, Auteur ; Mark J. TAYLOR, Auteur ; Paul LICHTENSTEIN, Auteur ; Brian M. D'ONOFRIO, Auteur ; Henrik LARSSON, Auteur ; Clara HELLNER, Auteur ; Linda HALLDNER, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 12 (2020) Mots-clés : Adolescent  Adult  Aged  Aged, 80 and over  Attention Deficit Disorder with Hyperactivity/complications/drug  therapy/epidemiology  Autism Spectrum Disorder/complications/drug therapy/epidemiology  Child  Child, Preschool  Humans  Methylphenidate/therapeutic use  Middle Aged  Pharmaceutical Preparations  Sweden/epidemiology  Young Adult Index. décimale : PER Périodiques Résumé : BACKGROUND: Clinical studies found that medication for attention-deficit/hyperactivity disorder (ADHD) is effective in coexisting autism spectrum disorder (ASD), but current research is based on small clinical studies mainly performed on children or adolescents. We here use register data to examine if individuals with ADHD and coexisting ASD present differences in the prescribing patterns of ADHD medication when compared to individuals with pure ADHD. METHODS: Data with information on filled prescriptions and diagnoses was retrieved from the Swedish Prescribed Drug Register and the National Patient Register. We identified 34,374 individuals with pure ADHD and 5012 individuals with ADHD and coexisting ASD, aged between 3 and 80 years. The first treatment episode with ADHD medications (≥ 2 filled prescriptions within 90 days) and daily doses of methylphenidate during a 3-year period was measured. Odds ratios (ORs) were calculated for the likelihood of being prescribed ADHD medication in individuals with and without ASD and Wilcoxon rank-sum test was used to compare group differences in dose per day. RESULTS: Individuals with ADHD and coexisting ASD were less likely to start continuous treatment with ADHD medication (ADHD 80.5%; ADHD with ASD 76.2%; OR, 0.80; 95% confidence interval, 0.75-0.86), were less likely to be prescribed methylphenidate, and were more commonly prescribed second line treatments such as dexamphetamine, amphetamine, or modafinil. No group difference was observed for atomoxetine. In adults with ADHD and coexisting ASD, methylphenidate was prescribed in lower daily doses over three years as compared to individuals with pure ADHD. CONCLUSIONS: The findings indicate that there are differences in the medical treatment of individuals with or without ASD. If these differences are due to different medication responses in ASD or due to other factors such as clinicians' perceptions of medication effects in patients with ASD, needs to be further studied. En ligne : https://dx.doi.org/10.1186/s11689-020-09352-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573

Optimal interpregnancy interval in autism spectrum disorder: A multi-national study of a modifiable risk factor / Gavin PEREIRA in Autism Research, 14-11 (November 2021)  

Public ISBD [article]  inAutism Research > 14-11 (November 2021) . - p.2432-2443 Titre : Optimal interpregnancy interval in autism spectrum disorder: A multi-national study of a modifiable risk factor Type de document : texte imprimé Auteurs : Gavin PEREIRA, Auteur ; Richard W. FRANCIS, Auteur ; Mika GISSLER, Auteur ; Stefan N. HANSEN, Auteur ; Arad KODESH, Auteur ; Helen LEONARD, Auteur ; Stephen Z. LEVINE, Auteur ; V.R. MITTER, Auteur ; Erik T. PARNER, Auteur ; Annette K. REGAN, Auteur ; Abraham REICHENBERG, Auteur ; Sven SANDIN, Auteur ; Auli SUOMINEN, Auteur ; Diana SCHENDEL, Auteur Article en page(s) : p.2432-2443 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/epidemiology  Birth Intervals  Female  Finland/epidemiology  Humans  Pregnancy  Retrospective Studies  Risk Factors  autism spectrum disorder  family planning services  longitudinal studies Index. décimale : PER Périodiques Résumé : It is biologically plausible that risk of autism spectrum disorder (ASD) is elevated by both short and long interpregnancy intervals (IPI). We conducted a retrospective cohort study of singleton, non-nulliparous live births, 1998-2007 in Denmark, Finland, and Sweden (N = 925,523 births). Optimal IPI was defined as the IPI at which minimum risk was observed. Generalized additive models were used to estimate relative risks (RR) of ASD and 95% Confidence Intervals (CI). Population impact fractions (PIF) for ASD were estimated under scenarios for shifts in the IPI distribution. We observed that the association between ASD (N = 9302) and IPI was U-shaped for all countries. ASD risk was lowest (optimal IPI) at 35 months for all countries combined, and at 30, 33, and 39 months in Denmark, Finland, and Sweden, respectively. Fully adjusted RRs at IPIs of 6, 12, and 60 months were 1.41 (95% CI: 1.08, 1.85), 1.26 (95% CI: 1.02, 1.56), and 1.24 (95% CI: 0.98, 1.58) compared to an IPI of 35 months. Under the most conservative scenario PIFs ranged from 5% (95% CI: 1%-8%) in Denmark to 9% (95% CI: 6%-12%) in Sweden. The minimum ASD risk followed IPIs of 30-39 months across three countries. These results reflect both direct IPI effects and other, closely related social and biological pathways. If our results reflect biologically causal effects, increasing optimal IPIs and reducing their indications, such as unintended pregnancy and delayed age at first pregnancy has the potential to prevent a salient proportion of ASD cases. LAY SUMMARY: Waiting 35 months to conceive again after giving birth resulted in the least risk of autism. Shorter and longer intervals resulted in risks that were up to 50% and 85% higher, respectively. About 5% to 9% of autism cases might be avoided by optimizing birth spacing. En ligne : http://dx.doi.org/10.1002/aur.2599 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 [article] Optimal interpregnancy interval in autism spectrum disorder: A multi-national study of a modifiable risk factor [texte imprimé] / Gavin PEREIRA, Auteur ; Richard W. FRANCIS, Auteur ; Mika GISSLER, Auteur ; Stefan N. HANSEN, Auteur ; Arad KODESH, Auteur ; Helen LEONARD, Auteur ; Stephen Z. LEVINE, Auteur ; V.R. MITTER, Auteur ; Erik T. PARNER, Auteur ; Annette K. REGAN, Auteur ; Abraham REICHENBERG, Auteur ; Sven SANDIN, Auteur ; Auli SUOMINEN, Auteur ; Diana SCHENDEL, Auteur . - p.2432-2443. Langues : Anglais (eng) in Autism Research > 14-11 (November 2021) . - p.2432-2443 Mots-clés : Autism Spectrum Disorder/epidemiology  Birth Intervals  Female  Finland/epidemiology  Humans  Pregnancy  Retrospective Studies  Risk Factors  autism spectrum disorder  family planning services  longitudinal studies Index. décimale : PER Périodiques Résumé : It is biologically plausible that risk of autism spectrum disorder (ASD) is elevated by both short and long interpregnancy intervals (IPI). We conducted a retrospective cohort study of singleton, non-nulliparous live births, 1998-2007 in Denmark, Finland, and Sweden (N = 925,523 births). Optimal IPI was defined as the IPI at which minimum risk was observed. Generalized additive models were used to estimate relative risks (RR) of ASD and 95% Confidence Intervals (CI). Population impact fractions (PIF) for ASD were estimated under scenarios for shifts in the IPI distribution. We observed that the association between ASD (N = 9302) and IPI was U-shaped for all countries. ASD risk was lowest (optimal IPI) at 35 months for all countries combined, and at 30, 33, and 39 months in Denmark, Finland, and Sweden, respectively. Fully adjusted RRs at IPIs of 6, 12, and 60 months were 1.41 (95% CI: 1.08, 1.85), 1.26 (95% CI: 1.02, 1.56), and 1.24 (95% CI: 0.98, 1.58) compared to an IPI of 35 months. Under the most conservative scenario PIFs ranged from 5% (95% CI: 1%-8%) in Denmark to 9% (95% CI: 6%-12%) in Sweden. The minimum ASD risk followed IPIs of 30-39 months across three countries. These results reflect both direct IPI effects and other, closely related social and biological pathways. If our results reflect biologically causal effects, increasing optimal IPIs and reducing their indications, such as unintended pregnancy and delayed age at first pregnancy has the potential to prevent a salient proportion of ASD cases. LAY SUMMARY: Waiting 35 months to conceive again after giving birth resulted in the least risk of autism. Shorter and longer intervals resulted in risks that were up to 50% and 85% higher, respectively. About 5% to 9% of autism cases might be avoided by optimizing birth spacing. En ligne : http://dx.doi.org/10.1002/aur.2599 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450

Parental and Perinatal Risk Factors for Autism: Epidemiological Findings and Potential Mechanisms / Sven SANDIN

Public ISBD in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Titre : Parental and Perinatal Risk Factors for Autism: Epidemiological Findings and Potential Mechanisms Type de document : texte imprimé Auteurs : Sven SANDIN, Auteur ; Alexander KOLEVZON, Auteur ; Stephen Z. LEVINE, Auteur ; Christina M. HULTMAN, Auteur ; Abraham REICHENBERG, Auteur Année de publication : 2013 Importance : p.195-202 Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : There is evidence that non-heritable familial pre- or perinatal factors play a role in the etiology of autism and autism spectrum disorders (ASD). According to current evidence from epidemiological studies, two groups of factors show a consistent relationship with ASD: advancing parental age and preterm birth and intrauterine growth restriction. Using a systematic review and meta-analysis of epidemiological studies incorporating a comprehensive assessment of risk factors, we have examined the evidence for an association between advancing parental age, low birth weight, preterm birth and being born small for gestational age, and risk for ASD in the offspring. Advancing maternal age (35 or older), and paternal age (40 or older), show a consistent relationship with ASD. Current evidence also supports a relationship between low birth weight (lt; 2,500 grams), preterm birth (lt; 37 weeks) and being born small for gestational age, and ASD. Future research should continue to examine these variables using large, population-based cohorts in order to offer a more refined modeling of risk and potential confounders, and to attempt to distinguish between autism and spectrum disorders. Identifying common and unique risk factors may be important to understand shared and non-shared etiologies. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Parental and Perinatal Risk Factors for Autism: Epidemiological Findings and Potential Mechanisms [texte imprimé] / Sven SANDIN, Auteur ; Alexander KOLEVZON, Auteur ; Stephen Z. LEVINE, Auteur ; Christina M. HULTMAN, Auteur ; Abraham REICHENBERG, Auteur . - 2013 . - p.195-202. Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : There is evidence that non-heritable familial pre- or perinatal factors play a role in the etiology of autism and autism spectrum disorders (ASD). According to current evidence from epidemiological studies, two groups of factors show a consistent relationship with ASD: advancing parental age and preterm birth and intrauterine growth restriction. Using a systematic review and meta-analysis of epidemiological studies incorporating a comprehensive assessment of risk factors, we have examined the evidence for an association between advancing parental age, low birth weight, preterm birth and being born small for gestational age, and risk for ASD in the offspring. Advancing maternal age (35 or older), and paternal age (40 or older), show a consistent relationship with ASD. Current evidence also supports a relationship between low birth weight (lt; 2,500 grams), preterm birth (lt; 37 weeks) and being born small for gestational age, and ASD. Future research should continue to examine these variables using large, population-based cohorts in order to offer a more refined modeling of risk and potential confounders, and to attempt to distinguish between autism and spectrum disorders. Identifying common and unique risk factors may be important to understand shared and non-shared etiologies. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189

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