Christelle Langley

Background: Artificial intelligence (AI), alongside emerging digital and neurotechnologies, is increasingly incorporated into mental health care, psychosomatic medicine, and psychotherapy. However, the clinical value of these tools cannot be judged by technical performance alone. These fields are characterized by diagnostic heterogeneity, reliance on language-based and self-reported information, complex biopsychosocial pathways, and substantial interindividual variability in treatment response. Clinically meaningful progress therefore requires integrating technological progress and biological markers with patients’ lived experience, personal history, and social context to catalyze person-centered precision assessment, decision-making and intervention. Summary: This review examines how AI and emerging technologies may contribute to mental health care across diagnostic assessment, biomarker development, treatment selection, personalized neuromodulation, adaptive interventions, and conversational agents. We argue that AI should support and improve, not replace, clinical assessments and care by integrating complex biopsychosocial data into precision person-centered decision making and intervention. Realizing this potential will require careful attention to clinical validation, safety, equity, commodification and governance. Key Messages: The clinical value of AI and emerging technologies will depend on their responsible integration into context-sensitive, person-centered mental health care. AI has the potential to strengthen diagnostic assessment, inform treatment selection, and expand therapeutic options while preserving the centrality of the human therapeutic alliance. Successful implementation requires combining computational precision with clinical judgment, ethical oversight, and demonstrated clinical benefit to improve clinical outcomes and quality of life.

Growing recognition of the importance of prevention in mental health has led to increased interest in modifiable lifestyle factors that support brain health, cognition, and well-being. This editorial examines evidence for an accessible and low-cost protective factor across the lifespan, namely reading for pleasure. Drawing on subjective surveys and objective studies using longitudinal, neuroimaging, and behavioral methods, we highlight converging findings that link reading engagement with improved brain and mental health, better cognitive performance, and reduced risk of cognitive decline. Survey data in adults suggested that reading was associated with reduced stress, greater empathy, enhanced well-being, and decreased loneliness. Longitudinal cohort studies further indicate that cognitively stimulating activities, particularly reading, are associated with a lower risk of dementia and slower cognitive decline, even among individuals with lower educational attainment. In childhood and adolescence, early reading for pleasure has been linked to better attention, memory, executive function, academic achievement, and fewer mental health problems. Neuroimaging findings suggest that reading is associated with structural and functional differences in brain regions supporting executive control, emotional regulation, and social cognition. Importantly, these benefits appear independent of socioeconomic background. Book club studies may suggest additional social benefits of reading in groups. Together, the evidence supports reading for pleasure and engaging in book clubs as scalable interventions, which may promote cognitive reserve, resilience, and lifelong mental well-being.

Background: Longitudinal studies of seed‐based functional connectivity (SBFC) in young adult Huntington's disease gene‐expanded (HDGE) individuals are rare, and none, to our knowledge, have examined adult cohorts decades from predicted clinical motor diagnosis. Objectives: To examine longitudinal functional connectivity (FC) changes over ~4.8 years in adult HDGE individuals before clinical motor diagnosis compared with matched controls, all selected from the HD Young Adult Study (HD‐YAS) cohort, focusing on bilateral caudate and putamen as seeds. Methods: A subset of 71 right‐handed individuals (43 HDGEs and 28 controls) from the HD‐YAS underwent resting‐state functional magnetic resonance imaging (fMRI) at two visits ~4.8 years apart. SBFC analyses focused on bilateral caudate and putamen seeds. Mixed‐effects analysis of variance (ANOVA) tested main effects of group, time, and group × time interactions, with false discovery rate (FDR) correction. Post hoc tests explored significant findings. Results: HDGEs showed reduced FC between the putamen and cerebellar vermis/lobules and brainstem ( P ‐FDR ≤ 0.01), alongside increased connectivity with precuneus ( P ‐FDR = 0.04), supramarginal, and angular gyri ( P ‐FDR = 0.04). Over ~4.8 years, HDGEs exhibited different FC trajectories compared with controls, displaying FC reductions between the right caudate and paracingulate, frontal ( P ‐FDR = < 0.001), occipital ( P ‐FDR = < 0.01), and striatal regions ( P ‐FDR = ≤ 0.03). Conclusions: These findings provide the first longitudinal evidence of early cortico‐striatal and cerebellar functional network changes in adult HDGEs decades before clinical motor diagnosis, alongside possible compensatory processes in key hubs of the default mode network. These early FC changes likely reflect a dynamic interplay between neurodegenerative processes and adaptive reorganization, a balance that may ultimately fail as pathology progresses. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Early detection and prevention of psychiatric disorders, particularly depression, remain as major global health challenges, yet reliable tools for identifying individuals before symptom onset are lacking. Here, we combine functional neuroimaging with computational modeling to identify a mechanistic biomarker of depression risk. In a population-based adolescent cohort (IMAGEN, N = 1332), we found that weakened neural representations of emotional signals were linked to depressive symptoms. Perturbation experiments in a brain-aligned deep learning model showed that this deficit reflects overregularized emotion perception, producing a negative perceptual bias. A neurocomputational signature of this mechanism predicted depression symptom onset up to 4 years later at the IMAGEN follow-up ( N = 725), was associated with both a genetic-risk variant and polygenic risk for depression, and improved depression classification in a patient cohort (STRATIFY, N = 411). These findings suggest a possible mechanism linking genetic vulnerability to altered emotion perception and future depression, and propose a predictive computational marker with potential for early detection and prevention.

Attention deficit hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental condition characterised by impairments in sustained attention, executive functioning, and emotional regulation, with significant lifelong consequences if untreated. Recent years have seen substantial increases in ADHD diagnoses and stimulant prescriptions across children, adolescents, and adults, alongside a parallel rise in the non-medical use of cognitive-enhancing drugs by neurotypical individuals. This review examines five key issues: factors driving rising ADHD diagnoses and prescriptions; the cognitive profile of ADHD and mechanisms of pharmacological treatments; reasons for increasing cognitive enhancer use in neurotypical populations; evidence for their efficacy in neurotypical individuals; and associated ethical implications. We review evidence implicating digital technology, parenting styles, educational incentives, and diagnostic practices in rising ADHD prevalence. Cognitive studies demonstrate that ADHD is associated with deficits in sustained attention, working memory, inhibitory control, and emotional regulation, underpinned by fronto-striatal dysfunction. Stimulant medications such as methylphenidate and lisdexamfetamine effectively improve 'cold' cognitive functions and change dysfuntional neural circuitry to a more typically developing pattern, though emotional dysregulation may persist. In neurotypical individuals, drugs such as methylphenidate and modafinil produce small-to-moderate improvements in cognition, particularly by increasing cognitive effort and motivation, with greatest benefits in those operating below optimal levels. However, their growing use raises ethical concerns regarding safety, fairness, coercion, and regulation. We argue that careful risk-benefit evaluation, long-term research studies, and informed policy are urgently needed to guide responsible use.

Background: Menopause is a natural physiological process, but its effects on the brain remain poorly understood. In England, approximately 15% of women use hormone-replacement therapy (HRT) to manage menopausal symptoms. However, the psychological benefits of HRT are not well established. This study aims to investigate the impact of menopause and HRT on mental health, cognitive function, and brain structure. Methods: We analyzed data from nearly 125,000 participants in the UK Biobank to assess associations between menopause, HRT use, and outcomes related to mental health, cognition, and brain morphology. Specifically, we focused on gray matter volumes in the medial temporal lobe (MTL) and anterior cingulate cortex (ACC). Results: Menopause was associated with increased levels of anxiety, depression, and sleep difficulties. Women using HRT reported greater mental health challenges than post-menopausal women not using HRT. Post-hoc analyses revealed that women prescribed HRT had higher levels of pre-existing mental health symptoms. In terms of brain structure, MTL and ACC volumes were smaller in post-menopausal women compared to pre-menopausal women, with the lowest volumes observed in the HRT group. Conclusions: Our findings suggest that menopause is linked to adverse mental health outcomes and reductions in gray matter volume in key brain regions. The use of HRT does not appear to mitigate these effects and may be associated with more pronounced mental health challenges, potentially due to underlying baseline differences. These results have important implications for understanding the neurobiological effects of HRT and highlighting the unmet need for addressing mental health problems during menopause.

BACKGROUND: Cognitive impairments are a hallmark of Huntington's disease (HD). METHODS: Seventy‐one participants (43 HD gene‐expanded [HDGE], 28 healthy controls) from the HD‐Young Adult Study at two timepoints ≈ 4.7 years apart, completed the Cambridge Neuropsychological Test Automated Battery Rapid Visual Information Processing task and underwent resting‐state functional magnetic resonance imaging. We focused on predefined regions of interest that are involved in sustained attention. RESULTS: HDGE individuals showed significantly poorer sustained attention than controls ( p _adj = 0.007), with no significant change over time. Functional connectivity (FC) analyses revealed group differences in attention‐related networks, including the occipital–operculum and lentiform–orbitalis pathways. Time and group × time effects were also observed in frontal and parietal regions. DISCUSSION: These findings demonstrate early and persistent attention deficits in HDGE, linked to altered FC in attention‐related circuits. This supports the presence of early cognitive dysfunction in HD and highlights potential compensatory and pathological changes in brain networks prior to the onset of clinical motor symptoms. Highlights: We detail the discovery of early sustained attention deficits in Huntington's disease (HD) gene‐expanded (HDGE) young adults. These sustained attention deficits do not measurably decline over a 4.7‐year period. Altered functional connectivity was observed in attention‐related brain networks. Alterations in regions include occipital, opercular, lentiform, and frontal areas. Findings support attention as an early cognitive biomarker in HDGE young adults.