搜索结果：Social neuroscience

Physical abuse in childhood and adolescence results in long lasting effects on mental and physical health in adulthood. The prefrontal cortex of adults exposed to abuse in childhood shows both functional and structural abnormalities in comparison to healthy controls. However, the changes in prefrontal innervation of specific downstream targets as a result of early life abuse are unclear. Here we used a novel abbreviated early adolescent chronic social defeat stress paradigm (5 day eaCSDS) to assess changes to prefrontal innervation in adult male and female C57BL/6 J mice. We injected control and defeated mice with virally encoded GFP in the prelimbic region of prefrontal cortex (PL) and examined axon density in basolateral amygdala (BLA), nucleus accumbens (NAc) and ventral tegmental area (VTA). We find that both male and female mice show robust but seemingly opposing changes in social interaction after 5 day eaCSDS. We found significantly decreased PL innervation of BLA and increased fragmentation of PL axons in BLA. Males, but not females, also show increased fragmentation of PL axons in NAc. Interestingly, PL innervation of BLA significantly correlates with adult social behavior in males and females. Our findings suggest that PL innervation of downstream targets is dramatically affected by early life social defeat in both a regional and sex-specific manner. This differential change in innervation across regions and sexes may underlie the social behavioral deficits seen after early life social defeat.

This study aimed to explore associations between social isolation, loneliness, and hypothyroidism risk, and whether genetic susceptibility modifies these links. It enrolled 434,628 hypothyroidism-free participants from the UK Biobank. Social isolation was assessed via 3 dichotomous questions, loneliness via 2 revised UCLA Loneliness Scale questions, and hypothyroidism cases via hospital/death records. Hypothyroidism polygenic risk scores (PRSs) were calculated using related genetic loci, with Cox proportional hazards models for analysis. Over a median 12.3-year follow-up, 9,873 hypothyroidism cases occurred. Demographically adjusted models showed social isolation (HR = 1.25, 95% CI 1.17-1.33) and loneliness (HR = 1.38, 95% CI 1.27-1.50) linked to higher risk. After full adjustment, only loneliness remained significant (HR = 1.12, 95% CI 1.02-1.24), while social isolation's association became insignificant. No significant interactions between loneliness/social isolation or loneliness/PRS were found. Joint analysis revealed highest risk in those with high PRS and loneliness. Findings indicate loneliness, not social isolation, is an independent hypothyroidism risk factor, regardless of genetic susceptibility and other factors.

In this Perspective, we suggest combining physiological, neurobiological, behavioural, and social data from multiple marine mammal species to create evolutionary models of the emergence of social vocal coordination. Marine mammal sound production mechanisms have evolved to manage vocalizing and breathing in an aquatic environment, potentially releasing functional constraints on the control of vocal timing. Intervals in rhythmic cetacean vocalizations cover a remarkable temporal range, from less than a millisecond in porpoise burst pulses to 10 s in sperm whale slow clicks. Many cetaceans demonstrate temporally coordinated social behaviour, while pinnipeds express high variability in vocal plasticity and social behaviour. The systematic variability of vocal production mechanisms, vocal rhythms, and sociality can be compared phylogenetically to generate models for the evolution of social rhythm in the vocal domain.

The dense and rapidly changing information conveyed through social interactions must be processed efficiently, allowing individuals to form impressions of others that guide social behavior. The present study summarizes over 100 functional magnetic resonance imaging studies on social impressions concerning stable attributes, highlighting overlapping and specific neural mechanisms for their different sub-types. We identified an extensive network involved in forming social impressions, including areas associated with person perception and emotional processing, alongside the mentalizing system in the medial prefrontal cortex and the semantic control network in the inferior frontal gyrus (IFG) and the pre-supplementary motor area. Implicit judgments appear to activate areas related to person perception such as the middle occipital cortex alongside the fusiform gyrus, while explicit judgments engage nodes of the mentalizing and the semantic control systems. Evaluating warmth involves the right IFG, possibly supporting the translation of inferences about others' warmth into social behavior. Additionally, attractive faces recruit the reward system. Psychological attributions involve left-hemispheric sectors of the mentalizing network, while physical attributions engage areas related to social categorization. Both physical and psychological attributions involve the insula, highlighting its potential role in the emotional facet of prejudice. The present results may guide the design of neuromodulation treatments.

Social gaze is a fundamental channel of primate communication, shaping dynamic interactions and fostering mutual understanding. While prior studies have mapped the behavioral correlates of social gaze across the prefrontal-amygdala circuits, the causal architecture of these interactions remains poorly understood. Here, we develop an algorithm to integrate independently recorded sessions from male macaques into "super-sessions", validated using ground-truth synthetic data, enabling the reconstruction of simultaneous multi-area recordings aligned to matched gaze sequences. Applying Dynamic Bayesian Network analysis to these super-sessions, we uncover temporally structured, behavior-dependent causal interactions among the amygdala, orbitofrontal cortex, dorsomedial prefrontal cortex (dmPFC), and anterior cingulate cortex. When macaques were the targets of social gaze, the brain-behavior network exhibited positive temporal modulations, with the dmPFC emerging as the dominant source and the amygdala as a primary recipient of influence. When macaques directed their gaze toward their partners, the dmPFC and amygdala retained their respective roles. Prefrontal regions positively modulated one another, while the amygdala acted solely as a downstream target receiving exclusively negatively modulated prefrontal inputs. These findings reveal previously unknown directional interactions in the primate social brain and highlight distinct causal architectures underlying the bidirectional dynamics of social attention.

Hoxa5 encodes a transcription factor essential for embryonic patterning and organogenesis, with sustained expression in hindbrain precerebellar nuclei during postnatal development. Given prior evidence implicating HOXA5 in synaptogenesis and early postnatal circuit maturation, we investigated whether its inactivation during this critical developmental window contributes to neurodevelopmental disorder (NDD)-related phenotypes. Using previously generated transcriptomic data, we identified multiple deregulated genes classified as autism spectrum disorder (ASD) risk genes in the SFARI database, several of which are associated with a cerebellar phenotype in mice. We then performed a comprehensive behavioral assessment across motor, social, stereotypical, anxiety-related, and attentional domains in a postnatal inactivation mouse model (Hoxa5-cKO). Motor coordination, learning, gait, and sensorimotor functions were preserved. Social behavior assays yielded no consistent genotype-dependent effects, although results were sensitive to analytical methods and cohort variability. In contrast, Hoxa5-cKO mice exhibited increased stereotypical behaviors, including elevated scratching and marble burying, in the absence of anxiety- or locomotion-related confounds. Importantly, interpretation of social and cognitive phenotypes was impacted by well-known constraints of behavioral neuroscience. We discuss these downfalls and propose additional guidelines. Altogether, our findings indicate that postnatal Hoxa5 deficiency selectively enhances stereotyped behaviors without broadly affecting motor or social functions. The data support a model in which HOXA5 acts as a modulator of postnatal precerebellar circuit connectivity and/or function, with subtle behavioral consequences that require further research in specific genetic or environmental contexts.

Cancer advances are not distributed equitably among many segments of the population. Specifically, individuals with serious mental illness (SMI) face compounded disparities in cancer detection, treatment, and survival. SMI, characterized by conditions such as schizophrenia, bipolar disorder, and severe major depression, is associated with significant functional impairment and a two-to-three-decade reduction in life expectancy. Patients with SMI encounter unique challenges when navigating cancer care, including fragmented care pathways, less access to cancer therapeutics, limited psychosocial support, stigma, heightened vulnerability to diagnostic overshadowing where symptoms are attributed to their psychiatric rather than a medical or oncologic condition, and underrepresentation in therapeutic clinical trials. This review explores the intersection of SMI and cancer care starting with the conceptual background and its importance related to cancer outcomes and the delivery of ethical care to highlight unmet needs and a multitude of barriers. The paper proposes practical recommendations to improve cancer care for individuals with SMI who develop cancer including adopting the collaborative care model, enhancing psychosocial and psychiatric integration in oncology settings, and addressing biases inherent in clinician training. Interventions targeting individual, interpersonal, health system, and policy levels are essential to comprehensively mitigating disparities and developing durable cancer delivery strategies. Equitable cancer care for patients with SMI is both a moral imperative and a cornerstone of advancing social justice in oncology. Thus, there is a critical need to prioritize the translation of research advances, to close the gap in cancer outcomes and mortality, and to improve patient outcomes and wellbeing.

Psychiatry is a distinct medical specialty that integrates biological, psychological, and social sciences to diagnose, treat, and prevent psychiatric disorders. Despite major advances in neuroscience, pharmacological treatments, psychotherapy, and service delivery, psychiatry often remains insufficiently recognized within the broader mental health discourse. Public awareness efforts have largely focused on mental health in general, while psychiatry as a medical discipline has received comparatively limited visibility. This has contributed to ambiguity regarding its identity and role within modern medicine. Many medical specialties have dedicated international observance days that strengthen professional identity, public awareness, and advocacy. In contrast, psychiatry currently lacks a dedicated global day of recognition. We therefore propose the establishment of a World Psychiatry Day, to be observed annually on February 20, the birth anniversary of Johann Christian Reil (1759-1813), the physician who coined the term Psychiatrie in 1808 and advocated for psychiatry as a distinct branch of medicine. The proposed observance would reinforce psychiatry's status as a core medical specialty, promote integration of psychiatric care with general healthcare, reduce stigma, strengthen advocacy and policy engagement, encourage research and innovation, and highlight the global burden of psychiatric disorders. Ultimately, World Psychiatry Day could enhance the visibility of psychiatry within medicine and reaffirm its indispensable role in improving health and wellbeing worldwide.

Recent cognitive neuroscience research has uncovered some similarities and some differences between general semantic memory (GS; e.g., knowledge about family in general) and personal semantic memory (PS; e.g., knowledge about my family in particular). To better understand the representational content and cognitive processes of PS and their relation to general semantics, we adapted a staple of General semantic memory research, the Property Generation task. In a first study, we randomly assigned 240 adult participants to a traditional General semantics perspective (e.g., listing the properties of families and bedrooms in general) or to a PS perspective (e.g., my family, my bedroom) in a between-subjects design. In a second, replication study, 124 participants completed the task in a within-subject design, taking each perspective for different concepts. Relative to the General semantics condition, the PS condition was associated with more features; these were more semantically distant from each other, and included adjectives more frequently and nouns less frequently. However, the two conditions had substantial (~46%) overlap in the frequency of their features. The findings contribute to the identification of the cognitive differences (e.g., semantic richness) and similarities (e.g., correspondence in semantic features) between personal and general semantic memory. Des recherches récentes en neurosciences cognitives ont mis en évidence des similitudes et des différences entre la mémoire sémantique générale (SG ; p. ex., les connaissances sur la famille en général) et la mémoire sémantique personnelle (SP ; p. ex., les connaissances sur ma propre famille). Afin de mieux comprendre le contenu des représentations et les processus cognitifs de la SP, ainsi que leur relation à la SG, nous avons adapté un outil classique de la recherche en mémoire sémantique générale : la tâche de génération de propriétés. Dans une première étude, 240 participants adultes ont été assignés aléatoirement à une perspective de sémantique générale (p. ex., lister les propriétés des familles et des chambres en général) ou à une perspective de sémantique personnelle (p. ex., ma famille, ma chambre), selon un plan inter-sujets. Dans une seconde étude de réplication, 124 participants ont réalisé la tâche avec un plan intra-sujets, en adoptant chaque perspective pour des concepts différents. Comparativement à la condition de SG, la condition de sémantique personnelle était associée à un plus grand nombre de propriétés de concepts, les propriétés étaient sémantiquement plus distantes les unes des autres, et comprenaient plus fréquemment des adjectifs et moins fréquemment des noms. Les deux conditions présentaient néanmoins un chevauchement substantiel (~46 %) dans la fréquence des propriétés produites. Ces résultats contribuent à cerner les différences cognitives (p. ex., la richesse sémantique) et les similitudes (p. ex., la correspondance des propriétés sémantiques) entre la mémoire des sémantiques personnelles et la mémoire des sémantiques générales.

This study examined the long-term effects of polyinosinic:polycytidylic acid (poly I:C), a synthetic double-stranded RNA and Toll-like receptor 3 (TLR3) agonist, on behavioral and immune outcomes in chronically stressed mice. Male C57BL/6J mice were exposed to 21 days of wet bedding stress followed by a poly I:C injection. Post viral fatigue syndrome (PVFS)-like symptoms were evaluated over 7 days post-injection using grip strength testing, the forced swim test, von Frey filament testing, the Morris water maze, the open field test, and the social interaction test. Body temperature and locomotor activity were continuously monitored via intraperitoneally implanted dataloggers. Serum concentrations of interleukin-6 (IL-6), IL-10, and C-X-C motif chemokine ligand 10 (CXCL10) were quantified. In separate cohorts, minocycline (a microglial activation inhibitor) or RU486 (a glucocorticoid receptor antagonist) was administered prior to poly I:C injection. Following IP injection of poly I:C, body temperatures in both stressed and unstressed mice were significantly elevated, indicating a polyphasic febrile response. At 7 days post-injection, stressed mice treated with poly I:C exhibited persistent fatigue, mechanical allodynia, depressive-like behavior, impaired spatial memory, increased anxiety-like behavior, and reduced social interaction. Serum levels of IL-6 and CXCL10 remained elevated and correlated with behavioral outcomes. Pretreatment with minocycline partially attenuated both the behavioral and immune responses, whereas RU486 pretreatment did not. These findings demonstrate that TLR3-mediated systemic inflammation induced by poly I:C produces persistent, multi-domain PVFS-like symptoms in chronically stressed mice. The attenuation by minocycline implicates neuroinflammation as a possible mechanism.

This study aimed to investigate whether the probiotic Lactobacillus rhamnosus GG (LGG) (alone or combined with high-intensity interval training (HIIT)) could improve cognitive, electrophysiological changes, oxidative stress and metabolic parameters in HFD-fed rats. Rats were randomly divided into four groups (n = 8): HFD group, HFD + LGG group, HFD+ HIIT group, and HFD + LGG+ HIIT group. Rats were fed HFD daily for a period of 16 weeks, during which LGG (1 × 1010 colony forming unit (CFU)/ rats, orally), and HIIT protocol were administered four times a week on alternating days. At the end of study, assessment of social behavior, memory function, and Long-term potential (LTP) were performed using three-chambered apparatus, Y-maze task, and electrophysiology technique, respectively. Next, oxidative stress, lipid profiles, and liver enzymes were evaluated with routine kits. Both LGG and HIIT alone or in combination improved working memory, social memory, and LTP in HFD-fed rats. In addition, both LGG and HIIT alone or in combination increased the hippocampal levels of superoxide dismutase, catalase, and increased the serum levels of high-density lipoprotein (HDL), and decreased the serum levels of leptin, triglyceride, cholesterol, low-density lipoprotein (LDL), aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) in HFD-fed rats. The combination of LGG and HIIT provides a multi-pathway intervention that improves HFD-induced memory impairments by concurrently targeting oxidative stress, dyslipidemia, and hippocampal synaptic function. This supports the potential of combined lifestyle and microbiome-based therapies for preventing metabolic and cognitive disorders.

Chronic pain and stress often co-exist and are driven by overlapping neurobiological, immunological, and psychosocial mechanisms. In this review, we provide a mechanistic and translational overview of the common pathways underlying chronic pain-stress comorbidity. We summarize key mechanisms, including dysfunction of the sympatho-adrenomedullary system and HPA axis, neuroimmune crosstalk, neurotransmitter imbalances (e.g., monoamines, neuropeptides, and cytokines), maladaptive neuroplasticity within the stress-pain matrix, as well as peripheral immune activation and autoantibody-mediated sensitization. Together these processes contribute to a bidirectional, self-perpetuating cycle observed in conditions such as fibromyalgia, complex regional pain syndrome, low back pain, irritable bowel syndrome, and rheumatoid arthritis. Current therapeutic options remain insufficient, with many patients showing resistance to traditional treatments. We highlight the importance of a multidisciplinary biopsychosocial strategy integrating pharmacological interventions targeting shared neurotransmitter systems (antidepressants, anticonvulsants), with non-pharmacological modalities (cognitive behavioral therapy, mindfulness, physical activity, neuromodulation). Furthermore, emerging mechanism-based targets, including the endocannabinoid system, neurotrophic factors, and stress-related hormonal pathways, are discussed as promising novel therapeutic approaches. In conclusion, chronic pain and stress should be conceptualized as interconnected neuroinflammatory disorders driven by common neuroimmune and neuroendocrine dysregulation. A mechanism-oriented, integrative framework may support the development of more effective, individualized therapeutic strategies to improve patient outcomes.

Understanding how human behavior relates to brain structure and function is a central goal of neuroscience. Autism spectrum disorder (ASD) is increasingly conceptualized as a disorder of connectome dysfunction; however, how morphological brain networks relate to behavioral profiles in children with ASD remains unclear. In this study, we collected a comprehensive battery of behavioral assessments and structural MRI data from 101 children with ASD and 67 typically developing (TD) children. Individual morphological brain networks were constructed by integrating four cortical features to estimate morphological connectivity (MC). We then applied sparse canonical correlation analysis (sCCA) to identify multivariate brain-behavior associations within each group. Using group-specific MC features, four distinct association modes were identified in TD children, none of which generalized to the ASD group. In ASD children, three modes were detected that captured comparable behavioral dimensions with three TD modes but were supported by largely distinct neural architectures. Within a unified MC framework, an autistic trait mode emerged in both groups; however, it was primarily supported by MC between the default and control networks in TD children, versus MC between the default and dorsal attention networks in ASD children. Notably, the prosociality mode present in TD children was consistently absent in the ASD group, regardless of the MC features used in sCCA. These findings reveal a reorganization of brain-behavior relationships in children with ASD and provide evidence for a neurodiverse neural architecture, in which similar behaviors arise from divergent neurodevelopmental pathways, moving beyond a simple continuum model of typical development.

Functional/dissociative seizures (FDS) are episodes of seizure-like behavior with a biopsychosocial basis. Emerging evidence has suggested executive dysfunctions in individuals with FDS. The Frontal Assessment Battery (FAB) has been widely used to assess executive functioning in neurologic conditions. We aimed to characterize FAB performance and executive screening profiles in FDS and to evaluate case-control differences between individuals with FDS and healthy controls. This study included individuals referred to epilepsy clinics affiliated with Tehran University of Medical Sciences who were diagnosed with FDS. Independent-samples t-tests were used to compare FAB scores between healthy controls and individuals with FDS. Moreover, receiver operating characteristic (ROC) curve analysis was conducted to assess the discriminative performance of the FAB. 50 healthy individuals and 50 with FDS were recruited in this study. The mean FAB score was significantly lower in individuals with FDS than in healthy controls (p&#xa0;<&#xa0;0.001). Similar differences between these groups were observed in most FAB subdomains, including conceptualization, mental flexibility, motor programming, sensitivity to interference, and inhibitory control (p&#xa0;<&#xa0;0.001). In the FDS group, FAB scores were positively associated with years of education (B&#xa0;=&#xa0;0.222, p&#xa0;=&#xa0;0.002). Finally, the FAB demonstrated strong case-control discriminative performance between individuals with FDS and healthy controls (AUC&#xa0;=&#xa0;0.909, 95&#xa0;% CI: 0.847 to 0.962). In conclusion, the FAB may serve as a practical bedside screening measure for executive dysfunction in FDS. Further studies are needed to evaluate its clinical utility in differentiating FDS from epileptic disorders.

Infant socioemotional development has important implications for later functioning, reflecting capacities for emotional regulation, stress responsivity, and social engagement. Stress and mental health during pregnancy and the postpartum can adversely influence infant socioemotional functioning. This study examined whether postpartum depressive and anxiety symptoms mediate associations between prenatal maternal hair cortisol concentration (HCC) and infant socioemotional development. A sample of 128 participants was followed from the third trimester of pregnancy to 6&#xa0;months postpartum. Maternal HCC was collected during the third trimester to reflect cortisol during the second half of pregnancy. Symptoms of depression and anxiety were measured at 2&#xa0;weeks postpartum, and infant socioemotional problems were assessed at 6&#xa0;months of age. Structural equation modeling tested postpartum depression and anxiety as parallel mediators. Results indicated that lower HCC in pregnancy predicted greater postpartum depression (B&#xa0;=&#xa0;-3.676, p&#xa0;=&#xa0;0.003) and anxiety (B&#xa0;=&#xa0;-3.41, p&#xa0;=&#xa0;0.009); depression was associated with greater infant socioemotional problems at 6&#xa0;months (B&#xa0;=&#xa0;1.900, p&#xa0;<&#xa0;0.001). HCC was not directly associated with infant socioemotional outcomes (B&#xa0;=&#xa0;1.071, p&#xa0;=&#xa0;0.792); however, the indirect effect, through depressive symptoms, was significant (B&#xa0;=&#xa0;-6.99, p&#xa0;=&#xa0;0.01). These findings suggest that prenatal physiological stress may influence infant socioemotional development indirectly through early postpartum depressive symptoms, highlighting the importance of integrated perinatal processes.

Xenopus laevis has long served as an important model for studies of embryonic development and is a cornerstone to our current understanding of cellular and molecular mechanisms underlying neurodevelopment, including the formation and refinement of neural circuits. In recent years, considerable efforts have been made to leverage the great accessibility and amenability of the Xenopus system to model neurodevelopmental and neurodegenerative disorders in humans for higher-throughput investigations of genetic and environmental risk factors. Behavioral paradigms are indispensable tools to assess functional output in whole animals. In this review, we summarize a range of behavioral paradigms established in Xenopus laevis and Xenopus tropicalis tadpoles to evaluate the functional development of the nervous system. We discuss the current understanding of neural substrates that give rise to specific behaviors, and how these paradigms have been used to evaluate the functional ramifications of cellular and molecular abnormalities in neural circuitry. We cover three categories of behavioral paradigms: innate and stable behaviors, experience-dependent and learned behaviors, and social behaviors. Each provides distinct functional readouts of the developing nervous system. We also include tips and suggestions for the implementation of these paradigms and discuss how insights from other aquatic animal models may inform the further development of behavioral paradigms in Xenopus tadpoles.

Pupil diameter is a non-invasive biomarker of brain state, correlating with arousal, attention, cognitive processing, and consciousness. However, existing pupillometry software often lacks scalability and robustness across diverse experimental conditions and species. We introduce Pupil-DLC, an open-source, offline, DeepLabCut-based pipeline for scalable, marker-less pupil tracking, primarily designed for mice. Trained on 21,750 manually annotated frames from over 140 videos of head-fixed mice spanning wakefulness and drug-induced states, including psychedelics and anesthesia, the dataset was deliberately selected to maximize pupil size variability and model generalization. Pupil-DLC implements a dual-model architecture: a General Model (GM) for high-throughput analysis and an Individual Model (IM) for session-specific optimization. Pupil-DLC captures pupil dynamics across awake, psychedelic, and anesthetized conditions with high agreement with ground truth and equal tracking fidelity during active locomotion and quiet rest. Confidence metrics aligned with human frame quality assessments, enabling principled tuning of accuracy-retention trade-offs. As a secondary demonstration, Pupil-DLC extends to unseen human videos across diverse conditions and frame rates, including daylight and smartphone recordings, without retraining. Pupil-DLC outperforms existing automated methods in accuracy and frame retention while maintaining computational efficiency comparable to real-time tools. These improvements stem from a learned keypoint-based representation robust to pupil shape variability, occlusions, reflections, and imaging artifacts. The GM/IM framework supports a tiered strategy balancing throughput and precision. Pupil-DLC provides a reproducible, adaptable platform for quantifying pupil-linked brain state dynamics across experimental paradigms and species, bridging basic mouse neuroscience and translational human applications.

BackgroundDuchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder causing progressive muscle loss and early death. Despite global evidence on its burden, data from Sweden remain limited.ObjectiveThis study described the natural history of DMD, treatment patterns, healthcare resource utilization, and direct medical and non-medical costs among patients with DMD and their caregivers in Sweden.MethodsA retrospective, observational matched cohort study was conducted using data from the Swedish National Registry for Neuromuscular Disorders linked to national health and social registers. Patients diagnosed with DMD and their caregivers were compared to matched population controls. Disease progression was classified into four stages based on the HERCULES model.ResultsA total of 211 DMD patients (mean age at diagnosis: 4.9 years) and 877 comparators were included. Patients experienced progressive loss of function, spending on average 3.8, 4.8, 4.8, and 7.4 years in stages 1-4, respectively. Glucocorticoid use was high (84% on either prednisolone or deflazacort). Annual direct medical costs were significantly higher for DMD patients (&#x20ac;14,590 vs. &#x20ac;660). Direct non-medical costs, predominantly for personal assistance, increased substantially with disease stage, representing 89% of total DMD-related costs (&#x20ac;135,671 annually).ConclusionsDMD is a severe disorder marked by prolonged time in the later stages of the disease and increasing need for support. DMD imposes a significant economic burden in Sweden, with direct non-medical costs far exceeding direct medical costs. These findings highlight the need for and value of early and effective interventions to delay disease progression and alleviate societal burden.

To compare the prevalence of food insecurity (FI) in adults with spinal cord injury (SCI) versus a matched control cohort without self-reported disability, identify demographic and socioeconomic correlates of food insecurity, and examine the association between FI and body mass index (BMI). Cross-sectional analysis. U.S. nationwide cohort from the All of Us Research Program. A cohort of 751 adults with SCI and a 1:3 age-, sex-, race-, and ethnicity-matched control cohort. Not applicable. FI, BMI. Overall, 19.0% of participants with SCI (n=143) experienced FI, which was higher than the prevalence observed in the control cohort (15.6%, p<0.05). In univariate analyses, risks of FI were elevated among participants who were Black or Hispanic, women, younger, unmarried, unemployed, had lower educational attainment, and lower income (all p<0.05). In multivariable logistic regression, higher income, being retired, and education beyond high school were associated with lower odds of FI, whereas race, ethnicity, sex, and marital status were no longer significant. In BMI analyses, FI was associated with higher BMI in unadjusted models, but this association attenuated after covariate adjustment. Exploratory analyses suggested effect modification by race: among White participants, FI was associated with higher BMI (+1.73kg/m&#xb2;; p<0.05), whereas among Black participants, FI was associated with lower BMI (-3.22kg/m&#xb2;; pinteraction=0.02). Sensitivity analyses using BMI&#x2265;25 or &#x2265;30kg/m&#xb2; yielded consistent racial-specific patterns. These findings highlight food insecurity as an important social determinant of health in SCI, shaped largely by socioeconomic conditions rather than demographic and injury characteristics. The association between FI and weight status in SCI may differ across racial groups, warranting further investigation into the pathways through which material hardship influences health in this population.