Background: Abnormalities in dopamine and norepinephrine signaling are implicated in cognitive impairments in bipolar disorder (BD) and attention‐deficit hyperactivity disorder (ADHD). This systematic review by the ISBD Targeting Cognition Task Force therefore aimed to investigate the possible benefits on cognition and/or ADHD symptoms and safety of established and off‐label ADHD therapies in BD.Methods: We included studies of ADHD medications in BD patients, which involved cognitive and/or safety measures. We followed the procedures of the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis (PRISMA) 2020 statement. Searches were conducted on PubMed, Embase and PsycINFO from inception until June 2023. Two authors reviewed the studies independently using the Revised Cochrane Collaboration's Risk of Bias tool for Randomized trials.Results: Seventeen studies were identified (N = 2136), investigating armodafinil (k = 4, N = 1581), methylphenidate (k = 4, N = 84), bupropion (k = 4, n = 249), clonidine (k = 1, n = 70), lisdexamphetamine (k = 1, n = 25), mixed amphetamine salts (k = 1, n = 30), or modafinil (k = 2, n = 97). Three studies investigated cognition, four ADHD symptoms, and 10 the safety. Three studies found treatment‐related ADHD symptom reduction: two involved methylphenidate and one amphetamine salts. One study found a trend towards pro‐cognitive effects of modafinil on some cognitive domains. No increased risk of (hypo)mania was observed. Five studies had low risk of bias, eleven a moderate risk, and one a serious risk of bias.Conclusions: Methylphenidate or mixed amphetamine salts may improve ADHD symptoms in BD. However, there is limited evidence regarding the effectiveness on cognition. The medications produced no increased mania risk when used alongside mood stabilizers. Further robust studies are needed to assess cognition in BD patients receiving psychostimulant treatment alongside mood stabilizers.

The placenta is increasingly recognized as a key mediator between the prenatal environment and long-term neurodevelopment. Emerging omics studies suggest that placental molecular profiles may predict neuropsychiatric outcomes, yet evidence has remained fragmented and rarely synthesized in a longitudinal framework. Here we present the first systematic review of longitudinal placental omics studies with direct placenta-child linkage, encompassing epigenomic, transcriptomic, and metabolomic approaches. A systematic search of PubMed, Scopus, and PsycINFO identified twelve eligible studies (total n = 1752 placentas), all of which followed children from birth to neurodevelopmental assessment in early or middle childhood. Across studies, specific loci and metabolites varied, but convergent signals consistently implicated three biological domains: immune signaling, oxidative stress, and metabolic regulation. Representative findings included replicated epigenetic alterations at DLL1, nutrient- and genotype-sensitive variation at CYP2E1 and IRS2, novel clusters at NHIP, transcriptomic integration involving LRRFIP1, environmentally responsive modules including GALC, AUTS2, and CSMD1, and metabolic shifts in fumarate, cystine, and 3-hydroxybutyrate. Notably, all longitudinal evidence to date centers on childhood outcomes, with the most robust associations reported for autism spectrum disorder, while links to schizophrenia and other adult psychiatric disorders remain speculative and are inferred indirectly from genetic or cross-sectional placental datasets. Together, these findings establish the placenta as a dynamic molecular interface where genetic background and environmental exposures converge to influence neurodevelopmental trajectories. By highlighting reproducible domains across omic layers, this review positions placental biology as a promising window into early biomarkers and mechanistic pathways of neuropsychiatric risk.

Esketamine has demonstrated efficacy in treatment-resistant depression (TRD), but medium-term real-world functional outcomes remain understudied. This study described 6-month depressive symptoms and functional trajectories during routine esketamine treatment, focusing on functional outcomes and remission correlates. In this prospective multicenter study, 60 patients with TRD initiating intranasal esketamine augmentation were assessed at baseline, Month 1, Month 3, and Month 6 using the Montgomery-Åsberg Depression Rating Scale (MADRS) and Sheehan Disability Scale (SDS). Mixed-effects models, Turnbull interval-censored time-to-remission analysis, logistic regression, and ROC analyses were performed. MADRS and SDS improved significantly at all follow-up time points (p < 0.001). At Month 6, symptomatic response and remission rates were 78.3 and 46.7%, while functional response and remission rates were 78.3 and 33.3%, respectively. Turnbull estimates showed cumulative functional remission rates of 5.0, 15.0, and 33.3% at Months 1, 3, and 6, respectively. MADRS-SDS correlations decreased over time, supporting partial symptomatic-functional dissociation. Higher baseline SDS (OR = 0.73, 95% CI: 0.59–0.89) and more previous antidepressant trials (ADTs; OR = 0.53, 95% CI: 0.35–0.82) were associated with lower odds of Month 6 functional remission; bootstrap internal validation supported coefficient stability. ROC-derived thresholds were considered sample-dependent and not clinically validated. Cumulative esketamine dosage was associated with functional response but not remission. Depressive symptoms and functioning improved progressively over 6 months during esketamine treatment in routine clinical care. Functional remission followed a slower trajectory than symptomatic remission and had partly distinct correlates, supporting functional monitoring as a distinct TRD outcome.