<strong>Background:</strong> The growth of the older adult population in Indonesia since 2019 has contributed to a 2.46% increase in dementia cases, with the number of cases projected to increase 2.5-fold by 2050. This trend is exerting a major impact on older adults and increasing the burden on caregivers. The current lack of systemic health support suggests that digital solutions—such as mobile health (mHealth) apps—have the potential to support caregivers and people living with dementia. However, to date, no mHealth initiatives have been developed through a participatory approach that involves users in the design process in accordance with the sociocultural conditions in Indonesia. <strong>Objective:</strong> This study aimed to identify the challenges faced by dementia caregivers in home care settings and to determine the functional requirements for an mHealth app to support them. <strong>Methods:</strong> The study adopted a qualitative participatory design, interviewing 12 health care workers, 2 employees of nongovernmental organizations, and 35 dementia caregivers. The qualitative data were analyzed using content analysis. The challenges identified by the interviewees were mapped onto the app design process as functional requirements. <strong>Results:</strong> The challenges identified in this study include a lack of education and awareness regarding the symptoms and treatment of dementia, the stress and mental strain experienced by caregivers, difficulties in monitoring the health and daily lives of people with dementia, barriers to access to health services, and declining cognitive function among older adults with dementia. To overcome these challenges, we identified corresponding functional requirements for the mHealth app, including diaries, music playlists, community forums, and quizzes and games for people with dementia, as well as dementia education videos and psychological assessments for caregivers. Aspects such as ease of use and the quality of information influenced the acceptance of the app by people with dementia and their caregivers. Educational materials, such as short videos, articles, and infographics, addressed dementia symptoms and steps that can be taken at home to care for people with dementia. Psychological assessments were developed using a validated tool. Quizzes and games helped caregivers design fun, relevant questions based on the personal experiences of adults with dementia. Music playlists highlighted songs that suited the mood of people with dementia, enhancing their personalized experiences without needing explicit guidance from the app. Community forums encouraged caregivers to voluntarily share their experiences and support others, strengthening their sense of belonging and emotional involvement in the caregiving process. Diaries could be used by caregivers to record the daily condition of people with dementia and their care. <strong>Conclusions:</strong> The challenges and functional requirements identified in this study provide a practical foundation for organizations and facilities to develop culturally appropriate health apps for dementia home care in Indonesia.
Attention-deficit/hyperactivity disorder (ADHD), marked by excessive activity and impulsivity, is linked to changes in the brain’s dopamine system, though the mechanisms remain unclear. Researchers at the University of Fukui have now found that in genetically modified, conditional knockout mice, loss of a protein called N-ethylmaleimide-sensitive factor (NSF)—which is linked to dopamine receptors—in D2 receptor-expressing cells led to lower dopamine levels and ADHD-like behaviors. Their results also pointed to a potential therapeutic strategy.
The team, headed by assistant professor Min-Jue Xie, PhD, at the Division of Development of Mental Functions, Research Centre for Child Mental Development, suggests that the results offer insight into how brain changes may contribute to ADHD and informing future treatments.
“This is basic research and will not immediately lead to a new treatment,” Xie acknowledged. “However, it provides important clues for understanding how dopaminergic dysfunction may contribute to ADHD. In the future, these findings may help develop new therapeutic strategies targeting D2R function and striatal dopamine signaling, especially for treatment-resistant ADHD.”
ADHD is a neurodevelopmental disorder that can affect attention, activity levels, and impulse control, with symptoms often beginning in childhood and sometimes continuing into adulthood. Although the exact causes of ADHD are not fully understood, changes in the brain’s dopamine system have long been linked to the condition. Dopamine is a chemical messenger that helps brain cells communicate and plays an important role in movement, motivation, and behavior.
While dopamine-related changes have been associated with ADHD, it remains unclear how the brain cells that respond to dopamine are maintained and how their disruption may contribute to ADHD-related behaviors. This is particularly relevant to dopamine D2 receptor (D2R)-expressing cells, which are found in the striatum, a brain region involved in movement and behavioral control. Understanding what helps these cells develop and function normally could provide new insights into the biological processes involved in ADHD. “Although D2R has been extensively studied, the upstream mechanisms regulating its function and localization remain unclear,” the authors wrote.
Against this backdrop, a research team from Japan, led by Xie, set out to investigate the role of NSF in these dopamine-related brain cells. NSF regulates membrane fusion, helping brain cells release chemical messengers and move proteins within their membranes. “NSF dysfunction is implicated in neuropsychiatric disorders, with reduced expression in autism spectrum disorder (ASD) and schizophrenia and aggregates in Parkinson’s disease,” the investigators noted.
“The motivation for this study came from previous findings suggesting that NSF may be involved in neurodevelopmental and neuropsychiatric disorders,” Xie explained. “NSF was known to interact with D2R; however, the role of this interaction in vivo remained unclear. Because ADHD is thought to involve reduced striatal dopaminergic function and D2R dysfunction, we hypothesized that NSF may be important for maintaining D2R-expressing neurons and dopaminergic function. This led us to initiate the present study.”
For their study the team created knockout mice in which NSF was removed specifically from D2R-expressing neurons. “… we generated D2R-specific Nsf conditional knockout (Nsf f/f;D2R-Cre) mice to examine NSF function in D2R-expressing cells in vivo,” they explained. They then studied the animals’ brain development, dopamine levels, and behavior. The team also tested whether drugs that affect dopamine signaling could reduce the behavioral changes seen in the modified mice.
The loss of NSF affected the developing brain, resulting in fewer dopamine D2R-expressing cells, increased early developmental cell death, and a smaller striatum. The mice also had markedly lower dopamine levels in this brain region. Together, these findings suggest that NSF helps maintain dopamine-related cells and supports normal development and dopamine function.
The brain changes were accompanied by ADHD-like behaviors. “Nsf f/f;D2R-Cre mice exhibited attention-deficit/hyperactivity disorder (ADHD)-like behaviors, including hyperactivity and impulsivity,” the team reported. The knockout mice were more hyperactive than control mice and showed more impulsive-like behavior in a test that measured how quickly they jumped from an elevated platform. By the end of the seven-minute test, 86% of the experimental group mice had jumped, compared with 31% of the control group mice. “These findings indicate that a reduction in D2R-expressing cells coincides with ADHD-like behaviors, suggesting a link between D2R dysfunction and these abnormalities.”
The researchers then explored whether these behaviors could be reduced by changing dopamine signaling. Methylphenidate, a medicine commonly used to treat ADHD, did not significantly reduce hyperactivity when given alone to the modified mice. However, when it was given together with quinpirole, a drug that activates D2R, the mice became less hyperactive and showed less impulsive-like behavior. During the seven-minute test, the proportion of knockout mice that jumped fell from 78% without treatment to 11% after the two drugs were given together. “Combined administration of methylphenidate and a D2R agonist, quinpirole, alleviated both behaviors, suggesting a potential complementary approach for ADHD treatment,” the investigators wrote.
“This study supports the translational relevance of the Nsf f/f;D2R-Cre model for ADHD and indicates that targeting D2R dysfunction, particularly in treatment-resistant ADHD, may be a promising therapeutic strategy.”
Personal narratives describing lived experiences of the entire spectrum of mental health challenges are now widely available to the public, including through autobiographies from public figures, thematic collections of narratives assembled by mental health organizations, and individual narratives published on video sharing services. Mental health lived experience narratives have been used as an “active ingredient” in interventions intended to create change, such as in campaigns against mental health stigma. In the narrative inquiry research approach, they are used to explore mental health phenomenology. Researchers and organizations working with mental health lived experience narratives have to contend with a wide range of legal and ethical challenges, such as how to handle narratives disclosing sensitive personal information about third parties and the ethical trade-off between preserving narrator autonomy over their presentation of personal identity and protecting narrators from harm due to mental health stigma if a narrator is identifiable in their narrative. In 2022, we formed the Interdisciplinary Consortium on Narratives in Context (ICONIC) of people with knowledge of narrative practices across disciplines. Members are engaged in health research, liberal arts, modern languages, history, and philosophy. In this viewpoint, we present four case studies of narrative practices by ICONIC members: (1) a narrative inquiry into the experiences of Ethiopian citizens with schizophrenia, (2) work to curate and share 2 collections of mental health recovery narratives, (3) an exploration of the use of poetic transcription to condense narrative interviews with mental health content, and (4) the development of safe approaches to working with personal narratives shared through an online mental health peer support service. In presenting these case studies, we focused on documenting decision-making on ethical and legal challenges as the best knowledge on ethical and legal decision-making regarding mental health lived experience narratives may come from integrating knowledge across disciplines. Through reflecting on these case studies, we identified cross-cutting challenges regarding consent processes, narrative analysis, and the interpretation and dissemination of data and findings. These challenges have transdisciplinary and disciplinary-specific features and can be used as a preliminary checklist in research design processes. In presenting what we learned, our intent was to demonstrate that greater knowledge on narrative practices can emerge through interdisciplinary contact and inform future decision-making on narrative practices by researchers working across disciplines. We conclude by contemplating interdisciplinary explorations with the potential to expand knowledge, including examining the use of pathographic narratives in philosophical inquiry.
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Background: Auditory verbal hallucinations (AVH) are among the most disabling symptoms of schizophrenia and often persist despite treatment. Virtual reality–assisted therapies (VRTs) are a new generation of relational interventions for AVH, but comparative evidence against active interventions is currently lacking. Objective: This study aimed to assess whether VRT (9 sessions) is superior to a short course of cognitive behavioral therapy (CBT) targeting AVH (9 sessions) in reducing AVH in individuals with treatment-resistant schizophrenia. Methods: In this assessor-blind, parallel-group randomized controlled trial conducted from 2019 to 2026 at an academic center in Montreal (Canada), adults with schizophrenia or schizoaffective disorder and persistent AVH were either referred by their health care team or self-referred. A total of 136 participants were randomly assigned 1:1 to VRT or CBT, stratified by sex and clozapine use status. Both 9-session interventions targeted maladaptive beliefs and relationships with voices and were administered by trained psychotherapists. The predetermined primary outcome was the evolution of AVH severity over time, measured at baseline, post treatment, and 3 months post therapy using the auditory hallucination subscale of the Psychotic Symptoms Rating Scale. Secondary outcomes notably included the general psychotic symptomatology measured using the Positive and Negative Syndrome Scale. Linear mixed-effects models were used to assess time-by-treatment interactions. Psychotherapy sessions and assessments were conducted primarily in person, with CBT being occasionally delivered via videoconferencing during the COVID-19 pandemic. Results: Participants had a mean age of 40.3 (SD 12.8) years, 63.2% (86/136) were male, and 56.6% (77/136) received clozapine. Intention-to-treat analyses (VRT, n=67; CBT, n=69) showed a significant time-by-treatment interaction favoring VRT (=.013) with a moderate effect size at 3 months post therapy (Cohen =0.614). Both therapies showed significant within-group improvements in the primary outcome, with large effect sizes for VRT (Cohen =0.81 post therapy and Cohen =1.17 at 3 months) and moderate for CBT (Cohen =0.58 post therapy and Cohen =0.39 at 3 months). While there were no between-group differences for secondary outcomes, within-group improvements were observed in psychotic symptoms, emotional regulation, and voice acceptance for both therapies, and VRT also reduced maladaptive beliefs about voices and improved self-esteem. Conclusions: VRT outperformed a targeted short course of CBT in reducing persistent AVH for up to 3 months after the intervention in a North American population with treatment-resistant schizophrenia. Improvements were also seen in some secondary outcomes, such as general psychotic symptomatology, and those were similar for both interventions. Overall, these findings support the value of VRT as a personalized and clinically effective intervention. Trial Registration: ClinicalTrials.gov NCT04054778; https://clinicaltrials.gov/study/NCT04054778
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Large language models are increasingly used within and alongside therapy. As large language models perform more therapy functions, questions arise about what the future might hold for therapists and what they will do. We argue that the enduring therapist role in the age of AI-assisted care is currently best understood through relational, adaptive, and accountability functions. These functions include therapeutic challenge, use of the therapeutic relationship as a mechanism of change, rupture detection and repair, bearing witness to suffering, calibration of pace and treatment burden, and clinical judgment under uncertainty across the broader care pathway. Drawing on psychotherapy theory, digital mental health research, the declarative-procedural-reflective model by Bennett-Levy, and our clinical experience, we propose a clinically informed, hypothesis-generating, relational-adaptive-accountability framework. This framework is intended to support further empirical testing and may have implications for workforce development, supervision, training, and service design.
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Over his short career, 44-year-old Sergiu Pașca, MD, has changed how scientists study the developing human nervous system.
It started in 2017, with Pașca and his Stanford University colleagues building more complex three-dimensional neural development models using human pluripotent stem cells (hPSCs). These organoids, the oft-misnomered “mini brains,” allowed researchers to observe human neurodevelopment in the lab and assemble neural regions into functional circuits.
In 2020, Pașca’s group reported fusing organoids of different lineages to create self-organizing 3D tissue models. One such assembloid was created by merging human cortical neuron organoids, spinal cord motor neuron organoids, and striated muscle organoids that translated cortical activity into muscle contraction. The textbook corticomuscular diagram of a white space with a brain, spinal cord slice, and muscle wired together came to life.
But such systems were limited because a brain doesn’t develop in a dish. Organoids lack sensory, vascular, immune, long-range circuitry, and behavioral outputs. Later in 2022, Pașca’s group transplanted human cortical organoids into newborn rats’ brains. The tissue grew and integrated with the host nervous system: human neurons responded to sensory input, extended projections through the rat brain, and could influence behavior when activated experimentally. The model has enabled researchers to study patient-derived human neurons in a living neural circuit and link molecular and cellular abnormalities to circuit and behavioral phenotypes.
That entire time, Pașca was working on a related project that was far more complex, both experimentally and ethically. In a new Nature study, Pașca and his colleagues describe xenocortication, an approach in which human cortical organoids are transplanted into mice genetically engineered so that most of the neocortex and hippocampus never form. By three months, human tissue took advantage of the space, generated diverse populations of human cortical cells, formed long-range connections with the mouse nervous system, and developed organized electrical activity.
By providing a large volume of developing human cortical tissue inside a living nervous system, the model potentially allows researchers to investigate human cells and circuits that are difficult to study in vitro. For proof-of-concept, Pașca’s group demonstrated several applications, including modeling neuropsychiatric disease and hypoxic injury. “This is not an all-in-one, universal system that is here to replace previous models, but rather to complement them,” Pașca told Inside Precision Medicine.
These hypoxic injury experiments highlighted, for Pașca, the degree of engraftment and functional integration between the human tissue and the host mouse. “When we induce hypoxia in the xenocortical mice, the microglia from the mouse react to hypoxia,” said Pașca. “But they’re not reacting to a hypoxic injury of the mouse cortex because there is essentially no mouse cortex there. They’re reacting to the injury of human cells.”
In six years, Pașca’s group has moved from assembling pieces of human neural circuitry in a dish to integrating them into a living rodent brain to redesigning the host brain itself to give human neural tissue room to grow.
Making room for human tissue
The work centers on immunodeficient “apallial” mice, which lack much of the dorsal and medial pallium, which gives rise to the neocortex and hippocampus. In cells expressing the pallial marker Emx1 on an immunocompromised SCID background, the team deleted Esco2, a sister chromatid cohesion gene. Creating mice without most of the neocortex and hippocampus gave researchers plenty of space to transplant human cortical organoids shortly after birth.
The engraftment of three different hPSC lines was effective, with 86.2% of the 29 transplanted animals showing successful engraftment. Graft volume increased 4.7-fold in two to three months after transplantation. Human-derived tissue made up 91.9% of cortical tissue volume after three months. “It’s still not a fully formed human cortex, but it contains a large diversity of cortical cell types, including astrocytes,” said Pașca.
Size wasn’t everything. The extra space seemed to affect how much human tissue could grow and how it connected to the nervous system. Human neurons projected organized axonal tracts toward the superior colliculus from subcortical structures. In contrast, mouse neurons from the paleocortex, thalamus, and pallidum projected into the human graft. Human-derived projections were even found in the cervical spinal cord, which were not seen when cortical organoids were transplanted into mice with intact cortex.
Map of estimated nerve-fiber pathways in the brain of a xenocortical (XCX) mouse. Dashed white lines outline the xenocortical graft. Colors indicate the main fiber direction: green, top to bottom; red, front to back; and blue, side to side. [S. Pasca lab / Stanford University]
Compared to previous cortical organoid transplantations, xenocortical grafts had three times more layer 5 extratelencephalic (L5-ET) projection neurons, which project far outside the telencephalon. Among them were cells with molecular and morphological features resembling von Economo neurons (VENs). These unusually large neurons are found in several large-brained mammals but are absent from rodents. VENs are implicated in neuropsychiatric and neurodegenerative diseases like frontotemporal dementia. “One unique application of this is the study of von Economo neurons in the context of frontotemporal dementia,” Pașca said.
Modeling disease and injury in human tissue
The researchers then examined graft cooperation. Wide-field calcium imaging showed synchronized events across human tissue, while electrophysiological recordings showed coordinated bursts throughout the graft. In mice, human graft activity correlated with orofacial movements.
That the model can go from human cellular phenotypes to circuits and behavior may be its most important feature. “Just because the neuron is hyperexcitable in a dish doesn’t mean they will result in a seizure or in the EEG changes that are characteristic of that condition,” Pașca said.
The distinction is crucial for studying neuropsychiatric disease. A cellular phenotype in vitro can reveal a key mechanism, but networks of interacting cells alter cognition and behavior to cause psychiatric disorders. “For many neuropsychiatric disorders, circuit and behavioral readouts are very important because psychiatric disorders are behaviorally defined,” Pașca said.
Xenocortication allows patient-derived human cells to be studied molecularly and physiologically while part of an animal’s circuitry. “We think these are a somewhat narrow but important set of applications,” Pașca said, “that capture a unique feature of the model.” The researchers also modeled severe hypoxia. After oxygen deprivation, human grafts showed strong HIF1α immunoreactivity, while adjacent mouse paleocortex did not show a similar signal. Injuries also altered motor behavior.
Pașca envisions xenocortication being used to investigate genetic and environmental perturbations, test therapeutics across relatively large volumes of human neural tissue, and potentially inform preclinical studies of cell therapies for conditions such as microcephaly or severe ischemic injury early in development.
Solving space, but not time
Despite expanding territory, xenocortication cannot eliminate another major drawback of cross-species transplantation. “While we create more space, we still don’t solve the problem of time,” Pașca said.
Neural development follows a human schedule. Grafted human glutamatergic neurons were transcriptionally comparable to the developing human cortex around mid-gestation 24 weeks after differentiation. “The cells are still progressing at their own pace,” Pașca said. The mouse nervous system, meanwhile, matures far more quickly. “The critical periods of the mouse are closing one by one over the ensuing weeks after transplantation,” he said.
That mismatch may limit how completely the two nervous systems can integrate. The human grafts lacked several hallmarks of mature cortical organization. There was no canonical cortical lamination, for example, although related neuronal populations showed evidence of local self-organization. “There’s no lamination in the human graft in the xenocortical animals,” Pașca said. “That’s partly because the cells don’t know where up and down really is. They’re not anchored in that way.”
There were, however, “attempts at cytoarchitecture,” he said, and the graft contained a broad diversity of human cortical cell types. The result is not a fully formed human cortex but rather developing human cortical tissue occupying an unusually large volume inside a living mammalian nervous system.
Yet anatomical connectivity alone does not establish what those human neurons are functionally contributing. Pathway-specific experiments will be needed to determine which graft-host connections are functional and whether particular human neuronal populations are necessary or sufficient for specific behavioral effects.
The experiment inside the experiment
Yet xenocortication also produced another finding, which goes back to the apallial mice and has relatively little to do with the human graft itself. Scientists created mice without most of the neocortex and hippocampus to accommodate human tissue. The mechanism is different from destroying a developed cortex, says Pașca. “This is not a depletion. It’s not an ablation,” he said. “This is sort of like a prevention of the formation. It’s a blockade.”
Those mice functioned far better than their anatomy might suggest. Apallial mice could move around their environment, see, hear, and smell. Gait, limb coordination, and spontaneous behavior were abnormal, but gross locomotion was preserved. Cognitive deficits also emerged.
The finding does not mean the cortex is dispensable. Pasca suggests that their nervous systems developed early around its absence, allowing other neural structures to compensate. “The nervous system therefore has to deal with the lack of cortex very early on,” Pașca said. “I think that probably creates some interesting opportunities for that plastic nervous system to compensate to some extent.” He suspects preserved subcortical structures may be assuming functions that would ordinarily involve cortical circuitry.
Xenocortication was built to ask what human cortical tissue can do when it is finally given room to grow. The mice required to make that experiment possible may now offer another model altogether: a way to ask how a developing nervous system reorganizes when the cortex that normally dominates it was barely there in the first place.
How far should xenocortication go?
As human neural grafts become larger and more integrated, the work also raises questions about how far such models should go. For example, one theoretical way to overcome the developmental mismatch in timing between neuronal and rodent cells is to use an animal with a longer developmental timeline or one that is evolutionary closer to humans. But Pașca is wary of that step. “If this were to be done in an animal where there is more space, or an animal that is evolutionarily closer to us, then the probability of integration is larger,” he said. “I don’t think it’s justified at this point.”
Pașca said the project underwent extensive ethical scrutiny, including consultation with an external committee, and the paper calls for proactive ethical engagement as researchers contemplate more mature or complex human neural grafts.
The immediate goal is to see what researchers can do with the platform they already have, and Pașca expects stem cell and animal model labs to adopt it without much technical difficulty. “You don’t need to request those because you can pretty much make them,” he said of the mice. “The Emx1-Cre mice already exist. You just cross them with the right line and then cross them to make them immunocompromised.” The human side of the system is increasingly accessible as well. Pașca said his laboratory has taught nearly 500 laboratories around the world to generate organoids.
Still, xenocortication is not a plug-and-play technique. “This is not like CRISPR that you can easily implement in lab,” Pașca said. “This is much more elaborate. It involves animals, live animals, human stem cells, and long-term experiments.”
But broad adoption was one reason for creating a reproducible system rather than a one-off experiment. “It’s not going to be a trivial experiment to do, and not many labs are going to do it,” Pașca said. “But hopefully others will do it, too. We built the system so others can also use it. We’re not going to be able to do everything.”
So, what’s next for Pașca? It may seem like he’s jumping from model to model, but he insists that it’s all been done to be a critical model for the field and his lab, not to push ethical or Frankensteinian boundaries. “My approach has always been quite utilitarian,” he said. “We have a specific goal in terms of disease, and then we model that in a specific way. We built a system for about seven years so that we can actually apply it, not to build the next one.”
BackgroundFunctional dyspepsia (FD) is a common gut–brain interaction disorder with suboptimal response to pharmacotherapy. Transcutaneous auricular vagus nerve stimulation (taVNS), a non-invasive neuromodulation targeting the vagus nerve, has emerged as a promising brain–gut axis therapy. This scoping review (PRISMA-ScR, JBI methodology) synthesizes clinical and preclinical mechanistic evidence on taVNS for FD.MethodsPubMed, Embase, Web of Science, and Cochrane Library were searched up to December 20, 2025, following PRISMA-ScR. Using PICOS (adults with FD; taVNS; sham/non-vagal/active controls; symptoms, gastric function, psychological outcomes, biomarkers; RCTs/clinical trials and controlled animal studies), two reviewers independently screened, extracted data, and assessed bias (RoB2 for RCTs, SYRCLE for animal studies). A narrative synthesis was performed due to heterogeneity.ResultsFour RCTs (n = 480) and eight preclinical rodent studies met inclusion. All RCTs showed significant improvements in dyspeptic symptoms, gastric accommodation, slow-wave normalization, and comorbid anxiety, depression, sleep disturbance versus sham/non-vagal control, sustained for 4–12 weeks. Stimulation parameters varied (10–30 Hz; 0.5–10 mA; 2–4 weeks); risk of bias low-moderate. Preclinical rodent evidence supported five interconnected candidate mechanisms: (i) autonomic balance and cholinergic modulation; (ii) α7nAChR/NF-κB anti-inflammatory pathway with duodenal barrier restoration; (iii) NGF/TrkA/PLC-γ/TRPV1-mediated visceral hypersensitivity suppression; (iv) HPA axis inhibition; (v) rebalancing of brain-gut peptides (motilin, CCK, GLP-1).ConclusionThis review characterizes taVNS as a safe, well-tolerated, mechanistically plausible non-invasive neuromodulation for FD acting on multiple brain–gut axis nodes. However, the small number of trials, parameter heterogeneity, and limited follow-up constrain definitive conclusions. Adequately powered, multicenter RCTs with standardized protocols and long-term follow-up are needed to confirm efficacy and define optimal regimens.
PurposeDepression and perceived stress are prevalent mental health problems worldwide, closely associated with physical health. Prior studies have suggested that both weight gain and loss may increase the odds of depression and stress, highlighting the need for clarification using national data.MethodsData from the Korea National Health and Nutrition Examination Survey in 2014, 2016, 2018, and 2020 were used. The final analytic sample included 21,599 adults aged ≥19 years. We identified weight change over the past year and categorized it into seven groups (≥10 kg loss, 6–<10 kg loss, 3–<6 kg loss, no weight change, 3–<6 kg gain, 6–<10 kg gain, and ≥10 kg gain). We analyzed the odds of depressive symptoms, self-reported physician diagnosis of depression, and perceived stress according to the change in weight.ResultsHigher odds of depressive symptoms, self-reported physician diagnosis of depression, and perceived stress were observed at both substantial weight loss and weight gain. Compared with participants reporting no weight change, the adjusted odds ratios (95% CIs) for weight loss ≥10 kg were 3.51 (2.30–5.34), 1.99 (1.17–3.78), and 1.83 (1.34–2.48) for depressive symptoms, self-reported physician diagnosis of depression, and perceived stress, respectively. The corresponding estimates for weight gain ≥10 kg were 3.82 (2.72–5.36), 2.80 (1.89–4.14), and 2.28 (1.82–2.85), respectively. No significant interactions were observed between weight change and sex, age, body mass index, or weight control status.ConclusionsSubstantial weight loss and weight gain were associated with elevated odds of adverse mental health outcomes.
Background and objectiveAttention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in childhood. Although mindfulness-based interventions (MBIs) have been proposed as promising non-pharmacological treatments, evidence regarding their efficacy in children and adolescents with ADHD remains inconsistent.MethodsA systematic search of PubMed, Embase, the Cochrane Library, Scopus, and Web of Science was conducted up to December 31, 2025, supplemented by manual screening of reference lists. Eligible studies were randomized controlled trials (RCTs) in which mindfulness-based intervention was the primary treatment for children or adolescents with ADHD, even alongside other therapies. Study selection followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Risk of bias was assessed using the Cochrane RoB 1.0 tool. Meta-analyses employed random-effects or fixed-effects models based on heterogeneity.ResultsFourteen randomized controlled trials were included in the meta-analysis. The results demonstrated that MBIs significantly alleviated core ADHD symptoms in children (standardized mean difference (SMD) = -1.30; 95% confidence interval (95% CI) [-2.14, -0.45]; p = 0.003). However, the heterogeneity was considerably high (I² = 91%), and publication bias could not be excluded (as suggested by funnel plot/Egger’s test, if available). Regarding neurocognitive functions, MBIs showed potential benefits in improving attention network function (SMD = 0.44; 95% CI [0.01, 0.87]; p = 0.04; I² = 88%) and executive function (SMD = 0.45; 95% CI [0.02, 0.88]; p = 0.04; I² = 84%), though the high heterogeneity (I² > 75%) and possible publication bias warrant cautious interpretation. No significant effects were observed on emotional problems, social problems, externalizing behavioral problems (including oppositional defiant, disruptive, and aggressive behaviors), or mindfulness skills.ConclusionsThis systematic review suggests that MBIs may improve core ADHD symptoms and neurocognitive functions (including attention and executive functions) in children and adolescents. Yet, effects on emotional health, social relationships, externalizing behaviors, and mindfulness skills remain inconclusive. While suggesting that MBIs hold promise as a potential adjunctive intervention alongside standard treatments, significant heterogeneity underscores the need for further high-quality research to confirm these therapeutic benefits.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251171407, identifier CRD420251171407.
AimTo identify, appraise, summarise, and synthesise current evidence on digital health strategies for postpartum depression (PPD) screening and management, and to develop practice-oriented recommendations to support evidence-informed clinical nursing practice.MethodsUsing the 6S evidence hierarchy to guide the retrieval sequence, we performed a wide literature search of clinical decision-support resources, guideline repositories, professional organisations’ websites, and major Chinese and international databases from their inception to May 1, 2026. Eligible evidence sources included clinical practice guidelines, evidence summaries, and systematic reviews relevant to digital screening, intervention, follow-up, or continuing care for PPD. Two trained reviewers independently screened the literature, assessed the methodological quality of the publications, extracted evidence statements, and synthesised the recommendations given. This evidence summary followed the reporting specifications of the Fudan University Center for Evidence-based Nursing, which are based on the methodological process of the Joanna Briggs Institute (JBI), including problem establishment, literature retrieval, literature screening, literature evaluation, evidence synthesis and grading, and formulation of practical recommendations. The study registration number is ‘ES202610615’.ResultsIn total, 16 publications were identified and included in the present study, comprising 2 guidelines, 13 systematic reviews, and 1 evidence summary. From these, 20 key evidence points were extracted and discussed, and 20 evidence statements were generated and then categorised into 5 domains: digital screening and assessment, delivery modalities, intervention components, continuity of care, and implementation issues.ConclusionDigital health technologies can extend the reach of PPD screening and management, but their implementation should be carefully adapted to address local service capacity, user needs, referral pathways, privacy requirements, and adherence risks. The 20 evidence statements summarised in this review could help guide the development of standardised, continuous, and patient-centred digital management models for PPD.
