Researchers at University of Utah Health reported a new finding on how Alzheimer’s disease may spread through the brain, identifying the protein Arc as a possible carrier that helps toxic tau move from damaged neurons into healthy ones. The study, published in Cell, was conducted primarily in mouse models and found that tau appeared to travel inside extracellular vesicles, small membrane-bound sacs used by neurons to exchange signals. The team also said it found extracellular vesicles containing both Arc and tau in human brain tissue, suggesting the same mechanism could exist in people, though it has not been confirmed.
In the experiments, researchers compared Alzheimer’s mouse models with and without Arc. They found that when Arc was present, toxic tau could attach to it inside extracellular vesicles and be transported into neighboring healthy cells, where it then triggered the formation of new tau tangles. When Arc was removed, the vesicles contained far less tau and the transfer of the protein between neurons was sharply reduced. The findings add to a broader body of research focused on tau, a protein that in Alzheimer’s disease can form clumps and interfere with normal cell function before neurons die.
The researchers said the results point to a possible therapeutic strategy based not on eliminating tau entirely, but on interrupting its movement into unaffected cells. At the same time, they cautioned that Arc appears to play a dual role. While it may help spread pathology, it also seems to help diseased neurons expel excess toxic tau. In mice lacking Arc, tau remained trapped inside already-damaged neurons and accumulated to more toxic levels, causing those cells to die more quickly. That led the team to suggest that blocking the uptake of tau-carrying vesicles by healthy cells may be a more promising approach than stopping diseased cells from releasing them.
The study’s authors emphasized that any clinical application remains distant. Jason Shepherd, the study’s senior author, said most of the work has been done in mice and that more research is needed before the mechanism can be tied definitively to human disease or translated into treatment. The findings also arrive within a wider Alzheimer’s research landscape in which the link between brain pathology and clinical decline has long been understood as complex. Long-running research including the Nun Study has shown that some people can retain strong memory and reasoning despite extensive plaques and tangles in the brain, underscoring that Alzheimer’s symptoms may be shaped not only by protein buildup itself but also by other biological factors and by cognitive resilience over a lifetime.