Search Results (9,626)

Metabolic syndrome (MetS) is associated with ectopic fat deposition, chronic systemic inflammation, oxidative stress, and increased susceptibility to organ dysfunction. While its cardiovascular consequences have been extensively studied, pulmonary al-terations remain less well characterized, particularly with respect to ferropto-sis-regulatory pathways. In this study, we evaluated ectopic fat deposition, TLR4/NF-κB signaling pathway, and ferroptosis-regulatory markers in a MetS rat model and analyzed the therapeutic potential of combined resveratrol plus quercetin (combined R + Q) supplementation. Rats were maintained for five months with 30% sucrose in drinking water to induce MetS and subsequently treated for 4 weeks with the R + Q combination (50 and 0.95 mg/kg/day, respectively). Lung tissue was analyzed by fluorescence microscopy to assess fat deposition, by colorimetric histology to evaluate hemosiderin-containing cells, including the quantification of hemosiderin-laden macrophages (HLMs), and by immunoblotting to determine TLR4, p-p65, and glutathione peroxidase 4 (GPX4), as well as cystine/glutamate antiporter SLC7A11 (xCT) protein expression. Lungs from MetS rats exhibited significantly higher fat deposits, pathological HLMs accumulation, upregulated TLR4/p-p65 signaling, elevated compensatory GPX4 expression, and depressed xCT levels compared with controls. Notably, the combined R + Q treatment markedly attenuated alterations in TLR4/NF-κB signaling and successfully restored xCT expression (p = 0.0116), stabilizing pulmonary redox homeostasis and limiting overall tissue susceptibility to lipotoxic injury. Full article

Continuous-variable quantum key distribution (CV-QKD) relies on efficient information reconciliation to establish identical secret key sequences from correlated modulation data and measurement outcomes. Accurate quadrature measurements are essential for reliable reconciliation, but residual phase mismatch between the signal and local oscillator distorts these measurements in coherent receivers and degrades decoding performance. To improve robustness against residual phase mismatch in homodyne-based CV-QKD, we propose a phase-aware multidimensional reconciliation method that jointly performs syndrome-based low-density parity-check (LDPC) decoding and expectation-maximization-based residual-phase refinement. We derive a discrete-time detection model that explicitly incorporates the receiver’s pulse-dependent quadrature-selection phase and construct phase-dependent virtual observations through multidimensional orthogonal mapping. The LDPC decoder provides posterior information for calculating the posterior spherical-symbol moments used in residual-phase refinement, while the refined phase is fed back to update the virtual observations and decoding likelihoods for the next iteration. Numerical results show that the proposed method achieves a lower residual-phase-estimation RMSE than disclosure-based cross-correlation estimation, BER and FER close to those under perfect phase compensation, and a higher finite-size secret key rate. Full article

Moringa oleifera Lam. seeds contain lectins that exhibit interesting bioactive properties, but their effects on metabolic syndrome (MetS) remain poorly understood. This work evaluated the effects of the water-soluble lectin from M. oleifera seeds (WSMoL) on metabolic, inflammatory, and histopathological alterations in a mouse model of MetS-like features. Male Swiss mice were fed a high-fat diet plus condensed milk solution for 11 weeks. Animals then received phosphate-buffered saline (negative control), orlistat (40 mg/kg), or WSMoL (1, 2, or 4 mg/kg, i.p.) for 14 days. A healthy group (Sham) received standard chow. The MetS-like protocol induced obesity, hyperglycemia, dyslipidemia, visceral adiposity, and systemic inflammation. WSMoL improved metabolic parameters at all doses, reducing visceral fat, attenuating hyperglycemia, and improving the lipid profile. It also decreased pro-inflammatory cytokines (IL-2, IFN-γ, TNF-α, and IL-6) while increasing IL-10 levels. WSMoL prevented hepatic steatosis and renal lipid accumulation, although inflammatory and degenerative tissue changes persisted. The 4 mg/kg dose showed efficacy but was associated with elevated AST and more frequent inflammatory alterations. In conclusion, WSMoL mitigated key features of MetS-like condition, although incomplete tissue recovery and signs of organ stress at the highest dose warrant caution regarding its potential therapeutic use. Full article

Takotsubo syndrome (TTS) is an acute and reversible heart failure condition characterized by transitional left ventricular systolic dysfunction without obstructive coronary artery disease. Although sympathetic hyperactivation is considered a key pathogenic mechanism, the contribution of gut-derived endotoxemia and oxidative stress is still unclear. Lipopolysaccharide (LPS), an endotoxin of Gram-negative bacteria, may translocate from the gut into the bloodstream and increase oxidative stress through activation of NADPH oxidase 2 (NOX2), nitric oxide (NO) depletion and endothelial dysfunction. This study aimed to evaluate circulating LPS levels in TTS and investigate their association with NOX2 activation, oxidative stress, and endothelial dysfunction. Twenty consecutive patients with TTS and 20 age- and sex-matched healthy controls were included. Within 48 h of admission, fasting blood samples were collected to assess soluble NOX2-derived peptide (sNOX2-dp), hydrogen peroxide (H₂O₂), NO metabolites (NOx), LPS, and zonulin. Endothelial function was assessed by brachial artery flow-mediated dilation (FMD). Compared with controls, TTS patients had significantly higher serum levels of sNOX2-dp, H₂O₂, LPS, and zonulin, lower NOx and impaired FMD. sNOX2-dp was positively correlated with LPS (Rs = 0.539, p < 0.001) and zonulin (Rs = 0.331, p = 0.037) and inversely correlated with FMD (Rs = −0.462, p = 0.003). NOx correlated negatively with H₂O₂, zonulin and LPS. In multivariable analysis, LPS was the only independent predictor of FMD (β = 0.498, SE = 0.126, p = 0.001) and sNOX2-dp (β = −0.572, SE = 0.034 p < 0.001); FMD (β = −0.347, SE = 0.455, p = 0.005), H₂O₂ (β = 0.445, SE = 0.155, p < 0.001), and zonulin (β = 0.298, SE = 2.309, p = 0.016) emerged as independent predictors of LPS (adjusted R² = 0.585). TTS is associated with low-grade endotoxemia, NOX2-driven oxidative stress, reduced NO bioavailability, and endothelial dysfunction. The independent association between LPS and NOX2 activation supports a potential gut–vascular axis in TTS pathophysiology. Full article

Metabolic syndrome (MetS) is a complex metabolic disorder characterized by central obesity, insulin resistance, dyslipidemia, hypertension, and chronic low-grade inflammation, all of which contribute to an increased risk of type 2 diabetes mellitus, cardiovascular disease, and premature mortality. Emerging evidence suggests that cellular senescence plays a central role in the pathophysiology of MetS by linking metabolic stress to chronic inflammation, immune dysfunction, as well as cell and tissue damage. Although senescence has traditionally been studied in tissue-resident cells, growing attention has focused on the role of blood-cell senescence in the initiation and progression of metabolic disease. This review summarizes current knowledge regarding the molecular and cellular mechanisms driving senescence in hematopoietic stem cells and circulating blood-cells (BCs) and how these mechanisms affect specific blood-cell populations leading to altered immune function, impaired tissue homeostasis, and persistent inflammatory activation. The link between clonal hematopoiesis to immunosenescence and cardiometabolic disease is also highlighted, providing additional insight into the complex interactions between hematopoietic aging and metabolic dysfunction. Full article

Background/Objectives: To evaluate the prevalence and distribution of taurodontism and pyramidal molar morphology in primary and permanent dentitions of children aged 6–16 years in Diyarbakır, Türkiye. Methods: A retrospective analysis of 1167 digital panoramic radiographs was conducted. Taurodontism was diagnosed according to the Shifman and Chananel criteria, while pyramidal molar morphology was evaluated as an independent anomaly. Prevalence, distribution, and symmetry were analyzed using Pearson’s chi-square test, Mann–Whitney U test, and Kappa test. Results: The individual and tooth prevalence of taurodontism was 6.60% and 2.44%, respectively, with significantly higher frequencies in the permanent dentition, maxilla, and permanent second molars (p < 0.001). Hypotaurodontism was the predominant subtype (81.5%). Pyramidal molar morphology was identified in 1.54% of individuals and 0.83% of teeth, with a significant female predominance (p = 0.022). Both anomalies exhibited high rates of bilateral involvement (85.7% for taurodontism and 72.2% for pyramidal molars). Pyramidal morphology was identified in 24 primary molars (0.58%). Among cases with available parental panoramic radiographs, the identification of the same morphology in at least one parent suggests potential familial aggregation, although further large-scale prospective genetic studies are required to confirm hereditary inheritance models. Conclusions: Taurodontism and pyramidal molar morphology are clinically significant developmental root variations in children. The quantitative documentation of pyramidal morphology in primary dentition addresses an important gap in the literature. Early radiographic recognition is essential for treatment planning and may serve as a helpful clinical indicator that prompts further genetic or systemic evaluation in suspected syndromic cases. Full article

Background: Methotrexate-induced neurotoxicity (MTX-NTX) is a severe complication during childhood acute lymphoblastic leukemia (ALL) treatment, yet its underlying pharmacogenetic determinants remain incompletely understood. Methods: A multicenter retrospective nationwide case–control study was performed including 71 pediatric ALL patients (34 MTX-NTX cases and 37 controls). Targeted next-generation sequencing of 17 genes involved in MTX transport, intracellular metabolism and folate pathways was performed. Results: Transport-related genes accounted for 61.4% of all detected variants and showed the highest number of nominally significant variants. Pathway-level burden analysis demonstrated a significant enrichment of transporter-related variants in patients with MTX-NTX compared with controls (FDR-adjusted p = 0.004), whereas the analysis for folate/metabolism-related genes did not remain significant after multiple-testing (FDR-adjusted p = 0.096). Similar findings were observed in the stroke-like syndrome (SLS) subgroup (FDR-adjusted p = 0.014 and 0.108, respectively). Gene-level burden analysis identified ABCG2 and ABCC4 as the predominant contributors, harboring both 18.4% of significant variants in the overall MTX-NTX analysis and 20.6% and 17.6%, respectively in the SLS phenotype. Moreover, the distribution of significant variants was strongly correlated between the overall MTX-NTX and SLS analyses (Spearman’s ρ = 0.549, p = 0.022). Volcano plot analysis revealed ABCG2 as the gene showing the most prominent pattern of nominal associations, containing both the variants associated with a protective direction (e.g., c.1728-46G>A, p = 2.6 × 10⁻⁴) and variants associated with increased risk, including c.34G>A and c.203+36A>G (p = 0.002) and c.263+10A>G (p = 0.0097). Phenotype-specific analyses revealed distinct genetic signatures across neurological manifestations, with transporter genes predominating in focal neurological deficits. Conclusions: Our findings suggest that genetic variability in ABC transporter genes may contribute to susceptibility to MTX-NTX, whereas folate metabolism genes may represent complementary phenotype-modifying factors. These findings are exploratory and require validation in larger, independent cohorts and functional studies. Full article

Background/Objectives: Sjögren’s Syndrome (SS) is an autoimmune disorder with impaired exocrine gland function. Its pathogenesis remains elusive, but aberrant innate/adaptive immunity and dysregulated interferon signaling are core features. Current SS research lacks exploration of innate immune mechanisms and therapeutic targets. Phloretin, a natural dihydrochalcone derivative, inhibits excessive innate immune activation, yet its role and mechanism in SS remain unreported. Methods: This study aimed to explore the therapeutic efficacy of phloretin against Sjögren’s syndrome (SS) and elucidate the regulatory mechanism underlying its effects on dendritic cells (DCs) and the Stimulator of Interferon Genes (STING)-driven innate immune cascade. Clinical specimens were utilized to analyze DC infiltration and STING expression in the labial glands of SS patients. In vivo experiments were conducted on NOD/Ltj SS mice with phloretin treatment, using hydroxychloroquine as a positive control. For in vitro studies, DCs were stimulated with poly I:C to verify the functional effects of phloretin and its regulatory role in the STING/TANK-binding kinase 1 (TBK1)/Interferon Regulatory Factor 3 (IRF3) signaling. Salivary secretion, glandular inflammatory responses, and systemic immune overactivation were evaluated in SS mice. In poly I:C-stimulated DCs, cell activation, migration, and co-stimulatory molecule expression were measured. The regulatory effects of phloretin on the STING signaling cascade and STING ubiquitin-mediated degradation were examined by Western blotting. Phloretin, initially identified as a candidate compound via virtual screening, was subjected to thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) and molecular dynamics simulation (MD) for direct binding verification with STING. The STING overexpression rescue experiment further corroborates that phloretin modulates innate immune responses in a STING-dependent manner. Results: Clinical results revealed obvious infiltration of CD11c⁺STING⁺ DCs and CD11c⁺p-TBK1⁺ DCs in labial gland lesions of SS patients. In NOD/Ltj SS mice, phloretin treatment recovered salivary secretion, relieved glandular inflammatory injury, and restrained excessive activation of innate and adaptive immune responses, showing comparable therapeutic effects compared with hydroxychloroquine. In vitro experiments confirmed that phloretin could alleviate poly I:C-induced abnormal activation and migration of DCs, as well as reduce the expression of co-stimulatory molecules. Mechanistically, phloretin was found to interfere with the STING signaling cascade, alter the ubiquitination level of STING protein, and further inhibit the abnormal activation of DCs, which may contribute to its protective effects against Sjögren’s syndrome. Notably, results from MD, CETSA and DARTS collectively validate the interaction between phloretin and STING protein, providing solid molecular-level evidence for its regulatory effect on STING signaling transduction. Conclusions: DCs and STING-driven innate immunity critically contribute to SS progression. Phloretin effectively ameliorates SS-related immune disorders by restraining DC overactivation and STING signaling, supporting it as a promising candidate agent for SS treatment. Full article

Cancer cachexia is a complex metabolic syndrome characterized by progressive skeletal muscle wasting and poor clinical outcomes. Previous studies have mainly focused on the association between cancer-derived extracellular vesicles and atrophy of differentiated myotubes, whereas their effects on myoblast differentiation markers have not been sufficiently elucidated. In this exploratory in vitro study, vesicle fractions isolated from MC38, CT26, MCA205, and B16F10 cancer cell lines under serum-deprived conditions were referred to as small extracellular vesicles (sEVs) and used to treat C2C12 myoblasts during differentiation. Compared with the control group, the sEV-treated groups showed reduced myotube diameter and differentiation area on day 6, while the mRNA expression patterns of MyoD, MyoG (Myogenin), MRF4, Myf5, Pax7, and several MHC isoforms showed time-dependent changes. GO/KEGG analysis of commonly identified proteins revealed enrichment of terms related to mRNA metabolism, the cell cycle, and the proteasome. These findings suggest that treatment with cancer cell-derived sEVs may be associated with impaired in vitro differentiation of C2C12 myoblasts. Full article

Background/Objectives: This study evaluated changes in PMS severity, nutrition knowledge, and eating attitudes over a 6-week online nutrition education programme delivered to female university students. Methods: This uncontrolled single-arm pretest/posttest study included 112 female university students recruited by convenience sampling from a women’s dormitory. Nutrition education was delivered daily for 6 weeks via WhatsApp as 42 informational cards. Measurements were taken before and after the programme. Attitudes and behaviours associated with disordered eating were screened using the Eating Attitudes Test-26 (EAT-26), nutrition knowledge using the Nutrition Knowledge Level Scale for Adults (NKLSA), and premenstrual symptom severity using the Premenstrual Syndrome Scale (PMSS). Results: No significant changes occurred in nutrition knowledge (p = 0.409) or eating attitudes (p = 0.654). The PMSS score significantly decreased (mean change = 14.28 ± 46.34; 95% CI 5.60–22.96; p = 0.001, d_z = 0.31, 95% CI 0.12–0.50), with decreases across eight subscales (d_z = 0.19–0.38; BH q < 0.05), whereas appetite changes were unchanged (p = 0.423); the largest standardized changes were observed for depressive mood and bloating. PMSS change was not correlated with knowledge (r = 0.001) or knowledge with eating attitudes (r = 0.057); PMSS and eating attitude changes were weakly positively correlated (r = 0.187, p = 0.048; exploratory, not corrected for multiplicity). Conclusions: Following a 6-week WhatsApp-based nutrition education programme, self-reported PMS severity decreased, particularly mood and somatic symptoms, without changes in nutrition knowledge or eating attitudes. The uncontrolled single-arm design precludes attributing these changes to the programme. Full article

Background: Opioid use during pregnancy is linked to preterm birth, fetal growth restriction, and Neonatal Opioid Withdrawal Syndrome. While the placenta is the primary regulator of the uterine environment, the precise molecular mechanisms by which opioids dismantle placental function remain poorly defined. Methods: The transcriptomic landscape of opioid-exposed human placentas from a unique Hawai’i-based cohort was characterized. Results: Transcriptional signatures were defined by genes involved in translational inhibition and metabolic attenuation. Integrative network modeling predicted a prominent stress-signaling hub centered on p38 Mitogen-Activated Protein Kinase and Extracellular Signal-Related Kinase 1/2, paralleling a broad suppression of ribosomal protein transcripts (Ribosomal Protein 27S, -29, and -39). This response was further characterized by the inhibition of the Myelecytomatosis Proto-Oncogene regulatory hub, predicting a loss of mitochondrial phosphate transport through associated genes (via Solute Carrier Family 25A3) and cell-cycle progression (via S-Phase Kinase-Associated Protein 1). Additionally, the genes in this model suggested upregulation of antisense regulatory brakes, such as RAP2C Antisense RNA 1, which might further reinforce this inhibitory state. Conclusion: The findings suggest that prenatal opioid exposure is associated with the disruption of placental homeostasis. This may be coordinated by protein synthesis and bioenergetic flux, as inferred from the modeled eukaryotic Translation Initiation Factor-mediated Integrated Stress Response. These findings establish a localized, clinical baseline of human placental stress, highlighting candidate molecular regulatory nodes to guide future mechanistic studies and biomarker discovery in exposed pregnancies. Full article

Although persistent neurological sequelae in long COVID are reportedly well associated with neuroinflammation, the underlying regulatory mechanisms remain poorly characterized. Previously, we identified dysregulated microRNA expression, including let-7a-5p, in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike S1-stimulated human microglial cells by RNA sequencing; however, how let-7a-5p regulates the S1-mediated neuroinflammatory processes remains undetermined. In the present study, we examined the functional role of let-7a-5p in alleviating S1-induced microglial inflammation in the CHME3 cell line as well as in human monocyte-derived microglia (MDMi) using a loss- and gain-of-function approach. Functional inhibition of let-7a-5p resulted in mitigating S1-induced inflammatory cytokine release and markers of pyroptosis. Mechanistically, we established SHIP-1 as a direct target of let-7a-5p using luciferase reporter assay validation. Interestingly, we noted upregulated expression of the TLR3 gene alongside TLR2/4 in S1-stimulated microglia. Although we could not establish exactly how TLR3 is stimulated in S1-induced neuroinflammatory processes, using siRNA-mediated inhibition and a pharmacological inhibitor in both CHME3 cells and MDMi, our study certainly provides evidence of TLR3 involvement during S1-induced microglial inflammation, which needs further investigation. Together, these in vitro findings demonstrate that the let-7a-5p/SHIP-1 axis regulates S1-induced inflammatory cascades in CHME3 and MDMi cells, providing mechanistic insight into its role in SARS-CoV-2-associated neuroinflammation and warranting further validation in appropriate in vivo/organoid models. Full article

Interstitial lung disease (ILD) is a frequent manifestation and a leading cause of morbidity and mortality in idiopathic inflammatory myopathies (IIM), particularly in antisynthetase syndrome (ASyS) and anti-melanoma differentiation-associated protein 5 (MDA5) dermatomyositis. Although these disorders share common features of interstitial lung diseases, they differ substantially in pathogenesis, clinical phenotype, prognosis, and therapeutic response. There is also variability amongst the different subtypes of IIM-ILD. Recognition of these distinctions is essential for accurate diagnosis and treatment; delays in care, especially in cases of rapidly progressive ILD (RP-ILD), can be associated with high mortality. This review focuses on ILD in IIM, focusing on ASyS and anti-MDA5 dermatomyositis, highlighting similarities and key differences in disease mechanisms, clinical presentation, diagnostic evaluation, prognostic biomarkers, and management strategies. Full article

Background/Objectives: Endometrial polyps are a prevalent pathological condition within the uterine cavity. While the majority of lesions are classified as benign, histopathological examinations indicate a potential for malignant transformation occurring in 0.5–5% of cases. The present study aimed to evaluate the prevalence of endometrial carcinoma and pre-malignant histopathological findings (glandular hyperplasia without atypia and atypical glandular hyperplasia) associated with endometrial polyps and to identify pertinent risk factors among Polish women undergoing hysteroscopic polypectomy under local anesthesia. Methods: A retrospective cohort study was conducted at the Outpatient Hysteroscopy Center of the Heliodor Swiecicki University Hospital of Gynecology and Obstetrics, affiliated with Poznan University of Medical Sciences. The study included patients treated using the GUBBINI mini-resectoscope under local anesthesia with the Hystero-Block system (Tontarra Medizintechnik GmbH, Wurmlingen, Germany) between December 2022 and July 2026. Statistical analysis of risk factors was performed using the Kruskal–Wallis H test and Fisher’s exact test. Odds ratios for potential risk factors were also calculated. Results: The study comprised 2588 patients. Endometrial carcinoma associated with endometrial polyps was identified in 16 women (0.62%). Additional histopathological findings included glandular hyperplasia in 360 patients (13.91%) and atypical hyperplasia in 35 patients (1.35%), with the remaining patients diagnosed with benign uterine polyps (84.12%). Patients with malignant and pre-malignant lesions were significantly older than those with benign polyps (p < 0.001). Regarding polyp size, patients diagnosed with glandular hyperplasia without atypia had significantly larger polyps than those with benign lesions (p < 0.001). Estimated postmenopausal status was associated with significantly higher odds of endometrial carcinoma (Odds Ratio [OR] = 6.56, 95% Confidence Interval [CI]: 2.12–20.30, p = 0.001) and atypical glandular hyperplasia (OR = 3.13, 95% CI: 1.41–6.96, p = 0.005) compared to benign polyps. Similarly, obesity increased the odds of glandular hyperplasia without atypia (OR = 1.32, 95% CI: 1.01–1.74, p = 0.045) and atypical glandular hyperplasia (OR = 3.33, 95% CI: 1.67–6.65, p < 0.001). Furthermore, hypertension was associated with higher odds of glandular hyperplasia without atypia compared to benign polyps (OR = 1.41, 95% CI: 1.02–1.97, p = 0.040). Other evaluated risk factors, including type II diabetes mellitus, infertility, abnormal uterine bleeding, breast cancer history, hypothyroidism and polyendocrine metabolic ovarian syndrome (PMOS), did not reach statistical significance (p > 0.05). This large cohort provides important data regarding the prevalence and risk factors of carcinoma associated with endometrial polyps and pre-malignant uterine lesions in Polish women. Conclusions: Endometrial carcinoma associated with endometrial polyps is a rare entity among Polish women undergoing outpatient hysteroscopy (0.62%). Nevertheless, the primary diagnostic value of this large-scale study lies in demonstrating that despite the low prevalence of malignancy in standard “see-and-treat” outpatient settings, systematic histopathological evaluation remains an absolute diagnostic mandate, as relying solely on visual or clinical parameters is insufficient to exclude malignancy. Furthermore, identified risk factors, such as age, polyp size, estimated postmenopausal status, obesity and hypertension, serve as critical diagnostic red flags, associated with increased odds of concurrent premalignant lesions or carcinoma. Full article

Early detection of canine cognitive dysfunction syndrome (CDS) is challenged by the limitations of single diagnostic tools, including owner-reported subjectivity and impractical behavioral testing protocols. This study examined a multidomain strategy integrating questionnaires, behavioral testing, and a circulating biomarker to identify measures associated with mild cognitive impairment in aged dogs. A total of 21 aged dogs were classified as cognitively normal (n = 9) or mildly cognitively impaired (n = 12) using the Canine Dementia Scale (CADES), and they were further assessed based on the Canine Cognitive Dysfunction Rating Scale (CCDR), a battery of behavioral tests across six cognitive domains, and serum brain-derived neurotrophic factor (BDNF) concentrations. The CADES scores differed significantly between the mildly cognitively impaired and cognitively normal groups (median 12.5 vs. 0, p < 0.01), whereas the CCDR scores did not (p = 0.114). Among the behavioral measures, the delayed match-to-sample task with a 20-s delay and the recognition index derived from novel object recognition testing were significantly associated with cognitive group classification; the other domains showed no significant associations. Serum BDNF concentrations did not differ between the groups or predict group membership. The results of this exploratory study show that targeted behavioral measures may be more strongly associated with mild cognitive impairment than circulating BDNF, thus supporting their potential utility for early cognitive screening in clinical settings. However, these findings should be interpreted with caution, and their diagnostic accuracy should be confirmed in larger cohorts with further validation. Full article