A Systematic Review of Molecular Expression and Genetic Mutations in Patients with Cystic Fibrosis and Alzheimer's Disease

Abstract

2019's progress in the development of highly effective modulating therapy has provided unprecedented clinical benefit to more than 90% of cystic fibrosis patients who are genetically eligible for treatment, leading to the identification of the disease-causing CFTR gene and our subsequent understanding of its mechanisms. The main disease in the pathogenesis of cystic fibrosis. In Alzheimer's disease, when the proteins inside the brain do not function properly, they cause disruption in the nerve cells of the brain. These disturbed cells secrete a toxic substance that damages the neurons and prevents the communication between the nerve cells of the brain. The present study was investigated by reviewing more than 79 articles with keywords including: "Molecular expression and genetic mutations", "Cystic fibrosis" and "Alzheimer". The results indicate that along with the progress of Alzheimer's disease, brain cells are disabled and communication between cells is lost. At this time, the cognitive symptoms of the disease begin to worsen. These drugs affect certain chemicals that exchange nerve messages between brain cells. In the case of cystic fibrosis, genetic defects cause dysfunction of a type of regulated chloride channel called CFTR. Dysfunction of this channel causes concentration and adhesion of lung, pancreas, liver, intestine, salivary glands and reproductive system secretions in these patients. Another complication of this disease is the increase in the amount of sodium and chlorine in the body, which causes more sweating. Because one of the main methods of early diagnosis of CF is to evaluate the amount of sweating.