Search Results (1,604)

Objectives: Attention-deficit hyperactivity disorder (ADHD) is the most prevalent neurodevelopmental disorder diagnosed during childhood, primarily characterized by continuous symptoms of inattention, hyperactivity, and impulsivity. The present study aimed to investigate the genetic association between polymorphisms in the serotonergic system-related genes, HTR1B and HTR2A, and the susceptibility to ADHD in a Korean sample. Methods: The study cohort consisted of 234 children diagnosed with ADHD and 1686 healthy controls. Clinical diagnosis was established based on the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria. Genetic analysis focused on single nucleotide polymorphisms (SNPs) within the serotonergic pathway: rs6296 in HTR1B, and three SNPs (rs6311, rs6313, and rs9534495) in HTR2A. Genotype and allele frequencies were analyzed using Chi-square tests. Risk estimates were calculated as odds ratios (OR) with 95% confidence intervals (CI) across dominant, recessive, and additive inheritance models. Results: A statistically significant association was observed between the HTR2A rs9534495 polymorphism and ADHD. Specifically, significant associations were identified under the dominant (OR 0.67, 95% CI 0.48–0.93, p = 0.017), recessive (OR 0.67, 95% CI 0.48–0.93, p = 0.016), and additive (OR 0.80, 95% CI 0.65–1.00, p = 0.046) models. However, these significant findings did not persist after applying the Bonferroni correction for multiple comparisons. Conversely, no significant associations were detected for the HTR1B (rs6296) and the other HTR2A (rs6311, rs6313) polymorphisms. Conclusions: These findings suggest that genetic variations in the serotonergic system, particularly within the HTR2A gene, may contribute to the genetic susceptibility to ADHD. This study confirmed gene SNIPs associated with the serotonergic system in the pathophysiology of ADHD. Future research involving large-scale multi-ethnic cohorts, functional assays, and gene–environment interaction analyses is warranted to further elucidate the underlying mechanisms of serotonergic genes. Full article

Accurate recognition of Line-of-Sight (LOS) and Non-Line-of-Sight (NLOS) signals is crucial for mitigating positioning errors and improving the positioning performance of Ultra-Wideband (UWB) localization systems. Current NLOS identification methods are limited to the specific measurement environments and fail to exhibit effective cross-domain adaptability, being unable to generalize to unseen environments. To address these challenges, we propose a novel NLOS identification strategy based on a Domain-Adversarial Neural Network (DANN). Firstly, aiming at the problem that traditional feature extraction methods fail to capture the deep nonlinear characteristics of Channel Impulse Response (CIR) data, we develop a CNN-DAE-MLP-Attention (CDM) hybrid model for high-quality channel feature extraction, which takes both raw CIR data and handcrafted channel features into account. Secondly, we integrate the CDM model into the DANN framework by replacing its original shallow feature extraction module to further propose the CDMD algorithm; by combining the robust feature representation capability of CDM with the excellent domain adaptation capability of DANN, the proposed CDMD algorithm achieves enhanced performance in cross-domain LOS/NLOS identification. Finally, the effectiveness of the proposed algorithm is verified using measured data from different scenarios. Results demonstrate that the proposed algorithm possesses strong generalization ability. For cross-domain NLOS recognition from underground parking garage to corridor and underground parking garage to lobby, the proposed method achieves accuracies of 77.00% and 72.84%, respectively. Moreover, the results indicate that only a limited number of target-domain samples are sufficient for the model to achieve accurate cross-domain transfer. Full article

Background: We investigated whether common variants in SCN1A are associated with antiepileptic drug (AED) non-response in Jordanian patients with epilepsy. Methods: We recruited 114 patients (105 successfully genotyped) and Sanger-sequenced five loci spanning rs6432860 and its flanking region of rs1531380, rs1531379, rs1531378, and rs10198801. Genotype–response associations were tested using contingency analyses and multivariable logistic regression adjusting for age at the time of the interview, number of AEDs, and carbamazepine use. Pre-specified secondary analyses included (i) stratification by AED class (voltage-gated sodium channel [VGSC]-acting vs. non-VGSC agents) and (ii) sensitivity analyses using alternative non-response thresholds (seizures > 0/year and ≥4/year). Linkage disequilibrium (LD) and exact Hardy–Weinberg equilibrium (HWE) tests were evaluated. Cohort minor allele frequencies (MAFs) were compared with global population estimates. Results: The four upstream previously cataloged intronic variant SNPs (rs1531380, rs1531379, rs1531378, and rs6432860) were in a complete pattern of LD association in this population (D′ = 1; r^{2 =} 1) whereas each upstream variant with rs10198801 showed D′ = 1 with inverse correlation (r ≈ −0.53). All loci conformed to the exact HWE tests. Upstream variants had novel associations with a non-response in unadjusted analyses and remained significant after adjustment (genotype aOR = 2.8; 95% CI = 1.1–7.2; p value = 0.03), alongside independent effects of carbamazepine use (aOR = 3.3; 95% CI = 1.3–8.0; p value = 0.009) and a number of AEDs (aOR = 0.17; 95% CI = 0.06–0.50; p value = 0.002). In AED-class stratification, upstream additional intronic variants had novel associations with a non-response among VGSC-treated patients (OR = 3.8; 95% CI = 1.1–13.6; p value = 0.03) whereas rs10198801 was associated among non-VGSC patients (OR = 7.9; 95% CI = 0.9–70; p value = 0.04). Findings were robust using a ≥4 seizures/year threshold (recessive model significant) but not using any seizures > 0/year. Cohort MAFs for upstream variants (~48.6%) exceeded European, African, and Asian estimates. Significance: SCN1A upstream intronic variation has a novel association with AED non-response in the Jordanian cohort, shows mechanism-aligned patterns by AED class, persists after covariate adjustment and under a clinically used seizure-frequency threshold, and warrants ancestry-informed replication and functional validation. Full article

Multimodal Named Entity Recognition (MNER) aims to integrate textual and visual information to identify entities with specific semantic categories. However, existing methods often suffer from insufficient intra-modal semantic modeling, coarse cross-modal alignment, and vulnerability to noisy or ambiguous expressions in social media. To address these challenges, we propose a Visual–Semantic Guided Interaction Network (VSGN), which improves multimodal representation learning from both semantic and structural perspectives. Specifically, we first design an adaptive visual–semantic fusion module that incorporates visual descriptions as semantic guidance, enabling more informative cross-modal interactions. To further enhance feature quality, we introduce a deviation-aware channel-wise inhibitory routing (CIR) mechanism, which jointly models channel importance and distributional deviation to suppress noisy or redundant visual signals. In addition, we propose a visual–semantic guided graph structure learning module (VSG), which explicitly captures structural dependencies across modalities. By enforcing distribution-level alignment between textual and visual graph representations, the model achieves structure-aware cross-modal interaction and reduces modality inconsistency. Extensive experiments on the Twitter-2015 and Twitter-2017 datasets demonstrate the effectiveness of the proposed method, achieving F1 scores of 76.72% and 87.86%, respectively. The results show that jointly modeling semantic enhancement and structural alignment leads to more robust and discriminative multimodal representations. Full article

Background/Objectives: Preterm infants are particularly vulnerable to nutritional deficiencies and electrolyte imbalances during the early stages of extrauterine life. To ensure optimal metabolic support, they often require the early initiation of “aggressive” parenteral nutrition (PN), which is a known risk factor for Refeeding Syndrome (RS), a potentially serious metabolic condition characterized by fluid and electrolyte disturbances, the most significant of which is hypophosphatemia. Hypophosphatemia can impair the metabolism, survival, and function of red blood cells, leading to a reduction in key intracellular metabolites and the development of a metabolic block that alters their quality and decreases their stability. It is therefore hypothesized that RS may contribute to the development of anemia of prematurity (AOP). At the same time, early enteral nutrition (EN) may promote metabolic adaptation and reduce exposure to the complications of prolonged parenteral support, potentially protecting against AOP. The primary aim of this study was to determine whether preterm infants who develop RS are at increased risk of AOP. A secondary aim was to evaluate whether early EN may act as a protective factor against the development of AOP. Methods: This retrospective observational study was conducted on infants with a gestational age ≤ 34 weeks and/or birth weight ≤ 1500 g, admitted to the Neonatal Intensive Care Unit of Policlinico Umberto I—Sapienza University of Rome, between January 2015 and November 2022. Infants diagnosed with AOP were classified as cases, while those without AOP served as the control group. Results: A total of 412 preterm infants were enrolled (110 cases, 302 controls). Refeeding Syndrome was significantly more frequent in infants with AOP (30.9% vs. 11.6%, p < 0.001). In the logistic regression model adjusted for gestational age, RS was independently associated with AOP (OR = 2.81; 95% CI: 1.55–5.10; p < 0.001), along with gestational age ≤ 34 weeks (OR = 7.10; 95% CI: 2.13–24.0; p = 0.001). Early enteral nutrition during the first week of life was associated with a significantly lower risk of AOP (OR = 0.12; 95% CI: 0.029–0.52; p = 0.005). The association between RS and AOP was confirmed in the model adjusted for birth weight (OR = 2.06; 95% CI: 1.16–3.79; p = 0.021). Infants with AOP showed significantly higher parenteral nutrition intake, delayed initiation of enteral feeding, and later achievement of full enteral nutrition compared with controls (all p < 0.001). Conclusions: RS is significantly associated with AOP in preterm infants, likely through pathophysiological mechanisms related to hypophosphatemia. Importantly, early EN may be a protective factor against AOP, suggesting that timely initiation and advancement in enteral feeding may counteract the metabolic derangements associated with intensive parenteral support. These findings support a nutritional approach that prioritizes early and progressive enteral nutrition as a strategy to reduce the risk of both RS and AOP. Further prospective studies are needed to confirm these associations and to define optimal EN protocols for this population. Full article

Although ombitasvir/paritaprevir/ritonavir plus dasabuvir (OPrD) therapy is highly effective for chronic hepatitis C (CHC), clinicians frequently encounter transient hyperbilirubinemia, which can be misidentified as hepatotoxicity. This study investigated the role of SLCO1B1 (OATP1B1) and SLCO1B3 (OATP1B3) genetic polymorphisms in predicting bilirubin spikes and distinguishing transporter-mediated interference from hepatocellular injury. In this prospective study of 65 patients with HCV genotype 1, genotyping for OATP1B1 (c.388A>G, c.521T>C) and OATP1B3 (c.334T>G, c.699G>A) was performed using PCR-RFLP and capillary electrophoresis (QIAxcel Advanced System). Clinical and biochemical parameters were monitored over a 12-week treatment period. Hyperbilirubinemia (total bilirubin >1.1 mg/dL) developed in 18.5% of the cohort, typically within the first month. A distinct ‘AST-dominant’ biochemical signature, elevated bilirubin and AST paired with stable ALT, was identified, suggesting transporter-specific interference rather than hepatocyte damage. Statistical analysis pinpointed the OATP1B3 c.699G>A (rs7311358) variant as the sole genetic driver (p = 0.007). Carriers of the c.699G>A allele faced a 6.3-fold higher risk of developing hyperbilirubinemia (OR: 6.30, 95% CI: 1.48–26.80, p = 0.032), while no significant associations were found for OATP1B1 variants. We conclude that OATP1B3 c.699G>A is a potent predictor of OPrD-induced hyperbilirubinemia. Identifying this genotype pre-treatment allows clinicians to anticipate transient, benign bilirubin elevations and prevent unnecessary drug discontinuation, thereby mitigating therapeutic inertia and ensuring treatment continuity for CHC patients. Full article

Background/Objectives: There is no consensus on standardized treatment algorithms for patients with acute ischemic stroke due to anterior circulation tandem occlusions. This study evaluated the outcomes of mechanical thrombectomy and carotid artery stenting in such patients, with a particular focus on a standardized, adaptive, and escalating antithrombotic strategy. Methods: This single-center retrospective study included patients with atherosclerotic tandem occlusion treated between January 2019 and July 2023 at our comprehensive stroke center. All patients underwent mechanical thrombectomy and carotid artery stenting and received a standardized antithrombotic regimen, including the administration of the GPIIb/IIIa antagonist eptifibatide as rescue therapy. Results: Sixty-seven patients were included in the analysis. Thirty-five patients (52.2%) received eptifibatide due to acute stent thrombosis. Subtotal to total revascularization (mTICI 2b-3) was achieved in 98.5% of patients. The carotid artery reocclusion rate was 3.4% at discharge. Symptomatic intracranial hemorrhage occurred more frequently in patients treated with eptifibatide (9.0% vs. 0%, p = 0.021) but was not associated with mortality or favorable outcome (mRS 0–2) at 90 days. In univariable regression analysis, eptifibatide administration was not significantly associated with symptomatic intracranial hemorrhage (OR 1.9, 95% CI 0.3–11.4; p = 0.465). Older age was associated with mortality. Conclusions: Our adaptive antithrombotic protocol demonstrated high revascularization and low carotid reocclusion rates. Rescue use of eptifibatide was not significantly associated with symptomatic intracranial hemorrhage; however, a clinically relevant risk cannot be excluded. These findings highlight the importance of tailored antithrombotic strategies in acute ischemic stroke to maintain stent patency while minimizing hemorrhagic complications. Full article

Background: Epilepsy is a chronic disorder with a higher prevalence in low- and middle-income countries. ATP-binding cassette superfamily B1 (ABCB1) not only has a potential influence on the resistance to antiepileptic drugs but also plays a possible role in the occurrence of epilepsy. Purpose: To evaluate the association of ABCB1 polymorphisms, c.1236C>T (rs1128503), c.2677G>T (rs2032582), and c.3435C>T (rs1045642), with epilepsy susceptibility in a Jordanian cohort. Subjects and methods: Eighty-six cases of patients with epilepsy were analyzed using polymerase chain reaction (PCR) for ABCB1 c.1236C>T, c.2677G>T, and c.3435C>T gene variants. The proportions of genotypes and alleles in the epilepsy group were compared with one hundred healthy controls who were previously also analyzed by PCR. Results: The C alleles of the ABCB1 polymorphisms c.1236C>T and c.3435C>T were more prevalent in the epilepsy group than in controls. The patients with epilepsy were less likely to have the TT genotype compared with controls (concerning ABCB1 c.1236C>T) (OR_{TT vs. CC} = 0.42; 95% CI = [0.19–0.91]; p = 0.019). The CC genotype of ABCB1 c.3435C>T was more frequent in epileptics than healthy people (OR_{CC vs. TT} = 4.3; 95% CI = [1.8–9.95]; p = 0.0007). No significant difference in ABCB1 c.2677G>T allelic and genotypic frequencies was observed between epileptic cases and healthy volunteers. Conclusion: Our findings suggest that ABCB1 c.1236C>T and c.3435C>T variants were associated with epilepsy susceptibility in this Jordanian cohort, whereas no significant association was observed for c.2677G>T. These findings should be interpreted cautiously because of the modest sample size and require validation in larger, independent studies. Full article

Background: Breast cancer (BC) is a leading cause of cancer-related mortality worldwide and a major public health concern in Mexico. Regulatory variants in KRAS, particularly within the 3′UTR and intronic regions, may influence gene expression through microRNA binding and transcriptional regulation. Methods: Five regulatory single-nucleotide variants (SNVs) in KRAS (rs12228277, rs1137196, rs8720, rs12587, and rs12245) were genotyped in BC patients and cancer-free controls. Associations were evaluated using odds ratios (ORs) with 95% confidence intervals (CIs), adjusting for age, alcohol, and tobacco use. Multiple testing was corrected using the Benjamini–Hochberg false discovery rate (FDR). Linkage disequilibrium (LD), multilocus combinations, and in silico functional analyses were also performed. Results: Variants rs12228277, rs1137196, rs8720, and rs12245 showed significant genotype-level associations with BC susceptibility, all remaining significant after FDR correction (pFDR < 0.05). No clinicopathological associations remained significant after correction in single-variant analyses. Multilocus analysis identified specific high-risk combinations (e.g., involving rs12228277, rs1137196, and rs8720) associated with increased BC susceptibility. At the nominal level, these combinations showed associations with clinicopathological features, including hormone receptor–positive status (PR and ER), proliferation markers, and Luminal B subtype; however, none remained significant after FDR correction. LD analysis indicated weak linkage among variants. In silico analyses suggested potential regulatory effects on microRNA binding and KRAS expression. Conclusions: Regulatory variants in KRAS are associated with BC susceptibility through independent effects and potential combinatorial patterns. These findings support the relevance of non-coding variation in cancer risk and warrant further functional and replication studies. Full article

Basal blood pressure (BP) is partly determined by systemic vascular resistance, which is modulated by vasoactive pathways, including gaseous messengers. Carbon monoxide (CO), continuously generated by the constitutive enzyme heme oxygenase-2 (HO-2) encoded by HMOX2, promotes vascular smooth muscle relaxation and may contribute to interindividual variability in resting BP. The functional single-nucleotide polymorphism rs4786504_T>C has been associated with higher HMOX2 expression in C-allele carriers, providing a plausible biological link between genetic variation in the HO-2/CO pathway and vascular redox signaling. We investigated this association in forty young, healthy, normotensive adults studied under controlled laboratory conditions during a 4-day sleep deprivation protocol, with repeated standardized daytime BP measurements (478 observations). Linear mixed-effects models were adjusted for major physiological and behavioral covariates. T-allele carriers (C/T + T/T) exhibited higher diastolic BP (β = +6.08 mmHg, 95%CI [1.32–10.84], p = 0.017) and mean arterial pressure (β = +5.28 mmHg, 95%CI [0.28–10.29], p = 0.046) than C/C homozygotes, with no effect on systolic BP or heart rate. The association remained consistent across sensitivity and additive genetic models. This hypothesis-generating study provides preliminary evidence in humans, albeit limited by sample size, of a link between a functional HMOX2 variant and resting BP, consistent with a possible contribution of constitutive HO-2 activity to BP regulation. Full article

Bacillus species are extensively studied, utilized, and commercialized biocontrol agents, demonstrating significant effectiveness in managing a variety of plant diseases. Bacillus possesses a robust intrinsic biosynthetic ability, capable of producing a diverse array of antimicrobial metabolites, including dipicolinic acid (DPA; 2,6-pyridinedicarboxylic acid), which exhibits antifungal properties and serves as a principal structural component of Bacillus spores. This study revealed that DPA exhibits significant antibacterial activity against the hazardous soybean pathogen Xanthomonas citri pv. glycines (Xcg), with an EC₅₀ value of 53.2 μg/mL. DPA inhibited Xcg swimming motility, extracellular protease activity, and biofilm formation, while inducing significant membrane irregularities in Xcg cells. DPA treatment downregulated the expression of several Xcg membrane integrity-related genes, including cirA, czcA, czcB, emrE, and tolC. The preventive and curative application of 500 μg/mL DPA reduced Xcg symptoms by 82.7% and 83.8%, respectively, and induced the accumulation of the isoflavone genistin in soybean leaves. DPA exhibited only weak toxicity in the zebrafish model, suggesting its potential suitability for agricultural commercialization. Overall, this study provides the first detailed characterization of the antibacterial mechanism of DPA against a phytopathogenic bacterium, Xcg, and identifies DPA as a previously underexplored antibacterial metabolite from Bacillus and Paecilomyces with potential for disease management. Full article

Background/Objectives: Musculoskeletal soft-tissue injuries are common among physically active individuals and arise from complex interactions between environmental and biological factors. Genetic variation in genes involved in extracellular matrix (ECM) organization may contribute to individual susceptibility to such injuries. This study investigated whether polymorphisms in aggrecan (ACAN, rs2351491 and rs1042631) and fibromodulin (FMOD, rs7543148) genes are associated with susceptibility to sports-related injuries. Methods: The study included 335 physically active Caucasians, comprising 202 participants with a history of non-contact sports-related musculoskeletal injuries and 133 uninjured controls. Genotyping was performed using real-time polymerase chain reaction. Results: No significant associations were observed between the analyzed polymorphisms and overall injury occurrence after correction for multiple comparisons. A nominal association was observed for ACAN rs2351491 in the overall injury comparison under the overdominant model (p = 0.0457), where CT heterozygotes were more frequent among injured participants. The ACAN rs1042631 variant showed nominal associations with anterior cruciate ligament (ACL) injury under the codominant (p = 0.0179), recessive (p = 0.0243), and overdominant (p = 0.0346) models, with the TT genotype associated with lower odds of ACL injury under the recessive model (OR = 0.15, 95% CI: 0.02–1.22). No significant associations were observed for FMOD rs7543148 or for haplotype analysis of ACAN variants. Conclusions: No robust associations were identified between the investigated variants and susceptibility to musculoskeletal soft-tissue injury after correction for multiple testing. Nominal signals observed for ACAN variants, particularly in ACL-focused analyses, warrant further investigation but should be interpreted cautiously and confirmed in larger, independent cohorts. Full article

Coronavirus disease-2019 COVID-19 exhibits marked inter-individual variability in susceptibility and clinical outcomes, suggesting a role for host genetic factors. Vitamin D exerts immunomodulatory effects through the vitamin D receptor (VDR), and genetic variation in the VDR gene may influence host responses to SARS-CoV-2 infection. This study aimed to investigate the association between VDR-gene polymorphisms—FokI (rs2228570), TaqI (rs731236), ApaI (rs7975232), and BsmI (rs1544410)—and COVID-19 susceptibility in the Kurdish population. The FokI polymorphism was significantly associated with COVID-19 susceptibility. Interestingly, the GG-genotype was more frequent among Patients than controls and was associated with increased odds of infection (OR = 9.00; 95% CI: 3.22–25.15; p < 0.0001), whereas the AG-genotype was associated with reduced susceptibility (OR = 0.33; 95% CI: 0.14–0.76; p = 0.001). Additionally, the G-allele was also more prevalent in Patients than controls (OR = 1.87; 95% CI: 1.21–2.89; p = 0.004). Similarly, the TaqI TT-genotype was more frequent among Patients and was associated with increased susceptibility (OR = 36.0; 95% CI: 11.2–115.8; p < 0.0001). In contrast, the ApaI AA-genotype was less frequent among Patients and was associated with reduced odds of COVID-19 susceptibility under a recessive model (OR = 0.15; 95% CI: 0.03–0.68; p = 0.003). Moreover, the BsmI polymorphism was monomorphic in both groups and therefore not informative. Genetic variation in the VDR gene, particularly at the FokI, TaqI, and ApaI loci, was associated with COVID-19 susceptibility in the case–control study, while BsmI showed no variations. These findings suggest that genetic variation in the VDR gene may contribute to inter-individual differences in susceptibility to SARS-CoV-2 infection in the Kurdish population. Larger studies incorporating functional validation and detailed clinical data are required to confirm these associations. Full article

Background: This study aimed to further explore the application of genetic risk assessments in 24 metabolic bariatric surgery (MBS) patients to predict weight loss outcomes three years after the procedure. Methods: Participants were assessed using the Genetic Addiction Risk Severity (GARS) test, which evaluates neurogenic polymorphisms linked to addiction and reward deficiency. Genetic and psychosocial data collected prior to surgery were analyzed in relation to post-operative weight loss measures, including weight change, body mass index (BMI), percentage of total weight loss (%TWL), and percentage of expected weight loss (%EWL). The analysis examined associations between specific genetic risk alleles, weight-related outcomes at three to four years post-surgery, and psychosocial trait scores. Results: Spearman’s correlations revealed that the DRD2 risk allele is negatively correlated with 3-year BMI (r_s = −0.481, p < 0.05, 95% CI: –0.746 to –0.083). One-way ANOVA indicated that there is a significant difference in 3-year BMI (p = 0.018) between 0 and 1 DRD2 risk allele copy. There is also a significant difference in ∆weight (p = 0.022), ∆BMI (p = 0.014), and %EWL (p = 0.032) among the different SNP expression values of the MAOA risk allele. In addition, Spearman’s correlation revealed that FCQ scores are negatively correlated with ∆BMI (r_s = −0.470, p < 0.05, 95% CI: −0.767, −0.005), %TWL (r_s = −0.561, p < 0.05, 95% CI: −0.814, −0.129), and %EWL (r_s = −0.533, p < 0.05, 95% CI: −0.800, −0.090) at 3 years post-surgery and positively correlated with 3-year weight (r_s = 0.576, p < 0.05, 95% CI: 0.151, 0.821) and 3-year BMI (r_s = 0.552, p < 0.05, 95% CI: 0.117, 0.810). Lastly, GARS scores are positively correlated with 3-year ∆weight (r_s = 0.422, p < 0.05, 95% CI: 0.010, 0.712). Full article

Background: Athletic performance is a multifactorial construct influenced by physiological, biomechanical, and psychological determinants. In recent years, genetic factors have been increasingly recognized as contributors to inter-individual variability in performance. In particular, polymorphisms in genes involved in neurobiological pathways have been associated with cognitive processes relevant to sport performance. However, the distribution of cognition-related genetic variants in elite athletes has not been systematically synthesized. Methods: This meta-analysis aimed to examine the distribution of selected candidate gene polymorphisms previously associated with cognition-related traits in elite athletes compared to control populations. A systematic literature search identified 17 eligible case–control studies investigating allele distributions of COMT rs4680, BDNF rs6265, DRD2 rs1800497, OPRM1 rs1799971, and HTR1A rs6295. Pooled analyses were performed using a fixed-effect model, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Results: Elite athletes demonstrated a significantly higher frequency of the G allele of COMT rs4680 (OR = 1.11; 95% CI: 1.02–1.21; p = 0.013) and the G allele of BDNF rs6265 (OR = 1.40; 95% CI: 1.10–1.77; p = 0.005) compared to controls. No significant differences were observed for HTR1A rs6295, DRD2 rs1800497, or OPRM1 rs1799971 polymorphisms (p > 0.05). Conclusions: This meta-analysis indicates that certain genetic variants previously associated with cognition-related traits, particularly COMT rs4680 and BDNF rs6265, are more frequently observed in elite athletes. These findings suggest a potential association between cognition-related genetic pathways and elite athletic status. However, as the present analysis is based on genetic distribution rather than direct cognitive assessments, the results should be interpreted within the context of association rather than causation. Full article