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Öğe Acute effects of high intensity interval training on cognitive function in smokers and nonsmokers(2025) Karakaş, Neşe; Özyalın, Fatma; Kartal, Mert; Kapikiran, Gurkan; Bayer, Ramazan; Kurt, Zeynep Eker; Keskinkılıç, KorhanThe use of tobacco is widespread among both active and inactive individuals. However, its adverse effects appear less pronounced in those who exercise regularly. Since smoking may differentially impact smokers and nonsmokers, this study examined the immediate effect of high-intensity interval training (HIIT) on cognitive performance in both groups. Forty inactive participants (20 smokers, 20 nonsmokers) were included, with mean ages of 20.35±1.26 and 20.15±1.38 years, respectively. The HIIT protocol involved five exercises. Cognitive performance was assessed immediately after the session using the Visual Cognitive Function Test (VCFT) and Auditory Cognitive Function Test (ACFT), each repeated five times, with results recorded in milliseconds. Pre-test VCFT scores were significantly higher in smokers (381.16±7.96 ms) compared to nonsmokers (372.24±11.17 ms, p=0.006). Post-test scores also differed (smokers: 607.50±43.33 ms; nonsmokers: 577.66±20.78 ms, p=0.007). The improvement from pre- to post-test was greater in nonsmokers (-48.39 ms, p < 0.001) than in smokers (-25.39 ms, p=0.021). In ACFT, no significant group differences were found at pre-test (p=0.080) or post-test (p=0.079), but both groups showed significant improvement following HIIT (p<0.001). These results suggest that smoking impairs visual cognitive performance more than auditory function after high-intensity exercise. The differences may stem from smoking-related vascular and neural plasticity deficits, which are critical for cognitive processing during and after exercise. Significance statement: This study highlights that smoking specifically reduces visual cognitive benefits from HIIT, while auditory function remains less affected. These findings emphasize the neurobiological consequences of smoking and support the role of exercise interventions in mitigating its adverse cognitive effects.Öğe Plasma free amino acids in Parkinson’s disease: An exploratory case–control study(Association of Clinical Biochemistry Specialists (Klinik Biyokimya Uzmanlari Dernegi), 2026) Kurt, Zeynep Eker; Aydin, Huseyin; Gokce, Seyda FigulObjectives: Parkinson's disease (PD) is associated with systemic metabolic alterations; however, reproducibility and methodological standardization remain ongoing challenges in metabolomics research. This exploratory case–control study aimed to evaluate whether targeted plasma free amino acid profiling reveals statistically robust differences between PD patients and healthy controls. Methods: Forty-three patients with PD and 43 age-and sex-matched healthy controls were included. Plasma free amino acids were quantified using a targeted triple quadrupole LC–MS/MS platform with Appendix 1 isotope-labeled internal standards. Between-group comparisons were performed with appropriate statistical tests. False discovery rate (FDR) correction and effect size (Cohen’s d) calculations were applied. Compound-based KEGG pathway enrichment analysis was conducted using FDR-significant metabolites. ROC analyses were performed for signal strength assessment only. Results: After FDR correction, alanine, arginine, aspartic acid, proline, taurine, threonine, and phenylalanine/tyrosine-related ratios remained significant, with moderate-to-large effect sizes. Compound-based KEGG enrichment demonstrated significant clustering within interconnected amino acid metabolism pathways, including arginine and proline metabolism, taurine and hypotaurine metabolism, glycine, serine and threonine metabolism, and alanine, aspartate and glutamate metabolism (pathway-level FDR <0.05). Exploratory ROC analyses showed moderate signal strength for proline (AUC=0.794), taurine (AUC=0.792), and threonine (AUC=0.780). Conclusion: Targeted plasma amino acid profiling revealed coordinated systemic alterations in amino acid metabolism in PD within a statistically disciplined analytical framework. These findings reflect peripheral metabolic variation and should be interpreted as exploratory and hypothesis-generating. The study primarily contributes an analytically validated and FDR-corrected dataset to the discussion on methodological rigor in PD metabolomics, rather than evidence of diagnostic or mechanistic inference. Validation in longitudinal, clinically well-characterized cohorts is required. © 2026, Association of Clinical Biochemistry Specialists (Klinik Biyokimya Uzmanlari Dernegi). All rights reserved.Öğe The importance of lipids in neurodegenerative diseases Neurodegenerative diseases and lipids(Bayrakol Medical Publisher, 2026) Kurt, Zeynep Eker; Ozyalin, FatmaLipids are vital for membrane structure, energy storage, and cell signaling. Balanced lipid intake is essential for brain health and function. PUFAs like DHA and AA make the brain prone to oxidative stress and inflammation. Lipid peroxidation contributes to neuronal damage and neurodegenerative diseases. Disrupted lipid metabolism is linked to Alzheimer's, Parkinson's, and schizophrenia. Studying brain lipid changes may uncover disease mechanisms and guide new therapies.












