Platelet glycogen synthase kinase 3β regulates plasma β amyloid and phosphorylated tau levels in chronic kidney disease patients with cognitive dysfunction; therapeutic role of erythropoietin

Introduction: Patients with chronic kidney disease (CKD) have increasingly been diagnosed cognitive impairment. Glycogen synthase kinase 3β (GSK3β) is directly causing both phosphorylated tau (pTau) and amyloid β (Aβ) accumulation in Alzheimer’s (AD). GSK3β expression more abundant human platelets than other blood cells. Recombinant erythropoietin (rHuEPO) a common medicine for treating anemia patients CKD, as well neuroprotective agent. Objectives: The goal of this research to find out how platelet regulates plasma Aβ, total Tau at threonine 181 (p-tau181) levels CKD dysfunction also the efficacy rHuEPO treatment. Methods: study included 60 participants, which consist 30 without based on neuropsychological examination. was evaluated using western blot Tau, pTau were quantified by ELISA. data compared statistically (P< 0.05) AD, normocytic normochromic anemic healthy patients. Results: In subjects, pTau181 significantly altered like AD when anemic, subjects. post (100 IU/kg, weekly twice, six months) treatment, protein abnormalities retrieved (P<0.05) pre-treatment. Conclusion: This established that are candidate biomarkers clinical utility inhibitor therapeutic agent has determined.