A new study linking Alzheimer's and infection may turn the scientific and medical community's understanding and treatment of the disease upside down. The study, published in Science Translational Medicine this past week, suggests that current therapies may be targeting the wrong culprit when it comes to treating the degenerative brain disorder.
Neurologists Rudolph Tanzi and Robert Moir headed the team of researchers from Harvard Medical School and Massachusetts General Hospital. Their study found that a protein that has previously been found to play an integral role in the development of Alzheimer's disease also acts to protect the brain from infection.
The processes involved in Alzheimer's disease are complex. The protein, which goes by the name amyloid beta, is generally believed among the researchers who specialized in Alzheimer's disease to be the root cause of the degenerative condition. Amyloid beta is a waste product, and as such, it was not believed to play any useful role in bodily functions.
As it accumulates in the brain, it builds up into the sticky plaque that damages nerve cells at the synapse, or where they communicate with each other. The declining memory and cognitive functions that are typically associated with Alzheimer's disease are the result.
Most current drug therapies for Alzheimer's disease target amyloid beta, with a view to clearing the brain of the protein, but the new study suggests that may not be the best approach.