Correlational Insights into Attention-Deficit/Hyperactivity Disorder in Lebanon.

Attention-Deficit/Hyperactivity Disorder (ADHD), a prevalent childhood neurodevelopmental disorder with complex etiology involving genetic and environmental factors, causes impairments across various life domains and substantial social and economic burden. Identifying correlates to prevent its onset and decrease its incidence is crucial. To our knowledge, our study represents the first case-control investigation of Lebanese ADHD patients to explore potential correlations between familial, maternal, and child health variables and ADHD to enhance understanding of its etiology and aid in prevention efforts. We recruited 61 Lebanese ADHD patients and 58 matched controls aged 6-24 years from all districts of Lebanon. The data to analyze were collected using a questionnaire. We employed statistical tests, including the independent samples t-test and the Chi-square test or Fisher's exact test. We conducted a multivariate logistic regression analysis to identify the statistically significant factors explaining ADHD likelihood. We observed male predominance (68.9%) among patients. Maternal anemia during pregnancy (OR = 3.654; 95% CI [1.158-11.529]), maternal self-reported stress during pregnancy (OR = 3.268; 95% CI [1.263-8.456]), neonatal jaundice (OR = 5.020; 95% CI [1.438-17.532]), and familial history of ADHD (OR = 12.033; 95% CI [2.950-49.072]) were significantly associated with increased odds of the disorder. On the other hand, breastfeeding (OR = 0.263; 95% CI [0.092-0.757]) was identified as a protective factor against ADHD. This pilot study shed light on risk and protective factors associated with ADHD in the Lebanese population. The results are relevant, as some identified correlates could be avoidable. Further rigorous investigation is required to expand upon the observed correlations and to assist in early detection, prevention, and intervention strategies targeting ADHD.

P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/hyperactivity disorder.

Introduction: Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder characterized by hyperactivity, inattention, and impulsivity that often persist until adulthood. Frequent comorbid disorders accompany ADHD and two thirds of children diagnosed with ADHD also suffer from behavioural disorders and from alteration of sensory processing. We recently characterized the comorbidity between ADHD-like symptoms and pain sensitisation in a pharmacological mouse model of ADHD, and we demonstrated the implication of the anterior cingulate cortex and posterior insula. However, few studies have explored the causal mechanisms underlying the interactions between ADHD and pain. The implication of inflammatory mechanisms has been suggested but the signalling pathways involved have not been explored. Methods: We investigated the roles of purinergic signalling, at the crossroad of pain and neuroinflammatory pathways, by using a transgenic mouse line that carries a total deletion of the P2X4 receptor. Results: We demonstrated that P2X4 deletion prevents hyperactivity in the mouse model of ADHD. In contrast, the absence of P2X4 lowered thermal pain thresholds in sham conditions and did not affect pain sensitization in ADHD-like conditions. We further analysed microglia reactivity and the expression of inflammatory markers in wild type and P2X4KO mice. Our results revealed that P2X4 deletion limits microglia reactivity but at the same time exerts proinflammatory effects in the anterior cingulate cortex and posterior insula. Conclusion: This dual role of P2X4 could be responsible for the differential effects noted on ADHD-like symptoms and pain sensitization and calls for further studies to investigate the therapeutic benefit of targeting the P2X4 receptor in ADHD patients.