Purpose of reviewHigh comorbidity rates across neurodevelopmental disorders (NDDs) may suggest shared pathogenic mechanisms rather than independent disease processes. This review synthesizes recent neuroimaging evidence (2024–2025) examining how comorbidity patterns reveal circuit-level convergence across traditional diagnostic boundaries.Recent findingsStudies of brain connectivity demonstrate that four core transdiagnostic dimensions of cognitive rigidity, sensory processing, repetitive behaviours, and social-emotional regulation show both circuit convergence and disorder-specific patterns across autism spectrum disorder, attention deficit hyperactivity disorder, obsessive compulsive disorder, Tourette syndrome and anxiety disorders. Analyses of how brain networks change over time clarify inconsistencies in earlier static studies, revealing that temporal network inflexibility predicts symptom severity better than anatomical connectivity alone. Developmental studies suggest circuit dysfunction emerges early (as early as 18 months for sensory processing) and creates cascade effects throughout maturation. Interventions targeting specific brain circuits produce transdiagnostic improvements, validating circuit-based approaches over disorder-specific supports.SummaryComorbidity patterns provide critical clues to shared pathogenesis, with circuit-level evidence supporting dimensional models over categorical diagnoses. The timing and of circuit dysfunction inform whether patterns reflect shared vulnerabilities, developmental cascades, or independent processes converging on similar phenotypes. These findings suggest that assessments and interventions targeting underlying brain mechanisms may be more effective than traditional categorical diagnosis-based interventions.

This narrative review synthesizes advances from the past 18 months on the etiology of autism spectrum disorder (ASD), integrating findings from genetics, neurobiology, environmental epidemiology, and developmental psychiatry. Given the profound clinical heterogeneity of ASD, improved etiologic clarity is essential for risk stratification, early identification, and targeted intervention. Extensive genomic and multiancestry studies are now further clarifying how both common polygenic and rare high-impact variants contribute to ASD. These studies reveal different patterns of genetic liability that underlie distinct ASD subgroups. In parallel, functional and multiomic research is highlighting shared pathways involving synaptic signaling, gene regulation, immune processes, and the balance between excitatory and inhibitory signals. Environmental research, especially on maternal immune activation and maternal metabolic factors, uses causal inference methods to clarify modest but plausible causal effects, tempering earlier claims. Longitudinal imaging and infant cohort studies continue to show that atypical connectivity and social-brain differences occur before behavioral diagnosis. Sex differences and global diversity underscore the need for etiology models to incorporate sex-specific genetic architecture and address significant gaps in ancestral representation. ASD arises from a dynamic interplay of genetic liability, early neurodevelopmental processes, and environmental exposures. Etiologic progress now depends on integrating multilevel and multiomic data - including genomic, transcriptomic, epigenetic, imaging, and epidemiologic information - toward stratified developmental models and better-tailored interventions.

This systematic review and meta-analysis evaluated mental and oral health outcomes among left-behind children (LBC) affected by urbanization-driven rural-urban labour migration. Although mental health impacts of parental migration are increasingly recognized, oral health outcomes remain underexplored. This review synthesizes available evidence, quantifies disparities, and identifies shared social and structural determinants. Thirty-three studies met inclusion criteria. Pooled analyses revealed significantly higher depressive symptoms among LBC compared to non-LBC peers [standardized mean difference (SMD) = 0.16, 95% confidence interval (CI): 0.03-0.29], with increased risk of elevated depressive symptoms [odds ratio (OR) = 1.36, 95% CI: 1.01-1.83]. LBC also experienced higher rates of permanent tooth caries (SMD = 0.15, 95% CI: 0.05-0.25) and were less likely to attend dental care in the past year (OR = 0.80, 95% CI: 0.67-0.94). Greater distress was observed in cases of shorter parental separation and when both parents had migrated. Factors such as caregiver education, quality of parent-child communication, and school climate consistently influenced outcomes across both mental and oral health domains. LBC experience a dual burden of psychological distress and unmet dental need, reflecting the effects of urbanization-related parental migration. These disparities are shaped by caregiving discontinuity, reduced access to preventive services, and socio-environmental stressors. Findings highlight the need for integrated responses, including caregiver training, school-based prevention, and equitable health entitlements. Addressing shared determinants across mental and oral health domains offers a feasible path toward improved outcomes and greater equity. PROSPERO ID: CRD420251152265.

Purpose of reviewThis review highlights three of the most promising mouse models of vascular cognitive impairment and dementia (VCID) that recapitulate chronic cerebral hypoperfusion. It also discusses therapeutic candidates evaluated using these models.Recent findingsThe three mouse models of chronic cerebral hypoperfusion induced by carotid artery manipulations are bilateral common carotid artery stenosis (BCAS), asymmetric common carotid artery surgery (ACAS), and gradual common carotid artery stenosis (GCAS). Altogether, these models reproduce white matter lesions and executive dysfunction. Notably, ACAS and GCAS exhibit gradual cerebral blood flow (CBF) reduction and motor impairments, addressing key limitations of BCAS, which induces abrupt CBF decrease and no motor deficits. Furthermore, ACAS uniquely demonstrates subcortical small infarcts, a hallmark feature of clinical VCID. These models have greatly contributed to elucidating VCID pathophysiology, including abnormal oligodendrocyte maturation, astrocytic dysfunction, and neuroinflammation. Several therapeutic strategies developed using these models – such as adrenomedullin and SIRT1 activator – are currently under investigation in clinical trials.SummaryThe three models are robust and complementary tools for exploring the VCID mechanisms. They have been instrumental in advancing our understanding of VCID pathogenesis and in facilitating the development of novel therapeutic approaches.

Purpose of this reviewThis narrative review provides an overview of functional cognitive disorder (FCD) as a cognitive subtype within the functional neurological disorder (FND) spectrum. It addresses the conceptual challenges, diagnostic criteria, and epidemiology of FCD, emphasizing the need for standardization of internal inconsistency and clearer diagnostic boundaries to improve clinical assessment and research.Recent findingsFCD is characterized by persistent cognitive complaints disproportionate to objective performance, underpinned by metacognitive, attentional, and cognitive-behavioural dysfunction. Emerging evidence supports a predictive processing framework in which maladaptive top-down priors and attentional dysregulation perpetuate subjective cognitive deficits despite preserved or inconsistent objective cognitive performance. Diagnostic criteria and FCD checklists show promise, although challenges remain in standardizing neuropsychological assessments and integrating patient-reported experiences. Epidemiological data highlight the stability of FCD and its distinctiveness from neurodegenerative conditions, with a nonprogressive trajectory in most cases.Summary statementDefining and refining FCD through standardized criteria and mechanistic models is crucial for enhancing diagnostic accuracy, patient care, and research validity. Advancing our understanding of the pathophysiology of FCD within the FND framework will facilitate targeted interventions and improve trial cohort purity in neurodegenerative disease research. Future studies should focus on objective biomarkers and therapeutic strategies that address attentional and metacognitive dysfunction in FCD.

The rapid urbanization in China has profoundly transformed social structures, environmental conditions, and public health landscapes within a relatively brief period. While driving economic growth, it has also generated complex mental health challenges. We explored the multifaceted relationships between urbanization and mental health in China, highlighting spatial and demographic disparities, impact pathways, and intervention strategies. Mental health outcomes are shaped not by a simple urban-rural divide but by many determinants such as age, gender, chronic illness, socioeconomic status, and stage of life. Vulnerable groups, including rural older adults, migrant workers, left-behind or migrant children, and urban youth, face elevated psychological risks from environmental stressors, social exclusion and institutional barriers. Key influences are likely to involve the physical environment, social system, economic factors and policy frameworks. In addition, intervention strategies emphasize both individual and structural approaches, such as community-based psychosocial support, urban greening, inclusive policy design, and integrated mental health governance. However, current research on their impacts remains constrained by methodological limitations. This review underscores the need for equity-oriented approaches, interdisciplinary research and policy innovations to support community mental health within China's urbanization trajectory. Aligning public mental health strategies with national initiatives like "Healthy China 2030" and dual carbon goals is imperative to building inclusive and healthy urban environments for population mental well being and resilience.

Early autism diagnosis is especially difficult when developmental history or caregiver input is unavailable (e.g., displaced, institutionalized, or orphaned children). We synthesize observation-first, clinician-led approaches and regulated, technology-enabled aids that minimize reliance on collateral history. Standardized direct observation (e.g., ADOS-2 modules that do not require a caregiver) can support diagnosis when history is limited, but feasibility hinges on training, cultural adaptation, and service capacity. Many legacy instruments predate DSM-5/DSM-5-TR, creating construct gaps. Recently cleared aids, an eye-tracking system for toddlers, and a software tool combining short videos, caregiver input, and clinician ratings, function as decision support rather than stand-alone diagnostics. Mobile and remote screening paradigms show promise but require independent, cross-cultural validation. Diagnostic equity necessitates pathways that are effective when medical histories are incomplete. We outline a minimum dataset and a pragmatic workflow that replace caregiver reports with structured observations, school/residential collateral, and carefully integrated objective measures, under clinician synthesis. Priorities include updating legacy instruments, publishing brief observational batteries with known accuracy bounds, and validating tools across languages and contexts.