Objectives The objective of this study is to assess the knowledge and awareness of epilepsy surgery among healthcare students and interns at King Abdulaziz University. By identifying gaps in understanding and perception, the study is aimed at informing future educational strategies to enhance awareness of surgical options for epilepsy management. Methods Data were collected using an online self‐administered questionnaire assessing participants′ awareness and knowledge of epilepsy surgery, drug‐resistant epilepsy (DRE), surgical referral timing, and perceptions regarding the risks and benefits of epilepsy surgery. Results Among 500 participants, only 25.8% (including 50.7% of medical students) knew that epilepsy could be treated surgically. Just 10.4% (17.3% of medical students) felt their medical training adequately covered epilepsy surgery. Only 10.6% (24.7% of medical students) correctly identified partial/focal epilepsy as surgically treatable, and 14.6% (30% of medical students) believed the benefits of surgery were high. “DRE” was correctly recognized by 44.2% overall (30% of medical students). Medical students had the highest knowledge scores (12.33 ± 4.04), followed by nursing (10.71 ± 2.87), pharmacy (9.94 ± 2.12), and laboratory students (9.85 ± 1.52). Conclusion A significant knowledge gap exists regarding epilepsy surgery among healthcare students and interns. Medical students demonstrated greater awareness than their nonmedical peers. Enhancing medical and allied health curricula could improve future referral practices and patient outcomes.
In the past two decades, advances in microbiomics and neuroimmunology have reframed the concept of "central immune privilege." Rather than simply proving a gut-brain connection, the translational challenge now lies in identifying how gut-derived signals are transmitted, filtered, amplified, or buffered across different neural, immune, metabolic, vascular, and barrier-related routes. Based on a structured narrative synthesis of experimental, translational, and clinical literature, this review presents barrier-immune-coupled gating failure as a working hypothesis and conceptual framework, rather than as a unifying explanation for all gut-brain interactions. Within this framework, three analytically separable but interacting dimensions are emphasized: (1) entry gating, referring to the threshold at which peripheral signals influence CNS boundary states; (2) boundary translation, in which signals are filtered or reshaped at interfaces such as the blood-brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB), and meningeal immune zones; and (3) clearance gating, involving CSF drainage, meningeal lymphatics, glymphatic exchange, and protein or inflammatory-signal clearance. We highlight how gut-derived signals-filtered by the intestinal mucosa and gut-associated lymphoid tissue (GALT)-interact with immune set points and structural barriers. These interactions are modulated by factors such as short-chain fatty acids (SCFAs) and metabolite load, influencing whether signals are buffered or amplified. Recent findings show that skull bone marrow can directly supply immune cells to the meninges via transcortical vascular channels (TCVs), forming a responsive border niche susceptible to intestinal inflammation. At the cellular level, the review focuses on boundary-associated macrophages (BAMs) and disease-associated microglia (DAM) states, which bridge peripheral disruptions and central neuroinflammation. In selected contexts, reduced boundary buffering or impaired clearance may increase the likelihood that interface inflammation extends toward the parenchyma, particularly in proteinopathies with persistent inflammatory or protein burden. Finally, we propose a biomarker matrix for mechanistic stratification, which may help prioritize hypothesis-guided evaluation of barrier repair, drainage enhancement, immune set-point modulation, and cell-state reprogramming, while acknowledging that current human intervention evidence remains modest, inconsistent, or context-specific. By defining its scope and testable predictions, this framework may help move selected gut-brain studies from broad association toward more stratified and mechanism-oriented investigation.
BACKGROUND:This bibliometric analysis is aimed at mapping global trends and research hotspots in postoperative depression, providing insights into the evolution and development of research in this field. METHODS:A comprehensive search was conducted in the Web of Science Core Collection database, focusing on literature from 1994 to 2024. Data extraction and visualization were performed using VOSviewer (Version 1.6.20), CiteSpace (Version 6.3.R1), and R (Version 4.3.3). RESULTS:This study encompassed 687 scholarly articles from 54 countries. The United States contributed the largest number of articles, followed by China and the United Kingdom. High-output institutions from the United States include the University of California System and Harvard University. The Journal of Psychosomatic Research and Epilepsy were among the top journals by h-index. Aalto Timo, Airaksinen Olavi, and Sinikallio Sanna were among the most productive authors. High-frequency keywords included "quality-of-life," "anxiety," and "symptoms." Recent burst keywords "risk," "elderly patients," and "double blind" indicate emerging trends in the field, pointing toward an increased interest in identifying factors that may precipitate postoperative depression, the unique vulnerabilities of older adults, and the methodological rigor of double-blind studies in assessing interventions. CONCLUSION:The research hotspots and trends in postoperative depression are centered around the impact of depression on surgical outcomes, the role of anxiety, and quality of life assessments. This study reveals a growing interest in predictors of postoperative depression and the exploration of novel therapeutic interventions, indicating an evolving and dynamic research area.
BACKGROUND:Social determinants of health (SDoH) have not been comprehensively studied in relation to Parkinson's disease (PD), although they are well known to be associated with other chronic diseases. Here we assessed the relationship of a multidimensional, comprehensive measure of SDoH with the prevalence of PD in US adults. METHODS:Among 48,637 adults in the National Health and Nutrition Examination Survey (NHANES) between 2001 and 2020, we identified PD cases based on self-reported antiparkinsonian medication use. We formed a weighted multidomain SDoH score from eight indicators that assessed economic security, education, healthcare access, and social environment. Both multivariable logistic regression and restricted cubic spline (RCS) were used to estimate odds ratios and dose-response relationships and were adjusted for demographic and lifestyle factors. RESULTS:More intensive adverse SDoH burden was significantly associated with higher PD prevalence (fully adjusted OR 1.31, 95% CI 1.16-1.47 per unit increase), and RCS analysis showed no evidence of nonlinearity (p for nonlinearity = 0.370). Unemployment (OR 4.15, 95% CI 2.70-6.40) and food insecurity (OR 1.96, 95% CI 1.39-2.76) were strongly associated with higher PD prevalence, whereas reported lack of health care access was associated with lower identified PD (OR 0.27, 95% CI 0.15-0. 49), pointing to likely ascertainment bias. When stratifying, we observed meaningful effect modification by age (p < 0.001), with stronger effects in middle-aged individuals (≤ 60 years: OR 1.35, 95% CI 1.13-1.61), compared with an attenuation in older individuals. CONCLUSION:Poor SDoH were independently associated with higher PD prevalence, particularly among adults aged 60 years and younger. Unemployment and food insecurity showed strong positive associations, whereas the inverse association with healthcare access likely reflects ascertainment bias. These findings are hypothesis-generating and suggest that SDoH may be relevant to PD screening and epidemiologic research. Longitudinal studies are needed to clarify temporality and causality.
Tobacco consumption has significantly increased globally, contributing to various degenerative diseases such as lung cancer and cardiovascular disorders. Nicotine, the primary addictive component in tobacco, exerts its effects by stimulating nicotinic acetylcholine receptors (nAChRs), leading to excessive dopamine release in the ventral tegmental area (VTA) and nucleus accumbens (NAc), which underlies its rewarding and addictive properties. Additionally, nicotine enhances orexin activity in the hypothalamus and prepro-glucagon expression in the nucleus tractus solitarius (NTS), further reinforcing addictive behaviors. This study is aimed at investigating the effects of liraglutide, a GLP-1 receptor agonist, on nicotine-induced reward. Male mice strain ddy were divided into four groups: control, nicotine, nicotine + liraglutide (50 μg/kg), and nicotine + liraglutide (100 μg/kg). The conditioned place preference (CPP) test was used to evaluate nicotine's rewarding effects, whereas RT-PCR assessed the expression of prepro-orexin and prepro-glucagon mRNA in the hypothalamus and NTS, respectively. The results confirmed that nicotine administration (0.5 mg/kg) significantly increased CPP scores, indicating enhanced reward-related behaviors. Correspondingly, nicotine elevated prepro-orexin and prepro-glucagon mRNA expression levels. Treatment with liraglutide (50 and 100 μg/kg) significantly reduced nicotine-induced CPP scores, suggesting an attenuation of addictive behavior. Liraglutide downregulated the expression of prepro-orexin and prepro-glucagon, with the 100 μg/kg dose demonstrating greater efficacy in normalizing prepro-glucagon levels. These findings indicate that liraglutide mitigates nicotine reward by modulating neuropeptide pathways, including orexin and glucagon signaling. The dual impact of liraglutide on behavioral and molecular markers highlights its potential as a therapeutic agent for treating nicotine induce reward-related behavior. Further research is warranted to explore its long-term efficacy and underlying mechanisms in addiction modulation.
