The most common form of dementia, Alzheimer’s disease, is a degenerative disease that causes a person to continually lose his or her memory as symptoms worsen over time. With Alzheimer’s, the cells of the nervous system are not able to carry out their jobs and the chemical signals surrounding them are not able to transfer properly. This is because the nerve cells are unable to send messages back and forth due to blocks in the nerve pathways called plaques and tangles. Plaques are portions of a built up protein called beta-amyloid (a-beta) and tangles refer to the twisted fibers of tau, another protein. As these road blocks build up in the brain, they interfere with the operation of the nerve cells, causing cell damage and even death. Generally speaking nerve cells do not have the ability to regenerate (but researchers are questioning this idea!) so there is no way for the brain to regain what it has lost. This is when memory loss and dementia begin.
In order to treat, or someday cure, Alzheimer’s, scientists must find out where the source of this deterioration is, and often they research nerve cells to figure it out. A new study, however, done by the Stanford University School of Medicine, looked at microglia and their function in Alzheimer’s in mice. Microglia are a type of support cell for the neurons in the nervous system. Microglial cells act as “doctors” or “garbage collectors” within the central nervous system. One of their functions is to reduce inflammation by getting rid of debris and toxic substances in the brain. To do this they use a process of phagocytosis to engulf the harmful material.
Beta-amyloid is one of the proteins that normally accumulates in the brain. When excess is present, it forms the plaques that are associated with Alzheimers. Normally, the microglia are in charge of breaking down the beta-amyloid protein, but in Alzheimer’s patients, microglial activity is reduced. For this reason, scientists looked into what was preventing the microglia from doing their job.
It turns out that one single molecule, a receptor protein, on the surface of microglia could be the key to curing Alzheimers. Researchers refer to this receptor protein as EP2. EP2 activation causes the deterioration of microglia, leading to and increase in inflammation and a buildup of plaque within the brain. During the study, older mice experienced greater EP2 activity when in the presence of the beta-amyloid protein, giving clue as to why older people are the ones experiencing memory loss due to Alzheimer’s. Once EP2 activity was blocked during the study, the memory of the mice was significantly improved.
The researchers of this study suggest that since this receptor has now been identified, it may be possible to manufacture drugs that interfere with EP2 and thus slow, or prevent, the accumulation of beta-amyloid plaques in the brain.
- Alzheimer’s Association: What is Alzheimer’s?
- Blocking receptor in brain’s immune cells counters Alzheimer’s in mice, study finds (Stanford Medicine, Dec 2014)
- Woodling N.S., P. G. Priyam, P. Larkin, J. Shi, J. U. Johansson, I. Zagol-Ikapitte, O. Boutaud & K. I. Andreasson (2014). Suppression of Alzheimer-Associated Inflammation by Microglial Prostaglandin-E2 EP4 Receptor Signaling, Journal of Neuroscience, 34 (17) 5882-5894. DOI: http://dx.doi.org/10.1523/jneurosci.0410-14.2014
Theresa Koos is a sophomore at Clarke University in Dubuque, Iowa where she is studying to be a Physical Therapist with a major in Biology.
- Alzheimers progression (top): By National Institute on Aging [Public domain], via Wikimedia Commons
- Microglia: By GerryShaw (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons