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    Deteriorated thiol-disulphide and oxidized-reduced glutathione status in blood in Alzheimer's disease
    (Pergamon-Elsevier Science Ltd, 2024) Akunal, Canan; Alisik, Murat
    Background: Alzheimer's disease (AD) is a steadily advancing neurodegenerative condition, the occurrence and prevalence of which are on the rise in various populations. Suspected factors contributing to its development encompass the buildup of amyloid (3 (A(3) plaques, the formation of neurofibrillary tangles induced by tau proteins, and heightened oxidative stress. In this study, we aimed to evaluate intra-cellular glutathione status and extracellular thiol-disulphide status in patients with AD. Methods: Adult patients (>60 years old) diagnosed with AD based on DSM-IV diagnostic criteria were included in the study. Patients were divided into 3 groups as mild, moderate and severe according to Mini Mental Status Examination (MMSE) and clinical findings. Extracellular thiol-disulfide and intracellular oxidized-reduced glutathione status parameters for patient and control groups were analyzed before and after reduction procedures by using reaction of thiol groups with DTNB. Results: The reduced forms of both balances (native thiol (NT) and reduced glutathione (GSH)) were significantly lower in the patient group than the control group (p = 0.031 and <0.001, respectively), while oxidized forms (disulphide (SS) and oxidized glutathione (GSSG)) and SS/NT and GSSG/GSH percent ratios were significantly higher (p < 0.05 for all). The disease duration and oxidative stress were significantly higher in the severe group of AD. There was a shift in intracellular and extracellular thiol balances towards the oxidized side, along with correlations between MMSE and these balances (rho = -0.412 for SS/NT and rho = -0.488 for GSSG/GSH), with GSSG/GSH identified as a significant predictive factor (odds ratio (95 % confidence interval): 1.352 (1.136-1.610) for the moderate group and 1.829 (1.451-2.305) for the severe group. Conclusions: These findings suggest that blood redox balance is disrupted in AD.