Risk factors for autism: perinatal factors, parental psychiatric history, and socioeconomic status.
ABSTRACT Research suggests that heredity and early fetal development play a causal role in autism. This case-control study explored the association between perinatal factors, parental psychiatric history, socioeconomic status, and risk of autism. The study was nested within a cohort of all children born in Denmark after 1972 and at risk of being diagnosed with autism until December 1999. Prospectively recorded data were obtained from nationwide registries in Denmark. Cases totaled 698 children with a diagnosis of autism; each case was individually matched by gender, birth year, and age to 25 controls. Analyses by conditional logistic regression produced risk ratios and 95% confidence intervals. Adjusted analyses showed that the risk of autism was associated with breech presentation (risk ratio (RR) = 1.63, 95% confidence interval (CI): 1.18, 2.26), low Apgar score at 5 minutes (RR = 1.89, 95% CI: 1.10, 3.27), gestational age at birth <35 weeks (RR = 2.45, 95% CI: 1.55, 3.86), and parental psychiatric history (schizophrenia-like psychosis: RR = 3.44, 95% CI: 1.48, 7.95; affective disorder: RR = 2.91, 95% CI: 1.65, 5.14). Analyses showed no statistically significant association between risk of autism and weight for gestational age, parity, number of antenatal visits, parental age, or socioeconomic status. Results suggest that prenatal environmental factors and parental psychopathology are associated with the risk of autism. These factors seem to act independently.
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ABSTRACT: Early-life stress is a key risk factor for the development of neuropsychiatric disorders later in life. Neuronal cell adhesion molecules have been strongly implicated in the pathophysiology of psychiatric disorders and in modulating social behaviors associated with these diseases. Neuroligin-2 is a synaptic cell adhesion molecule, located at the postsynaptic membrane of inhibitory GABAergic synapses, and is involved in synaptic stabilization and maturation. Alterations in neuroligin-2 expression have previously been associated with changes in social behavior linked to psychiatric disorders, including schizophrenia and autism. In this study, we show that early-life stress, induced by limited nesting and bedding material, leads to impaired social recognition and increased aggression in adult mice, accompanied by increased expression levels of hippocampal neuroligin-2. Viral overexpression of hippocampal neuroligin-2 in adulthood mimics early-life stress-induced alterations in social behavior and social cognition. Moreover, viral knockdown of neuroligin-2 in the adult hippocampus attenuates the early-life stress-induced behavioral changes. Our results highlight the importance of neuroligin-2 in mediating early-life stress effects on social behavior and social cognition and its promising role as a novel therapeutic target for neuropsychiatric disorders. Copyright © 2015 Elsevier Ltd. All rights reserved.Psychoneuroendocrinology 02/2015; 55:128-143. DOI:10.1016/j.psyneuen.2015.02.016 · 5.59 Impact Factor
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ABSTRACT: We examined trends in autism spectrum disorders (ASD) and the association of ASD with parental age among young New York City (NYC) children. Children born in NYC to resident mothers from 1994-2001 were identified through vital statistics records (N = 927,003). Records were linked to data from NYC Early Intervention (EI) Program through 2004. The independent parental age-specific odds of having an ASD before 36 months of age were estimated using multiple logistic regression controlling for risk factors. The increase in ASD attributable to changes in parental age at birth was examined. Births to mothers and fathers 35 years or older increased 14.9 and 11.5 %, respectively, between 1994 and 2001. ASD prevalence in EI increased significantly from 1 in 3,300 children born in 1994 to 1 in 233 children born in 2001. Children born to mothers ages 25-29, 30-34 and 35 or older had significantly greater odds of being diagnosed with ASD than children of mothers younger than 25 years (OR 1.5, 1.6, and 1.9, respectively). Children born to fathers ages 35 or older (OR 1.4) had greater odds of ASD than children of fathers younger than 25. The change in parental age accounted for only 2.7 % of the increase in ASD prevalence. Older paternal age and maternal age were independently associated with increased risk of ASD. However, while parental age at birth increased between the 1994 and 2001 birth cohorts in NYC, it did not explain the increase in number of ASD cases.
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ABSTRACT: Although now believed to be two distinct disorders, autism spectrum disorders (ASD) and schizophrenia spectrum disorders (SSD) share multiple phenotypic similarities and risk factors, and have been reported to co-occur at elevated rates. In this narrative review, we give a brief overview of the phenomenological, genetic, environmental, and imaging evidence for the overlap between ASD and SSD, highlighting similarities and areas of distinction. We examine eight possible alternate models of explanation for the association and comorbidity between the disorders, and set out a research agenda to test these models. Understanding how and why these disorders co-occur has important implications for diagnosis, treatment, and prognosis, as well as for developing fundamental aetiological models of the disorders. Copyright © 2015. Published by Elsevier Ltd.Neuroscience & Biobehavioral Reviews 05/2015; DOI:10.1016/j.neubiorev.2015.04.012 · 10.28 Impact Factor