The role of microglial cells in Alzhimer's disease
Suli Wang
Collingwood School
Floor Location : S 008 H

Alzheimer’s disease, one of the most feared disease among people of age, is a type of dementia that features a progressive brain cell deaths which causes memory lost and hinders one’s thinking process. With 44 million patients suffering, scientists from all over the world are now trying to formulate new ways to cure or alleviate the symptoms of this disease. In these reports, we will exam the effect of one of the possible solution: Microglial cells. Microglial cells are the main immune cells of human brains, plays a pivotal role in regulating neuro inflammation and deposition of Aβ. Under ordinary conditions, microglial cells are inactive and repeatedly monitor brain homeostasis. However, when Aβ level increases due to Alzheimer, microglial cells become overstimulated and produce inflammatory cytokines that that promote inflammation. Therefore, by stimulating autophagy in Microglial cells, we can decrease Aβ deposit which in turn alleviates symptoms.
By conducting western blotting, we proved that the given compound significantly decreases p62 protein expression in BV2 cultured cells. This opens up two possibilities: First, mRNA level is decreasing. (Since p62 mRNA codes for p62 proteins, its decrease will ultimately lower protein expression.)Second, the proteins themselves are degrading. (No protein = no respective expression). Therefore, by conducting RT-PCR, we eliminated the first explanation since mRNA level did not alter significantly. Therefore, the decrease in protein expression is certainly caused by protein degradation. By research, we learned that P62 protein degradation happens strictly under autophagy. Thus, the results from western blotting and RT-PCR affirms how the given compound stimulates autophagy in microglial cells.