Hesna Bektas

A novel oxidative stress marker in patients with Alzheimer’s disease: dynamic thiol–disulphide homeostasis

Objective The aim of this study was to evaluate the dynamic thiol–disulphide homeostasis as an oxidative stress parameter, using a newly proposed method, in patients with Alzheimer’s disease. Methods In total, 97 participants were included in the study. Among them, 51 had been diagnosed with Alzheimer’s disease, and the remaining 46 were healthy individuals. Total thiol (–SH+–S–S–) levels and native thiol (–SH) levels in serum of each participant were measured. The amount of dynamic disulphide bonds (–S–S–) and (–S–S–) ×100/(–SH), (–S–S–) ×100/(–SH+–S–S–), and –SH×100/(–SH+–S–S–) ratios were calculated from these values. The obtained data were used to compare Alzheimer’s disease patients with healthy individuals. Results The average total thiol and native thiol levels of patient with Alzheimer’s disease in the study were found to be significantly lower than those levels of healthy individuals. In addition, in the patient group, the –S–S–×100/–S–S+–SH ratio was found to be significantly higher, whereas the –SH×100/–S–S+–SH ratio was found to be significantly lower compared with healthy individuals. Total thiol and native thiol levels, dynamic disulphide bond amount, and –S–S–×100/–SH, –S–S–×100/–S–S+–SH, and –SH×100/–S–S+–SH ratios were not found to be correlated with mini mental state examination score or duration of disease. Conclusion Recent studies have shown that oxidative stress is the one of the molecular changes underlying the pathogenesis of Alzheimer’s disease. In this study, we have investigated the dynamic thiol–disulphide homeostasis in patients with Alzheimer’s disease, using a novel method.

Impairment of dynamic thiol–disulphide homeostasis in patients with idiopathic Parkinson’s disease and its relationship with clinical stage of disease

OBJECTIVE The aim of this study was to investigate dynamic thiol-disulphide homeostasis in patients with idiopathic Parkinsons disease and to determine its relationship with the clinical stage as assessed by the modified Hoehn and Yahr scale. DESIGN AND METHODS Fifty-two patients with Parkinsons disease (PD), diagnosed according to the United Kingdom Brain Bank Criteria for idiopathic PD, and 41 healthy individuals were included in the study. Clinical staging of patients was performed according to the Hoehn and Yahr scale. Peripheral blood samples were taken from all participants, and their native thiol and total thiol concentrations were measured using the newly developed automated method. In addition, their amount of disulphide bonds, disulphide/native thiol, disulphide/total thiol and native thiol/total thiol ratios were calculated. RESULTS Considering the data obtained from Parkinsons patients and the control group, both native thiol (-SH) and total thiol (-SH+-S-S) levels were found significantly lower in patients with Parkinsons disease. A negative and statistically significant relationship was found between both disease duration and disease stage and native thiol (-SH), total thiol (-SH+-S-S) levels and -SH/(-SH+-S-S-) ratio. A positive and statistically significant relationship was found between both disease duration and stage and -S-S-/-SH and -S-S-/(-SH+-S-S-) ratios. CONCLUSION In patients with Parkinsons disease, dynamic thiol-disulphide homeostasis is disrupted, according to disease stage and duration. This balance, easily measured by using the newly developed automated method, can be used in monitoring disease progression. To our knowledge, our study will be the first report in the literature.

Impaired thiol-disulphide homeostasis in patients with axonal polyneuropathy

Abstract Objective: The objective of this study is to examine thiol-disulphide homeostasis in patients with polyneuropathy dominated by diabetic or non-diabetic axonal degeneration. Materials-methods: Fifty-four patients diagnosed with polyneuropathy dominated by axonal damage and 41 healthy subjects were included in the study. The patients were grouped into two groups according to whether or not they had diabetes. The native thiol and total thiol concentrations were measured with the newly developed automated method. Results: While there was no significant difference between the patients with diabetic and non-diabetic polyneuropathy in terms of native thiol and total thiol levels (p > 0.05), the native thiol and total thiol levels of the groups with both diabetic polyneuropathy and non-diabetic polyneuropathy were significantly low compared to the control group (p < 0.01). The level of disulphides in the patients with diabetic polyneuropathy was significantly higher than that of the patients with non-diabetic polyneuropathy and the healthy individuals (p < 0.05). The loss in the sural nerve sensory neural action potential amplitude was positively correlated with the decrease in the levels of both native thiol and total thiol (p < 0.05). Discussion: In our study, we observed that the thiol-disulphide balance was also impaired in patients with non-diabetic polyneuropathy similar to patients with diabetic polyneuropathy, and we therefore considered that impaired the thiol-disulphide homeostasis could be the last common path in patients with polyneuropathy with axonal damage, regardless of the aetiology. Therefore, fortification of thiol deficiency with N-acetyl cysteine or alpha-lipoic acid can fix the thiol-disulphide balance and help decelerate the axonal damage.

Rhabdomyolysis Related to Dyskinesia in Parkinson’s Disease

Rhabdomyolysis is a life threatening syndrome. It accounts for an estimated 8% to 15% of cases of acute renal failure and is associated with a mortality rate of 5%. In movement disorders, various causes of rhabdomyolysis have been reported including status dystonicus, myoclonus, generalized chorea and parkinsonism-hyperprexia syndrome in Parkinson’s disease (PD). Levodopa-induced dyskinesia leading to rhabdomyolysis is a very rare phenomenon in PD. We report a case of 76 years old PD patient with dyskinesia and rhabdomyolysis.