Neurodevelopmental disorders have been associated with hearing problems (HP) later in life, but there is limited information regarding their shared biology.

We leveraged large-scale genome-wide datasets to estimate genetic correlation (global and local), polygenic overlap, and locus-specific pleiotropy among HP, autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and Tourette syndrome (TS). Then, we investigated shared molecular functions, biological processes, and cellular components, and performed a drug-repurposing analysis to identify compounds that may target the pathogenic processes linking neurodevelopmental disorders to HP.

We observed high genetic correlation of HP with ASD (rg = 0.22) and TS (rg = 0.22). With respect to HP-ADHD polygenic overlap, 34% of the causal variants were shared between these conditions, with only 74% of them showing concordant effect directions. We also identified nine chromosomal regions with evidence of ADHD-HP local genetic correlations with pleiotropic effects on other outcomes, such as smoking initiation, brain-imaging phenotypes, and bilirubin levels. With respect to HP-ASD, we observed an inverse local genetic correlation within CD33 chromosomal region. Pleiotropy among HP, ASD, and ADHD was also identified in two variants (rs325485 and rs2207286) included within 95% credible sets related to neuropsychiatric conditions, altered hearing function, and other traits such as risk taking and insomnia. Drug-repurposing analyses identified anisomycin for HP-ASD shared biological mechanisms and five compounds related to HP-ADHD pleiotropy.

Our findings provide evidence that the comorbidity between neurodevelopmental disorders and HP is at least partially due to shared pathogenic processes acting through intrinsic and extrinsic factors.

Polygenic risk scores (PRSs) capture genetic vulnerability to psychiatric conditions. However, PRSs are often associated with multiple mental health problems in children, complicating their use in research and clinical practice. The current study is the first to systematically test which PRSs associate broadly with all forms of childhood psychopathology, and which PRSs are more specific to one or a handful of forms of psychopathology.

The sample consisted of 4717 unrelated children (mean age = 9.92, s.d. = 0.62; 47.1% female; all European ancestry). Psychopathology was conceptualized hierarchically as empirically derived general factor (p-factor) and five specific factors: externalizing, internalizing, neurodevelopmental, somatoform, and detachment. Partial correlations explored associations between psychopathology factors and 22 psychopathology-related PRSs. Regressions tested which level of the psychopathology hierarchy was most strongly associated with each PRS.

Thirteen PRSs were significantly associated with the general factor, most prominently Chronic Multisite Pain-PRS (r = 0.098), ADHD-PRS (r = 0.079), and Depression-PRS (r = 0.078). After adjusting for the general factor, Depression-PRS, Neuroticism-PRS, PTSD-PRS, Insomnia-PRS, Chronic Back Pain-PRS, and Autism-PRS were not associated with lower order factors. Conversely, several externalizing PRSs, including Adventurousness-PRS and Disinhibition-PRS, remained associated with the externalizing factor (|r| = 0.040–0.058). The ADHD-PRS remained uniquely associated with the neurodevelopmental factor (r = 062).

PRSs developed to predict vulnerability to emotional difficulties and chronic pain generally captured genetic risk for all forms of childhood psychopathology. PRSs developed to predict vulnerability to externalizing difficulties, e.g. disinhibition, tended to be more specific in predicting behavioral problems. The results may inform translation of existing PRSs to pediatric research and future clinical practice.

Few studies have assessed the characteristics of spousal psychopathologies among parents of schoolchildren with and without psychological disorders (PD) in China.

Parental symptoms were measured using the General Health Questionnaire (GHQ) in 275 mothers and 278 fathers of 298 schoolchildren with PDs diagnosed in a population survey and in 825 mothers and 834 fathers of 894 schoolchildren without PDs as a 1:3 matched comparison group. Spousal GHQ scores were compared. Childhood PD type, presence of childhood comorbidities, and multiple parental and family characteristics were examined as predictors for parental GHQ scores by multiple linear regression analyses.

The GHQ scores were significantly higher among mothers and fathers of children with any PD. Maternal GHQ scores were higher than paternal scores and significantly correlated with paternal GHQ scores in both groups. Spousal GHQ, personal PD history, and childhood PD comorbidity were significant independent predictors of both parents’ GHQ scores. There were also significant associations among parental chronic disease, low family income, and paternal and maternal GHQ score, as well as among low maternal education, less common disorder (LCD) prevalence in children and maternal GHQ score. The rate of GHQ score ≥3 for both parents was significantly higher in the study group than the control group (15.1 vs.7.0%).

Parents of children with any PD type demonstrate significantly elevated psychopathologies, and psychopathology tends to occur concomitantly and resemble that of the other spouse. Screening and treatment of parental psychiatric symptoms will benefit all family members.