Because amyloid plaques can build up in the brain and trigger a cascade response, leading to cognitive decline and neurodegeneration, they have previously been thought of as only harmful. As such, plaques have been the target of pharmaceutical companies in the development of drugs—remove amyloid plaques, the logic goes, and one can halt the destruction occurring in the brain as a result of Alzheimer’s disease. All of these prospective drugs have failed.
New research is revealing that amyloid may play more nuanced part in the function of the brain. Evidence suggests that amyloid plays a role in innate immunity, and that it can protect against a wide range of infectious agents. Amyloid has the capacity to form fibrils that trap pathogens in an infected brain. As infections in the brain increase, the build-up of amyloid demonstrates the double-edged sword of this peptide. On the one hand, amyloid initially traps the infection, keeping the brain safe—on the other hand, this leads to an accelerated build-up of the plaque that can contribute to the pathology associated with Alzheimer’s disease.
This would suggest that total clearance of amyloid from the brain is not an appropriate therapy; instead, it should be regulated and not removed completely.