Scientists have found that tau, a protein usually tied to Alzheimer’s, also helps the brain keep memories for a long time. This new insight could guide future dementia treatments.
The research was led by Flinders University together with experts from the University of New South Wales and Macquarie University. Their work was published in Nature Communications. It shows that tau organizes and steadies memories so they last.
Researchers looked at "remote memory" in mice – memories that are recalled days or weeks after an event. They saw that tau isn’t needed to learn something new or remember it right away. Instead, tau is key for making those memories stay strong over time.
Because the experiments were done with mice, the results can’t be copied directly to humans or to Alzheimer’s disease. Still, the findings give useful clues for future dementia research.
Tau’s Role in Long‑Term Memory
"Why some memories stay while others fade has puzzled scientists for years. Our study shows tau is a big part of that puzzle," says Associate Professor Ittner. "Without tau, memories can form, but they are weaker."
The team studied special brain cells called engram cells. These cells hold the physical record of a memory. When a new experience happens, only a few engram cells are chosen to store it.
During this crucial stage, tau becomes active. It helps decide which engram cells are picked, shaping a clear and lasting memory trace.
How Tau Keeps Memories Clear
Tau also quiets down extra brain noise while memories are forming. By reducing this background chatter, tau lets a specific group of cells join the memory, making the memory sharper and more stable.
The scientists discovered a tiny chemical change called phosphorylation that tau undergoes during learning. This change helps coordinate the activity of engram cells.
While abnormal tau phosphorylation is a hallmark of Alzheimer’s, the study shows that a low, normal level of this change is actually needed for healthy brain function.
What This Means for Alzheimer’s
Even when tau was missing, memory traces still existed and could be brought back by directly stimulating engram cells. This suggests tau isn’t needed to store memories themselves, but it helps link everyday cues—like sights and sounds—to the act of recalling those memories.
The researchers also found that disease‑related forms of tau mess up memory in two ways. If abnormal tau is present while learning, it blocks new memories from forming. If it appears after memories are already made, it hampers the brain’s ability to retrieve them.
These problems were linked to strange brain activity patterns, indicating that memory loss in dementia may stem from both lost memories and disrupted memory organization.
"Understanding how tau supports memory formation and recall can reveal what goes wrong in memory loss," says Associate Professor Ittner.
Future work aims to test these ideas in human brains and see how they apply to dementia treatment.
Overall, the study suggests we should view tau not just as a culprit in Alzheimer’s, but also as a key player in how the brain stores, organizes, and retrieves lasting memories. This fresh perspective could deepen our grasp of both healthy memory and the changes that lead to Alzheimer’s disease.