Article Link: http://www.nytimes.com/2016/05/26/health/alzheimers-disease-infection.html
Although this is not viral hemorrhagic fever news, I thought that this new study was too interesting to pass up a chance to discuss. Essentially, researchers at Harvard are hypothesizing that the plaques that form in the brain that are a hallmark feature of Alzheimer’s Disease form because of a viral or bacterial particle that passes the blood brain barrier. It has been noted that the barrier gets “leakier” with age, and certain infectious particles have a higher likelihood of getting in to the brain.
Scientists had previously noted that the structure of the beta amyloid protein was similar to innate immune system proteins, even though the reigning theory about the proteins is that they are garbage that builds up in the brain with age. The lead investigator, Dr. Moir of Harvard Medical School, hypothesized that these proteins in the brain were actually reacting to invading particles, and forming a cage around them to prevent them interacting with the brain. This is also how the immune system deals with threats in other parts of the body. However, the once the particle dies, what is left is the cage of protein, which is essentially the characteristic plaque of AD. The scientists have found supportive evidence for this hypothesis in petri dish neurons, yeast, round worms, fruitflies and mice.
This is a fascinating new turn for Alzheimer’s Disease, and it’s very interesting how this new theory helps explain a lot of interesting findings in the past that we did not know what to do with. Previously, researchers found that patients who developed AD had higher numbers of antibodies to Herpes virus, but found a causative link to be too much of a stretch – this might begin to explain that finding. Honestly, it’s also amazing to me how paradigms for research can change with a single study, which is what is happening right now in this field. It will be really interesting to see the follow up research done in response to this!