Complement in Alzheimer’s Disease.

Alzheimer's disease (AD) is a devastating disease that affects over 55 million of people worldwide, causing memory loss, cognitive decline, and ultimately, a loss of independence. This number is projected to nearly triple by 2050, posing significant economic and social challenges. While the exact causes of AD are still not fully understood, recent research has highlighted the significant role that inflammation may play in the development and progression of this disease.
My proposal aims to explore how inflammation contributes to AD. The part of the inflammatory pathway that I explore here is called the complement system. Complement is part of the immune system, it is the body's natural response to injury or infection, but when it becomes chronically active, it can lead to harmful effects in many organs, including brain. In the context of AD, chronic brain inflammation may damage brain cells and disrupt the normal functioning of neural networks, leading to the disease. The cognitive decline seen in AD patients can be partially attributed to inflammation, which is driven by the complement system. This system comprises an army of proteins in the blood that exist to counter pathogens. One critical component of this army, the Membrane Attack Complex (MAC), functions like a pinprick in a balloon, poking holes in bacteria and human cells, leading to cell leakage and inflammation. Divisions of this complement army include the classical, lectin, and alternative pathways, which recruit additional reinforcements to combat invaders. Normally, these reinforcements enhance the army's strength, aiding in repelling invaders. However, if complement becomes excessively activated, rather than helping, it become problematic. The defenders begin to attack self-cells. Although it is unclear why this breakdown occurs – potentially due to a lack of communication within the system - this "friendly fire" can drive disease by promoting a hyperinflammatory state, leading to brain...