Inflammation’s Role In Developing Alzheimer’s Disease


Inflammation is a natural and necessary healing response produced by the body, but what role might it have in developing Alzheimer’s disease? Inflammation has been getting much attention as it is found to have many negative effects on the body and it is being deemed the culprit causing many diseases. Recent research by William Banks, MD may provide a “one-two punch in giving clues on how Alzheimer’s disease develops and could be treated.” It seems that increased accumulation of a protein in the brain causes detriment and results in the negative affects seen by the disease. This protein is usually present in the body and brain, but it can exit the brain and becomes absorbed by the blood stream. Because it leaves the brain, it does no damage and thus a person’s cognition and brain function remains unaffected. With the presence of inflammation, the pump that pushes this protein out does not function as is required. A broken pump means excessive protein build up and therefore more damage.

If Inflammation Is Decreased Does Alzheimer’s Disease Disappear?

According to the research, keeping inflammation at bay means that the protein pump works and thus the culprits causing Alzheimer’s can exit the brain. William Banks feels that anti-inflammatory drugs can be used to help prevent the development of the disease. He further “supports using indomethacin, an anti-inflammatory medication, as a buffer to protect LRP from being turned off.” The LRP is the pump that shuts down and allows the build of excess protein. Research performed on rats showed that they had challenges with memory and learning as the protein build up increased. They responded to the indomethacin medication and were able to flush out the brain of excess proteins. This research provides some hope for patients and doctors. Anti-inflammatory drugs are to be considered when exploring treatments for this disease.

Saint Louis University. “Inflammation May Trigger Alzheimer’s Disease.” ScienceDaily 9 July 2009. 21 July 2009 <>.

