The Possible Role of Kallikrein-6, 7, and Potassium Channel Proteins in Alzheimer’s Disease

Abstract

Objective: Although the formation mechanism of Alzheimer’s Disease (AD) is not known with certainty, two major proteins, beta amyloid of senile plaques and tau protein of neurofibrillary tangels are responsible for AD. One of the major factors in the development of the disease is the formation of in soluble amyloid deposits, and the other one is the increased tau phosphorylation. Kallikreins (KLK’s) are a sub-family of serine proteases that play a role in the etiology of AD which is characterized by neuronal damage and loss of function.Kallikrein (KLK)-6 and KLK-7 are known to be age-related protease and are found at high levels in the central nervous system (CNS). It was previously shown to be involved in proteolysis of extracellular proteins implicated in neurodegenerative diseases such as AD. In this study, we aimed to investigate the possible role of KLK-6 and KLK-7 in the pathogenesis of AD and the relationship between potassium channel proteins. Methods: A total of 35 Alzheimer’s patients over the age 65 years, followed-up by Polatlı Duatepe Government Hospital and 35 healthy individuals (control group) admitted to the neurology clinic for routine screening with cognitive status considered normal were included in this study. After a 12-hour hunger, KLK-6 and KLK-7 were measured with inwardly rectifying potassium channel protein (KCNJ3), and two-pore potassium channel protein (KCNK9) levels were measured by the Enzyme-Linked Immuno Sorbent Assay (ELISA) in the serum of the blood samples which were taken from the antecubital vein after centrifuging for 10 minutes at 2500xg. The differences between the two groups were tested by T- test. A value of p<0.05 was considered statistically significant. Results: All the groups were matched for age and gender, but not statistically significant difference was observed (p>0.05). According to our findings, serum KLK- 6 and KLK-7 levels of Alzheimer’s group were significantly increased (p<0.05). A significant difference was not detected when the levels of serum KCNJ3 and KCNK9 of the Alzheimer’s group compared with the control group (p>0.05). Conclusion: It is thought that the failure in preventing the abnormal protein folding and accumulation leads to AD in the brain. According to the findings of the present study, a positive correlation was detected between the levels of KLK-6 and KLK-7 and AD’s pathology. © 2021. All Rights Reserved.