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Tau protein has a well-earned reputation as one of the villains of Alzheimer’s disease. Tangles of the abnormal form of the protein build up inside brain cells as dementia takes hold, and for decades researchers have studied tau mainly as a marker of damage. But a new study has found the same protein does something researchers did not expect; helping healthy brains build memories that last.
The findings, published in Nature Communications, come from a team at Flinders University working with the University of New South Wales and Macquarie University in Australia. Rather than focusing on tau’s destructive role, the researchers examined what tau does inside normal, healthy neurons—and found it is central to turning a fleeting experience into a memory that survives weeks later.
A Protein Doing Double Duty
The study looked at mice and what scientists call “remote memory”—memories recalled days or weeks after something happens, as opposed to memories recalled minutes later. The team found tau is not needed for an animal to learn something new or to remember it a short time afterward. Its job comes later, making sure that memory holds up over the long term.
That work happens inside a small set of brain cells called engram cells, which store the physical record of an experience. Out of the many neurons available, only a small number are chosen to hold onto any given memory. According to the study, tau is active precisely when that selection happens, helping determine which cells take on the job.
“Our findings show that tau helps determine which cells are selected to store a memory, shaping how an experience forms a lasting memory trace,” Renée Kosonen, one of the study’s lead authors, said in a statement.
Cutting Through the Noise
The researchers also found tau limits background activity in the brain during memory formation. By quieting that extra “noise,” tau allows a smaller, more defined group of cells to lock in the memory, producing a clearer and more stable trace rather than a fuzzy one.
Behind this process is a subtle chemical change called phosphorylation, in which a phosphate molecule attaches to the tau protein. Abnormal phosphorylation of tau is a hallmark of Alzheimer’s disease, but the study found that a controlled, low-level version of this same process is a normal and necessary part of healthy memory formation.
“Studying the protein tau’s role in dementia is good because it relates to memory consolidation, and its role is timing in the brain, not just storage,” physician and author John La Puma told Newsweek. “Healthy tau in mice organizes memory in the brain, and the brain’s clock runs on light.
“The brain’s cleaning system, called the glymphatic system, clears tau proteins at night during deep sleep. Whether you get enough deep sleep depends on daytime bright light in the morning most people never get. But the problem with this study is that we’re ignoring the biological signal from daylight that [determines] whether the brain gets the deep sleep to consolidate anything at all.”
Implications for Alzheimer’s Research
Because the work was done in mice, the results cannot be applied directly to human memory or to Alzheimer’s disease. Even so, the researchers say the findings offer a new angle for future dementia research, suggesting that treatments might eventually need to preserve tau’s normal function rather than simply eliminating the protein altogether.
Reference
Kosonen, R., Stefanoska, K., Lin, Y., Edwards, S., Prikas, E., Bertz, J., Poljak, A., Ittner, L. M., Ittner, A. (2026). Tau T205 phosphorylation modulates engram cell recruitment and remote memory in mice. Nature Communications. https://doi.org/10.1038/s41467-026-73207-9.
Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang
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