Projenitör nöral hücrelerden geliştirilen alzheimer hücre modelinde kompleman sistemi elemanlari C5a ve C5aR'nin rolü

Alzheimer's disease (AD) is a neurodegenerative disease characterized by plaques and neurofibrillary tangles (NFT) resulting from the accumulation of amyloid beta peptides. According to data from the World Health Organization (WHO) (2020), there are currently more than 55 million people worldwide suffering from AD. The complement system, consisting of more than 25 proteins, is one of the important components of inflammatory responses. C5a, a complement system anaphylatoxin, is one of the inflammatory mediators of the innate immune system. C5aR1 (CD88), the classical receptor of C5a, is also known to play a role in neurodegenerative diseases. Demonstration of complement components and activation in the brain of Alzheimer's patients has led to various speculations regarding the role of this inflammatory pathway in neurodegenerative mechanisms. It is not clear how the role of the complement system affects the pathogenesis of the disease. The aim of this study was to determine how C5a caused a change in AD characteristics in an Alzheimer's cell model developed from human progenitor neural cells. There was no previous study on the complement system relationship with an Alzheimer's cell model developed from human progenitor neural cells. The effect on the presence and inhibition of C5a by exposing cells to C5a and then suppressing it with a C5a antagonist, PMX53, was examined in an Alzheimer's cell model developed in immunology lab of Yeditepe University. It was also analyzed whether the antagonist, PMX53, had an effect alone. Alzheimer's cell groups had much higher C5aR1 expression than the control group. When C5a was added to the cells, no significant difference was observed in the C5aR1 level compared to the Alzheimer group. When PMX53 was added, C5aR1 level decreased, but when C5a and PMX53 were added together, there was an increase in C5aR level. While some of the results were compatible with the literature, some were contradictory, but they proved that the complement system has a significant effect on Alzheimer's disease.