Prenatal Maternal Infections and Children’s Neurodevelopment in the UK Millennium Cohort Study: A Focus on ASD and ADHD

Objective: No clear answer has yet been attained as to the influence of prenatal exposure to infection on autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), either alone or as co-occurring issues. The current study examined links between hospital-recorded and maternal-reported prenatal infections and ASD, ADHD, and co-occurring ASD and ADHD. Methods: Participants were n = 15,462 children and mother pairs from the Millennium Cohort Study (MCS), a population-representative UK sample. Results: Findings show associations between maternal-reported infections and ASD, and some evidence of links with ADHD and co-occurring ASD and ADHD. Hospital-recorded infections were not found to be associated with ASD, ADHD, or their co-occurrence. Agreement between hospital-recorded and maternal-reported infections was low, which may explain the discrepant findings. Conclusion: Prenatal maternal infections may be associated with increased odds of ASD and ADHD. Findings point to the importance of drawing on multiple sources of information when ascertaining prenatal infection status.

A Proof-of-Concept Study of Maternal Immune Activation Mediated Induction of Toll-Like Receptor (TLR) and Inflammasome Pathways Leading To Neuroprogressive Changes and Schizophrenia-Like Behaviors in Offspring.

Infection, particularly prenatal infection leads to an enhanced risk of schizophrenia in the offspring. Interestingly, few data exist on the pathway(s) such as TLR and inflammasome, primarily involved in sensing the microorganisms and inducing downstream inflammatory responses, apoptosis and neuroprogressive changes in the prenatal infection-induced risk of schizophrenia. Herein, we aimed to discern whether prenatal infection-induced maternal immune activation (MIA) causes schizophrenia-like behaviors through activation of TLR and inflammasome pathways in the brain of offspring. Sprague Dawley rats (n=15/group) were injected either with poly (I:C) or LPS or saline at gestational day (GD)-12. Significantly elevated plasma levels of IL-1β, IL-6, TNF-α and IL-17A assessed after 24 hours were observed in poly (I:C) and LPS-treated rats, indicating MIA. The offspring rats of poly (I:C)-and LPS-treated dams displayed increased anxiety-like behaviors, deficits in social behaviors and prepulse inhibition. The hippocampus of offspring rats showed increased expression of TLR3, TLR4, NLRP3, IL-1β, and IL-18 of poly (I:C) and TLR3, TLR4, NLRP3, Cas1, IL-1β, and IL-18 of LPS-treated dams. Notably, the expression of these genes showed a positive correlation with apoptotic and a negative correlation with neuroprotective genes. Furthermore, TLR and inflammasome genes had significant impact on social deficits and impaired prepulse inhibition in offspring rats. The results suggest MIA due to prenatal infection perhaps trigger TLR, inflammasome and apoptotic pathways leading to the induction of schizophrenia-like behaviors in the later stages of life. Prenatal infections seem to drive neuroprogression and subsequently schizophrenia-like symptoms through a common central pathway involving TLR, inflammasome and apoptosis.

Prenatal maternal infections and psychopathology in childhood and adolescence: Findings from the ALSPAC birth cohort

Aims: Studies have suggested that exposure to prenatal infections may be a risk factor in the aetiology of neurodevelopmental disorders such as schizophrenia and autism, but that its effects may differ by timing of exposure. Evidence on other psychiatric outcomes, however, is scarce and mixed. The aims of this study were to examine whether exposure to infections, at any point in gestation and during each trimester, is associated with increased odds of psychiatric disorders (pervasive developmental disorders, attention-deficit hyperactivity disorder, behavioural disorders and emotional disorders) at ages 7 and 14. Methods: Participants were n = 8859 mother and child pairs from the UK Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Exposure to prenatal infections was assessed for each trimester using maternal self-reports. Children’s psychiatric status was assessed using the parent-reported Development and Well-being Assessment (DAWBA). Logistic regressions were used to examine links between prenatal infections and child outcomes. Results: Half of the mothers reported an infection at some point during pregnancy and 7% of children were reported to have a psychiatric condition. Increased odds of children having any psychiatric disorder at age 14 were found in association with infections at any point during pregnancy, OR = 1.27 (95% CI 1.04, 1.55) and in the third trimester specifically, OR = 1.28 (95% CI 1.02, 1.61), after adjusting for the effects of potential confounds and other covariates. No other links were found in adjusted models. Conclusions: Findings suggest that associations between prenatal infections and children’s psychiatric disorders are weak to non-existent, after adjusting for the effects of other factors.

Prenatal maternal infections and children’s socioemotional development: findings from the UK Millennium Cohort Study

Previous research suggests that prenatal maternal infections may be associated with increased odds of children having a neurodevelopmental disorder. However, little evidence exists on associations with broader child outcomes, especially subclinical symptoms. Participants were the N = 14,021 members of the population-representative UK Millennium Cohort Study. We examined associations between prenatal maternal infections, both maternal-reported and hospital-recorded, and children’s socioemotional development, using the Strengths and Difficulties Questionnaire (SDQ) at age three. Maternal-reported prenatal infections were associated with increased emotional symptoms, after adjusting for several potential confounds and covariates. Hospital-recorded prenatal infections were not associated with children’s socioemotional outcomes, after adjusting for potential confounding and covarying factors. Findings suggest that prenatal maternal infections, particularly those which the mothers remember months later, may be associated with increased emotional problems in early childhood. This emphasises the need for screening for and preventing infections during pregnancy. Further, the occurrence of prenatal infection indicates the potential need for early intervention for children’s emotional difficulties.

Prenatal maternal infections and children's socioemotional outcomes

Previous research suggests that prenatal maternal infections may be associated with increased odds of children having a neurodevelopmental disorder. However, little evidence exists on associations with broader child outcomes, especially subclinical symptoms. Participants were the N = 14,021 members of the population-representative UK Millennium Cohort Study. We examined associations between prenatal maternal infections, both maternal-reported and hospital-recorded, and children’s socioemotional development, using the Strengths and Difficulties Questionnaire (SDQ) at age three. Maternal-reported prenatal infections were associated with increased emotional symptoms, after adjusting for several potential confounds and covariates. Hospital-recorded prenatal infections were not associated with children’s socioemotional outcomes, after adjusting for potential confounding and covarying factors. Findings suggest that prenatal maternal infections, particularly those which the mothers remember months later, may be associated with increased emotional problems in early childhood. This emphasises the need for screening for and preventing infections during pregnancy. Further, the occurrence of prenatal infection indicates the potential need for early intervention for children’s emotional difficulties.

Prenatal maternal infections, ASD and ADHD

No clear answer has yet been attained as to the influence of prenatal exposure to infection on autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), either alone or as co-occurring issues. We examined links between hospital-recorded and maternal-reported prenatal infections and ASD, ADHD and co-occurring ASD and ADHD in a large population-representative UK sample. Significant associations between maternal-reported infections and ASD, ADHD and co-occurring ASD and ADHD were found, but no significant associations were found with hospital-recorded infections. Agreement between hospital-recorded and maternal-reported infections was low, which may explain the discrepant findings. Results point to the importance of drawing on multiple sources of information when determining whether or not a prenatal infection is present.

Screening on prenatal infections in the South and Southwest macro-regions in the State of Bahia, Brazil: detected on paper filter

Objectives: to estimate the detection rate on prenatal screening pathologies on paper filter in the South and Southwest in the State of Bahia, as well as to delineate the epidemiological profile of these pregnant women, calculate and estimate the rate of adherence and the coverage of the Program. Methods: a descriptive study was carried out from August 2013 to August 2015, and the data were obtained from the Labimuno/ICS/UFBA. Results: 64,743 pregnant women were included; the mean ages were 25 years for the Southwest macro-region and 23 for the South. The results on the screening tests showed positivity of 0.13% and 0.29% for HBsAg, 0.17% and 0.22% for cytomegalovirus, 0.07% and 0.09% for HCV, 0.13% and 0.38% for HTLV, 0.04% and 0.19% for HIV, 1.2% and 2.84% for syphilis, and 0.54% and 0.73% for toxoplasmosis in the Southwest and South macro-regions, respectively. The estimates on coverage were considered satisfactory. Sickle cell anemia showed positivity of 0.02% and of 0.04% and 5% and 6.3% presented sickle cell trait in the Southwest and South macro-regions, respectively. Conclusions: the frequencies of infections in maternal-fetal health were considered low, highlighting on syphilis and the presence for sickle cell trait.