Proteins involved in amyloid plaque formation in Alzheimer's disease

Alzheimer's disease is a progressive and challenging neurodegenerative disorder that leads to memory loss, cognitive dysfunction, difficulty in performing daily activities, and, in advanced stages, the loss of basic life functions. The disease can only be diagnosed after symptoms have begun due to the underlying pathophysiological mechanisms, and the diagnostic methods are not practical from the patient's perspective (such as PET scans and other imaging techniques). Additionally, there is no protocol for early diagnostic methods, which places a significant burden on the economies of countries. As a result, patients, caregivers, and social states providing healthcare face considerable challenges. There is currently no treatment option that completely reverses the pathology of the disease and heals the patient. For many years, symptomatic treatments have been applied in the clinic (including galantamine, rivastigmine, donepezil, memantine, and combination therapy with donepezil/menantine), and these symptomatic treatments only have a mild alleviating effect on the syndromes. Two molecules recently approved by the FDA (aducanumab and lecanemab) can alleviate the course of the disease, provided that they are used in the early stages of the disease. The two most important mechanisms underlying the disease are amyloid beta cascade and tau pathology. The two most important mechanisms underlying the disease are amyloid beta cascade and tau pathology. Amyloid beta forms senile plaques in the spaces between nerve cells in the brain tissue, and phosphorylated tau forms neurofibrillary tangles within the nerve cells. Senile plaques consist of amyloid beta-42, and neurofibrillary tangles consist of phosphorylated tau. There is no diagnostic method approved by health authorities yet to diagnose these proteins based on plasma. The aim of our thesis is to determine by ELISA method whether the proteins that are thought to increase in plasma in Alzheimer's disease create a significant difference between the control and patient groups. In our study conducted with 37 controls and 24 Alzheimer's patients, Aβ40, Aβ42, BACE-1, t-Tau and p-Tau concentrations were measured. In addition, demographic data were evaluated along with consent forms obtained from volunteers and patients' guardians. As a result of the evaluation, it was found that the risk of Alzheimer's increased with increasing education level; there have been findings that increased tea consumption reduces the risk of Alzheimer's. It was found that Aβ40, Aβ42, BACE-1, t-Tau and p-Tau concentrations detected in plasma by ELISA method generally increased in the patient group compared to the control group, but this increase was not a statistically significant difference. A review of the literature reveals the significance of diagnosis based on plasma in large-scale studies conducted worldwide; the measurement of Aβ40, Aβ42, BACE-1, t-Tau, and p-Tau proteins in plasma using the ELISA method is being conducted for the first time in our country. It is anticipated that studies with more participants will contribute to the development of the plasma-based diagnostic method.