Samenvatting

Alzheimer's disease is a complex neurodegenerative disease and the most prevalent form of dementia. It affects every 14th person after the age of 65, thus making it a serious concern in modern society. Furthermore, currently available treatment is restricted only to symptomatic and is not highly effective. Neuroinflammation has been increasingly reported to play a crucial role in underlying the disease pathology, thus becoming a promising therapeutic target. However, different aspects of neuroinflammation, including the exact time point of its occurrence, are still not entirely understood. The focal point of this research was to investigate the developments of neuroinflammatory changes in the APP/PS1 Alzheimer's disease mouse model. Notably, the expression of markers (TREM2 and Clec7a) associated with disease-associated microglia, cells considered the primary neuroinflammation mediators, was investigated, as well as the phagocytic capacities of the brain cells. The results
demonstrated significantly elevated expression of TREM2 in 3-day-old APP/PS1 mice. Similarly, border associated macrophages in the APP/PS1 mice of this age showed significantly increased phagocytic capacities. Taken together, these findings indicated that the neuroinflammatory changes might occur earlier than was previously accepted and pointed to the need for further study of diverse aspects of neuroinflammation in the early stages of the disease process. Further discoveries in this area might reveal strategies to detect and modulate the disease in the earlier stages, leading to better clinical outcomes.