1. The Connection
The excessive buildup of plaques which are highly composed of amyloid-beta proteins is a factor that is present in incarnations at least two of these diseases. In the case of IBM, it seems that the amyloid-beta triggers an immune response that then attacks the muscles, which leads to the weakness that characterizes the disease. This theory is somewhat supported by research where a vaccine to counter potentially associated retroviruses worked to help protect mice from IBM. While there’s certainly a long way to go, but there is other research suggesting the ability of Amyloid-beta to migrate, which sheds more light.
This evidence of ‘migration’ comes from a study in which healthy mice were kept in physical contact with mice who produced significant levels of amyloid-beta proteins. In the end, the healthy mice developed symptoms of Alzheimer’s disease. If this indeed is a case of migration, then it’s not entirely unreasonable assumption that the Amyloid-beta proteins could migrate through a single body. After all, amyloid-beta is not produced only in the brain; as evidenced by its presence in manifestations of IBM and perhaps DLB, there are other parts of the body that produce it, such as muscles, platelets and blood vessels.
With all that being said, there is still simply too much that is conjecture at this time. Perhaps the links uncovered among these diseases and amyloid-beta proteins are clues into the nature and origin of Alzheimer’s. Perhaps it can start in the brain or the body, or at the very least, start in the brain based on a bodily trigger. If it is a matter of whole-body amyloid-beta protein presence, perhaps we can develop a more effective means to identify and treat this before Alzheimer’s appears. Only time and more research will be able to uncover those answers for us.Related: 11 Predictors of Alzheimer’s You Didn’t See Coming