Last year, the idea that brain cells affected by Alzheimer's disease might "infect" neighboring cells made big news, reaching national and international news audiences. In these studies, researchers at Columbia University Medical center, and BrightFocus-funded researchers at Massachusetts General Hospital showed that tau, a protein long implicated in Alzheimer's disease, could migrate from one cell to another, propagate, and cause a wave of Alzheimer's-like symptoms, which ultimately overtakes the brain.
Before these mice studies, there was BrightFocus-funded work in isolated cells, which set the stage for these later experiments by documenting tau spreading in simpler systems.
This week, Dr. Marc Diamond, the researcher responsible for the earlier BrightFocus-funded study, reported that the affected cell is not wholly responsible for spreading tau. Rather, the neighboring cells also have a role in receiving the bad tau through a gateway into the cell that is normally used for regulating movement of many molecules between cells.
This view of tau spreading has a definitive up-side when it comes to thinking about preventing the spread of bad tau. First, the cellular machinery that creates these gateways is amenable to being controlled by drugs. Second, these proteins seem to be shared between several diseases. Thus, research investment in drugs that prevent tau spreading might pay off in new treatments for Alzheimer's, as well as other diseases such as Parkinson's.