Biology subjects

Dalman, C.

Publications and source records attributed to Dalman, C..

3 recordsLinked to original sources

bioRxiv2020

Neonatal levels of acute phase proteins and risk of autism spectrum disorders

BackgroundImmune signaling pathways influence neurodevelopment and are hypothesized to contribute to the etiology of autism spectrum disorders (ASD). We aimed to assess risk of ASD in relation to levels of neonatal acute phase proteins, key components of innate immune function, measured in neonatal dried blood spots. MethodWe included 924 ASD cases, 1092 unaffected population-based controls, and 203 unaffected siblings to ASD cases in this case-control study nested within the register-based Stockholm Youth Cohort. Concentrations of nine different acute phase proteins were measured in eluates from neonatal dried blood spots from cases, controls, and siblings using a bead-based multiplex assay. ResultsC reactive protein was consistently associated with odds of ASD in case-control comparisons, with higher odds associated with the highest quintile compared to the middle quintile (OR 1.50, 95% CI 1.10 - 2.04) in adjusted analyses. In contrast, the lowest quintiles of alpha-2-macroglobulin (3.71, 1.21 - 11.33), ferritin (4.20, 1.40 - 12.65), and Serum Amyloid P (3.05, 1.16 - 8.01) were associated with odds of ASD in the matched sibling comparison. Neonatal acute phase proteins varied with perinatal environmental factors and maternal/fetal phenotypes. Significant interactions in terms of risk for ASD were observed between neonatal acute phase proteins and maternal infection in late pregnancy, maternal anemia, and maternal psychiatric history. ConclusionsIndicators of the neonatal innate immune response are associated with risk for ASD, though the nature of these associations varies considerably with factors in the perinatal environment and the genetic background of the comparison group.

molecular biology↗

bioRxiv2020

Maternal antibodies to gliadin and autism spectrum disorders in offspring - A population-based case-control study in Sweden

ObjectiveIndividuals diagnosed with autism spectrum disorders (ASD) are reported to have higher levels of antibodies directed towards gliadin, a component of wheat gluten. However, no study has examined such antibodies in etiologically-relevant periods before diagnosis. The objective of this study is to investigate if maternal levels of immunoglobulin G antibodies directed at gliadin, during pregnancy and at the time of birth, are associated with ASD in offspring. MethodsIn this population-based study set in Sweden with 921 ASD cases and 1090 controls, we analyzed levels of anti-gliadin antibodies (AGA) in archived neonatal dried blood spots (NDBS, as maternal IgG is transferred to the fetus) and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations to any ASD diagnosis and considering common comorbidities (i.e. intellectual disability [ID] and attention-deficit/hyperactivity disorder [ADHD]). We compared 206 ASD cases to their unaffected siblings to examine the potential for confounding by shared familial factors. ResultsHigh levels ([≥]90th percentile) of maternal AGA were associated with decreased odds of ASD, particularly ASD with comorbid ID, when measured in NDBS (OR 0.51, 95% CI 0.30-0.87) with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of maternal AGA were similarly associated with lower odds of ASD with ID in the sibling comparison. ConclusionsThis first study of exposure to AGA in the pre- and perinatal periods suggests that high levels of maternal AGA are associated with lower odds of ASD with ID.

molecular biology↗

bioRxiv2017

Gestational Age At Birth And Risk Of Intellectual Disability Without A Common Genetic Cause: Findings From The Stockholm Youth Cohort

BackgroundPreterm birth is linked to intellectual disability and there is evidence to suggest post-term birth may also incur risk. However, these associations have not yet been investigated in the absence of common genetic causes of intellectual disability (where risk associated with late delivery may be preventable) or with methods allowing stronger causal inference from non-experimental data. We aimed to examine risk of intellectual disability without a common genetic cause across the entire range of gestation, using a matched-sibling design to account for unmeasured confounding by shared familial factors.\n\nMethods and FindingsWe conducted a population-based retrospective study using data from the Stockholm Youth Cohort (n=499,621) and examined associations in a nested cohort of matched siblings (n=8,034). Children born at non-optimal gestational duration (before/after 40 weeks 3 days) were at greater risk of intellectual disability. Risk was greatest among those born extremely early (adjusted OR24 weeks=14.54 [95% CI 11.46-18.44]), lessening with advancing gestational age toward term (aOR32 weeks=3.59 [3.22-4.01]; aOR37 weeks=1.50 [1.38-1.63]); aOR38 weeks=1.26 [1.16-1.37]; aOR39 weeks=1.10 [1.04-1.17]) and increasing with advancing gestational age post-term (aOR42 weeks=1.16 [1.08-1.25]; aOR42 weeks=1.41 [1.21-1.64]; aOR44 weeks=1.71 [1.34-2.18]; aOR45 weeks=2.07 [1.47-2.92]). Associations persisted in a nested cohort of matched outcome-discordant siblings suggesting they were robust against confounding from shared genetic or environmental traits, although there may have been residual confounding by unobserved non-shared characteristics. Risk of intellectual disability was greatest among children showing evidence of fetal growth restriction, especially when birth occurred before or after term.\n\nConclusionsBirth at non-optimal gestational duration may be linked causally with greater risk of intellectual disability. The mechanisms underlying these associations need to be elucidated as they will be relevant to clinical practice concerning elective delivery within the term period and the mitigation of risk in children who are born post-term.

epidemiology↗