Background: Major depressive disorder (MDD) is a prevalent psychiatric condition with limited biological markers to guide diagnosis and treatment. While reduced brain creatine concentrations have been implicated in MDD pathophysiology, the role of circulating creatine remains unclear. Objective: To examine whether circulating creatine concentrations differ between individuals with MDD and non-MDD comparators in a large, population-based cohort, and to explore demographic correlates of systemic creatine status. Methods: We conducted a cross-sectional exploratory analysis within the All of Us Research Program, an NIH-led cohort of U.S. adults. MDD cases were identified from electronic health records using standardized OMOP concept identifiers. Circulating creatine concentrations were extracted from curated laboratory data, and participants with end-stage renal disease were excluded. Group comparisons were performed using Welch’s t-test, and associations with age and sex were evaluated. Results: Circulating creatine concentrations did not differ significantly between individuals with MDD and non-MDD participants. Of the 63,162 individuals diagnosed with MDD, creatine measurements were available for 94, and 81 participants were included in the final analysis after excluding those with renal pathology (mean age: 53.7 ± 13.8 years; 54% male). Mean creatine concentrations in the MDD group (1.02 ± 0.36 mg/dL) were similar to those in the non-MDD reference group (n = 121; mean age: 52.4 ± 15.4 years; 1.01 ± 0.40 mg/dL; P = 0.86). Within the MDD group, creatine concentrations were not significantly correlated with age (r = 0.18, P = 0.12). However, serum creatine levels were significantly higher in men than in women (1.16 ± 0.36 mg/dL vs. 0.81 ± 0.24 mg/dL; P < 0.0001). Conclusions: In this population-based exploratory analysis, circulating creatine concentrations were comparable between individuals with and without MDD but showed pronounced sex-related differences. These findings highlight the importance of considering sex as a biological variable in creatine research and underscore the need for longitudinal and mechanistic studies to clarify the relationship between peripheral and central creatine homeostasis in depression.
Background: The quality of life and academic performance are severely impacted, particularly in females, due to higher anxiety and lower Control. Issues regarding perceived BMI contribute to anxiety levels; however, the relationship remains unknown. Studies regarding the association between anxiety and perceived BMI have reported contradictory results. Objective: The study aims to examine the relation between perceived weight status, Body Mass Index (BMI) discrepancy, and anxiety control. Methods: The study used a cross-sectional design and a survey questionnaire, completed by 362 medical students at King Abdulaziz University (KAU). Perceived anxiety control was evaluated using the Anxiety Control Questionnaire (ACQ). For calculating BMI, data was collected. Statistical analysis included weighted Kappa for agreement on BMI perception, while multiple linear regression assessed anxiety and perceived BMI relationships. To determine the difference in ACQ scores, ANOVA and sample t-tests were conducted across different predictor levels. Results: Moderate to substantial agreement was observed between calculated BMI and perceived BMI category (weighted Kappa = 0.62, 95% CI: 0.56–0.68), with a mean anxiety control score of 78.1 ± 18.5. Compared to those perceiving a normal weight, students who perceived themselves as overweight or obese had significantly lower ACQ scores (adjusted β = –8.28, p = 0.01; β = –27.49, p = 0.001. Discussion: Respectively, after adjustment for GPA, smoking, and BMI category. Conversely, students who underestimated their BMI (perceived themselves thinner than actual) had significantly higher ACQ scores (adjusted β = 8.54, p = 0.02 Conclusion: The present study denotes the need to address perceived BMI concerns to overcome anxiety with selective measures and awareness initiatives to enhance the overall quality of life and mental health of the female medical population.
Traumatic Brain Injury (TBI) is a major global health concern with complex pathophysiology and long-term neurological, cognitive, and psychosocial consequences. Although advances in neuroimaging, biomarkers, and neurorehabilitation have improved diagnosis and management, outcomes remain variable due to injury heterogeneity and limited targeted therapies. This review summarises current evidence on TBI mechanisms, diagnostic tools, management strategies, rehabilitation practices, and emerging technologies, while highlighting key gaps and future priorities. A comprehensive literature search of peer-reviewed articles, clinical guidelines, and contemporary research databases was conducted. Studies addressing acute care, monitoring, surgical intervention, rehabilitation, and advanced technologies such as Brain-Computer Interfaces (BCIs) were evaluated. Recent progress underscores the utility of multimodal neuroimaging, such as diffusion tensor imaging and quantitative MRI, for detecting microstructural injury and supporting clinical decisions. Blood-based biomarkers, including GFAP, UCH-L1, and NFL, offer promise for rapid assessment and prognosis. Current management continues to focus on preventing secondary injury through optimised ventilation, hemodynamic stability, hyperosmolar agents, and stepwise intracranial pressure control, while surgical interventions are guided by clear radiological thresholds. Rehabilitation benefits from coordinated multidisciplinary care that integrates physical, cognitive, and behavioural therapies. Emerging rehabilitation tools, such as BCIs, robotic- assisted systems, and virtual-reality platforms, show early promise for enhancing functional recovery, though evidence remains limited and requires larger, standardised studies. Despite important diagnostic and rehabilitative advances, TBI management still lacks unified biomarkers, standard imaging criteria, and robust evidence for emerging therapies. Coordinated multicentred research and personalised, technology-integrated care models remain essential to improve long-term outcomes.
It has come to our attention that in the published version of this article [1], references 27 and 50 contained errors in their DOI link. These errors have now been corrected. The original article can be found online at: https://www.benthamscience.com/article/148494. Details of the correction are provided below: Original: [27] Mollaahmadi L, Keramat A, Changizi N, Yazdkhasti M, Afshar B. Evaluation and comparison of the effects of various cognitive-behavioral therapy methods on climacteric symptoms: A systematic review study. J Turk Ger Gynecol Assoc 2019; 20(3): 178. http://dx.doi.org/10.4274%2Fjtgga.galenos.2019.8.0170 [50] Sharma P, Kapoor S. Impact of husband’s attitude towards menopause on severity of menopausal symptoms among women in IndiaPankhuri Sharma. Eur J Public Health 2015; 24(2): 1-10. http://dx.doi.org/1093/eurpub/cku161.065 Corrected: [27] Mollaahmadi L, Keramat A, Changizi N, Yazdkhasti M, Afshar B. Evaluation and comparison of the effects of various cognitive-behavioral therapy methods on climacteric symptoms: A systematic review study. J Turk Ger Gynecol Assoc 2019; 20(3): 178. http://dx.doi.org/10.4274/jtgga.galenos.2019.2018.0170 [50] Sharma P, Kapoor S. Impact of husband’s attitude towards menopause on severity of menopausal symptoms among women in IndiaPankhuri Sharma. Eur J Public Health 2015; 24(2): 1-10. http://dx.doi.org/10.1093/eurpub/cku161.065 The article has been updated to reflect this correction.
Introduction: Autism Spectrum Disorder (ASD) may increase vulnerability to premature mortality, but the magnitude of risk and sex-specific differences remain unclear. Methods: A systematic search of PubMed, Web of Science, Scopus, and Google Scholar was conducted up to January 13, 2025. Studies comparing premature mortality risk between ASD and non-ASD populations were included. Pooled Hazard Ratios (HRs) and 95% Confidence Intervals (CIs) were calculated using a random-effects model. Heterogeneity was assessed using I². Results: Six cohort studies (5,814,167 participants) were included. ASD was associated with a significantly increased risk of premature mortality (RR = 2.06; 95% CI: 1.44–2.69; I² = 97.1%). The risk was higher in females (RR = 3.41; 95% CI: 1.95–4.86; I² = 87.0%) than in males (RR = 2.33; 95% CI: 1.63–3.02; I² = 86.2%). Discussion: These findings confirm that ASD confers a more than twofold risk of premature death, with females disproportionately affected. The high heterogeneity reflects variations in causes of death (e.g., epilepsy, suicide) and study populations. Importantly, many contributing factors are potentially preventable through early comorbidity screening, integrated mental and physical healthcare, and psychosocial support. The elevated risk in females may stem from diagnostic delays and under-recognition of ASD. Clinicians and policymakers should prioritize proactive, life-course-oriented strategies to reduce this mortality gap. Conclusion: ASD is associated with substantially increased premature mortality, especially among females. Targeted prevention and improved healthcare access are urgently needed.
