Cognitive dysfunction has been increasingly recognized in chronic kidney disease (CKD) patients. Senile plaques are important pathophysiological characteristic of cognitive dysfunction. The major component of plaques is the amyloid β (Aβ) peptide released from proteolytic cleavage of amyloid precursor protein (APP). Plasma Aβ has been a focus of the growing literature on blood based biomarkers for cognitive dysfunction. Oxidative stress is prevalent in CKD and it plays an important role in cognitive dysfunction. Increased oxidative stress leads to cause cleavage of APP and Aβ production. The aim of this study is to assess the antioxidant status and Aβ42 levels in plasma of CKD patients with cognitive dysfunction compared to CKD without cognitive dysfunction. A total of 60 subjects divided into 30 CKD without cognitive dysfunction and 30 CKD with cognitive dysfunction based on neuropsychological assessment tests. To compare antioxidant status and Aβ42 levels in plasma, the following groups such as healthy subjects (n = 30), normocytic normochromic anemia (n = 30) and Alzheimer's disease (AD, n = 10) patients were also maintained. Plasma Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Reduced glutathione (GSH) and lipid peroxidation (LPO) were determined by spectrophotometrically. Aβ level was determined by immunoblotting method. The parameters were statistically compared with healthy, normocytic normochromic anemia and AD subjects. Like AD subjects, significantly increased Aβ and LPO level while decreased SOD, CAT, GPx and GSH levels were observed in plasma of CKD patients with cognitive dysfunction when compared to healthy, CKD without cognitive dysfunction and normocytic normochromic anemic subjects. Results suggest that elevated plasma oxidative stress and Aβ were seen in CKD patients with cognitive dysfunction may be attributed to pathological changes within the brain.
1 November 2019 in Journal of Clinical Neuroscience
Introduction: Patients with chronic kidney disease (CKD) have increasingly been diagnosed with cognitive impairment. Glycogen synthase kinase 3β (GSK3β) is directly causing both phosphorylated tau (pTau) and amyloid β (Aβ) accumulation in Alzheimer’s disease (AD). GSK3β expression is more abundant in human platelets than in other blood cells. Recombinant human erythropoietin (rHuEPO) is a common medicine for treating anemia in patients with CKD, as well as a neuroprotective agent. Objectives: The goal of this research is to find out how platelet GSK3β regulates plasma Aβ, total Tau and tau phosphorylated at threonine 181 (p-tau181) levels in CKD patients with cognitive dysfunction and also the efficacy of rHuEPO treatment. Patients and Methods: The study included 60 participants, which consist of 30 CKD without cognitive dysfunction and 30 CKD with cognitive dysfunction based on the neuropsychological examination. The expression of GSK3β in platelets was evaluated using a western blot and plasma Aβ, total Tau, pTau 181 levels were quantified by ELISA. The data were compared statistically (P< 0.05) to AD, normocytic normochromic anemic and healthy patients. Results: In CKD with cognitive dysfunction subjects, platelet GSK3β expression and plasma Aβ, total Tau and pTau181 levels were significantly (P< 0.05) altered like AD when compared to normocytic normochromic anemic, healthy and CKD without cognitive dysfunction subjects. In post rHuEPO (100 IU/kg, weekly twice, six months) treatment, the altered protein abnormalities were retrieved significantly (P<0.05) compared to pre-treatment. Conclusion: This study established that platelet GSK3β expression and plasma Aβ, total Tau, pTau181 are the candidate biomarkers for cognitive dysfunction in CKD patients. The clinical utility of rHuEPO as a GSK3β inhibitor and therapeutic agent for cognitive dysfunction in CKD has been determined.
12 September 2023 in International Archives of Occupational and Environmental Health
Diabetic patients with depression or anxiety are more likely to develop diabetic complications and have a lower quality of life. The aim of the study is to determine the prevalence of depression and anxiety among type 2 diabetic patients and to identify the associated factors. A cross-sectional, observational study of type 2 diabetes mellitus outpatients, with diabetes-related conditions who attended the hospital from January to April 2023, was conducted by interviewing them using the Patient Health Questionnaire-9 for depression and Generalised Anxiety Disorders-7 for anxiety. Descriptive statistics, bivariate analysis, and multivariant regression were performed for statistical analysis. Out of 450 type 2 diabetic patients, 90% were between ages 30 and 45, 50.2% were male, 60% were living in rural areas, and 76.5% literate; most of them belong to the upper middle class (64%) and they live in joint family (32.7%). Depression and anxiety were observed among 65.3% and 62.4% of type 2 diabetic patients, respectively. When observing the severity, 47.8% of patients had mild depression, and 38.7% had minimal anxiety. Age group, socioeconomic status, treatment type, and years of diabetes were found to be factors associated with depression and family type is associated with anxiety. Hospitalized diabetics have higher depression and anxiety rates for multiple reasons. Therefore, diabetes management programmes should include regular depression and anxiety screenings to quickly identify and treat high-risk patients in healthcare facilities.