Parkinson’s disease (PD) screening can identify people needing clinical assessment but does not itself provide continuing care. Drawing on Thailand’s smartphone-based CheckPD implementation and selected literature, this conceptual review proposes CheckBRAIN, a platform linking screening to personalised brain-health care. All CheckPD participants would be offered voluntary entry, while clinician-led assessment would proceed without delay when clinically indicated. Concerning screening results, new or progressive symptoms, clinically defined high-risk syndromes, diagnostic uncertainty or medication-related problems would trigger clinical review, while people with established PD could enter directly. A personal brain-health portfolio links multidomain functioning, systemic and environmental context, priorities, actions, responsible persons or services and review dates. The six-domain SHAPES framework supports priority setting without creating another diagnostic score. Actions may include diagnostic assessment, medication review or pharmacotherapy, rehabilitation, cue-linked daily habits, social support, and service-level responses to practical barriers such as transport, digital access, referral navigation or unavailable services. Primary-care teams would coordinate longitudinal review, community workers would support assisted or non-digital participation, and specialists would contribute according to clinical need. Intended benefits include understandable next steps, fewer unresolved referrals, support for everyday function and participation, and clearly defined roles for care partners with the participant’s consent. We outline staged co-design and evaluation of feasibility, safety, functioning, participation, caregiver burden, equity, service use and costs. CheckBRAIN is not intended as a population registry and has no fixed national enrolment target. It remains a proposed care architecture, not a validated intervention or evidence of PD prevention or cost saving. Its intended contribution is accountable continuity between identified needs, appropriate care and reviewed outcomes.
Atypical Parkinsonian Syndromes (AP), such as Progressive Supranuclear Palsy (PSP), Multiple System atrophy (MSA), are characterized by motor and non-motor symptoms. Although cognitive impairment is a core feature of AP, its differential profile across AP syndromes has been inadequately understood, particularly in underrepresented populations like in India. To compare cognitive and neuropsychological profiles in PSP and MSA and examine their clinical correlates. In this cross-sectional study, AP patients underwent cognitive assessment using the Frontal Assessment Battery (FAB), the Montreal Cognitive Assessment (MoCA), the Addenbrooke’s Cognitive Examination-III (ACE-III), and selected neuropsychological tests from the NIMHANS Neuropsychology Battery for the elderly (NNBE). Between-group comparisons were conducted using age-adjusted ANCOVA. Partial correlations examined associations between cognition and clinical variables within each group. A total of 159 patients were included in which PSP (n = 98, mean age 62.5 ± 7.4 years) was older than MSA (n = 61, 58.6 ± 7.8 years). Groups were gender-matched (p = 0.48). After age adjustment and FDR correction, PSP showed significantly lower scores than MSA on FAB, MoCA, and ACE-III Total, as well as on fluency, attention, visuospatial construction, and visuospatial working memory measures (all corrected p < 0.05). In PSP, cognitive performance correlated with education, motor severity (UPDRS-III, PSPRS), and mood (all p < 0.05), whereas in MSA, cognition correlated only with education and multilingualism, with no significant association with motor or symptom severity. PSP demonstrates greater global and domain-specific cognitive impairment than MSA, particularly in fluency and working memory, with cognition more closely tied to motor and mood burden. In MSA, cognition is more closely tied to premorbid reserve (education, multilingualism) than to disease severity. Routine cognitive screening may aid early differentiation and clinical management of AP.
Abnormal brain iron levels are implicated in several neuropsychiatric illnesses, including schizophrenia spectrum disorders (SSD). However, current evidence on subcortical iron changes in chronic SSD remains limited, with the majority of studies conducted in early psychosis. We recruited 20 chronic SSD patients and 19 healthy controls from the Centre for Addiction Mental Health (CAMH) in Toronto, Canada. Participants underwent quantitative susceptibility mapping (QSM) with a 3T MRI to estimate brain iron levels. Magnetic susceptibility was significantly elevated in the left hippocampus (dadj = 1.108, pFDR = 0.02) and nearing significance in the left putamen (dadj = 0.86, pFDR = 0.068) of SSD patients compared to controls, while accounting for age and sex. Interestingly, there was a significant, positive age-by-illness effect in the aforementioned areas, indicating a stronger age-related iron accumulation in SSD (L-putamen: β = 0.0006, p = 0.01; L-hippocampus: β = 0.0005, p = 0.001). We demonstrate elevated subcortical magnetic susceptibility, likely corresponding to elevated iron, in chronic SSD and a more pronounced age-related iron deposition associated with the illness. In conclusion, the expected age-related accumulation of subcortical iron levels appears to be disrupted in SSD and should be considered as a confounding factor in future analyses.
Neurodevelopmental disorders (NDDs) are clinically and genetically heterogeneous conditions often studied through diagnostic categories, causal genes, synaptic dysfunction or end-stage phenotypes. Although these approaches remain essential, they do not fully capture the developmental nature of NDD pathophysiology. This review proposes a trajectory-first framework in which NDDs are interpreted as disorders of altered developmental progression. From this perspective, the key question is not only which gene, pathway, cell type, or synapse is affected, but when, where and how neurodevelopment begins to diverge. We discuss mechanisms of trajectory divergence, including altered developmental timing, cell-state and lineage disruption, selective cellular vulnerability, epigenetic and signaling dysregulation, cytoskeletal and morphogenetic abnormalities, synaptic maturation defects, excitability changes and network-level alterations. We then examine how human systems, including fetal and post-mortem atlases, iPSC-derived models, cortical organoids, assembloids, functional readouts and patient-level phenotypes, can be integrated to reconstruct developmental trajectories across biological scales. Representative NDD genes and syndromes illustrate that distinct divergence points may later converge on shared functional or clinical outcomes, including altered excitation/inhibition balance, abnormal network activity, epilepsy, language delay, intellectual disability, autism spectrum disorder features or motor dysfunction. Finally, we discuss limitations and perspectives for trajectory-based stratification and biomarker discovery. Rather than acting as static diagnostic readouts, future biomarkers should aim to capture developmental state, timing, divergence, convergence, compensation and response to intervention.
Tardive dyskinesia (TD) remains an under-recognised medication safety issue in many Asian countries, compounded by fragmented care between psychiatry and neurology and underpinned by a lack of cross-discipline professional education. The multidisciplinary expert recommendations proposed here have been developed jointly by a panel of psychiatrists and neurologists representing selected Asian healthcare settings (Thailand, Japan, Korea and China), and suggest a practical, structured education and competency framework to help close this gap and improve multidisciplinary management. The recommendations emphasise the need for collaborative educational initiatives focused on rational antipsychotic prescribing, proactive monitoring, standardised assessment and diagnosis, patient and caregiver education, and timely specialist referral. The proposed joint neurology–psychiatry educational framework is informed by real-world expert perspectives and spans undergraduate education, residency training, and continuing medical education, encompassing interdisciplinary curricula, collaborative workshops, with locally adapted multilingual resources. It is suggested that implementation of such a framework should be supported by national professional societies and development of shared-care pathways, with key outcomes monitored. Strengthening cross-disciplinary knowledge, skills, and attitudes in this way may improve TD detection, reduce avoidable progression, and promote coordinated, patient-centred care in selected Asian regions.
