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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 β (Aβ) 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Thiol-disulphide homeostasis (TDH) is a new parameter indicating oxidative stress that plays a role in the pathogenesis of various clinical disorders. Our study planned to investigate TDH in COVID-19 patients. Age and gender-matched healthy subjects (n = 70) and COVID-19 patients (n = 144) were included in the study. In addition to the routine laboratory parameters of the groups, their native thiol (NT), total thiol (TT) and disulphide levels were measured. Primarily, we compared COVID-19 patients to the healthy control group for inflammatory parameters, NT, TT and disulphide levels. Then, COVID-19 patients were divided into two groups according to the severity of the disease as mild to moderate and severe COVID-19, and the three groups were compared with each other. Predictive value of thiol parameters in the diagnosis of COVID-19 and in the determining its severity, and its correlation with presence and duration of symptoms were investigated. Severe COVID-19 patients had lower NT and TT levels compared with healthy controls and mild to moderate patients (P < 0.001 for both). The results of ROC analysis show that the greatest AUC was IL-6 and NT (AUC = 0.97, AUC = 0.96, respectively) between control and COVID-19 patients, while it was CRP and NT (AUC = 0.85, AUC = 0.83) between mild to moderate and severe patients. A negative correlation was found between duration of symptoms of dyspnoea, cough, fever, and sore throat and NT (r = -0.45, P = 0.017, r = -0.418, P < 0.001, r = -0.131, P = 0.084, r = -0.452, P = 0.040, respectively). NT and TT levels have a strong predictive value in the diagnosis of COVID-19 and in determining disease severity. Our results support that changing TDH parameters appears to have an important role in disease pathogenesis and it can be used in clinical management of patients., (Copyright © 2021 Elsevier Inc. All rights reserved.)