Babies have more of this Alzheimer’s-linked protein than dementia patients – study raises hope for future treatments

A protein long blamed for the brain damage seen in Alzheimer’s disease has now been found in astonishingly high levels in healthy newborn babies, challenging decades of medical dogma.

The discovery could transform our understanding of both brain development and Alzheimer’s disease itself. The protein, called p-tau217, has been viewed as a hallmark of neurodegeneration – yet a new study reveals it’s even more abundant in the brains of healthy infants.

Rather than being toxic, p-tau217 may be essential for building the brain during early development.

To understand why this matters, it helps to know what tau normally does. In healthy brains, tau is a protein that helps keep brain cells stable and allows them to communicate – essential functions for memory and overall brain function. Think of it like the beams inside a building, supporting brain cells so they can function properly.

But in Alzheimer’s disease, tau gets chemically changed into a different form called p-tau217. Instead of doing its normal job, this altered protein builds up and clumps together inside brain cells, forming tangles that impair cell function and lead to memory loss typical of the disease.

For years, scientists have assumed high levels of p-tau217 always spell trouble. The new research suggests they’ve been wrong.

An international team led by the University of Gothenburg analysed blood samples from over 400 people, including healthy newborns, young adults, elderly adults and those with Alzheimer’s disease. What they found was striking.

Premature babies had the highest concentrations of p-tau217 of anyone tested. Full-term babies came second. The earlier the birth, the higher the protein levels – yet these infants were perfectly healthy.

These levels dropped sharply during the first months of life, remained very low in healthy adults, then rose again in people with Alzheimer’s – though never reaching the sky-high levels seen in newborns.

The pattern suggests p-tau217 plays a crucial role in early brain development, particularly in areas controlling movement and sensation that mature early in life. Rather than causing harm, the protein appears to support the building of new neural networks.

Rethinking Alzheimer’s disease

The implications are profound. First, the findings clarify how to interpret blood tests for p-tau217, recently approved by US regulators to aid dementia diagnosis. High levels don’t always signal disease – in babies, they’re part of normal, healthy brain development.

More intriguingly, the research raises a fundamental question: why can newborn brains safely handle massive amounts of p-tau217 when the same protein wreaks havoc in older adults?

If scientists can unlock this protective mechanism, it could revolutionise Alzheimer’s treatment. Understanding how infant brains manage high tau levels without forming deadly tangles might reveal entirely new therapeutic approaches.

The findings also challenge a cornerstone of Alzheimer’s research. For decades, scientists have believed p-tau217 only increases after another protein, amyloid, starts accumulating in the brain, with amyloid triggering a cascade that leads to tau tangles and dementia.

But newborns have no amyloid buildup, yet their p-tau217 levels dwarf those seen in Alzheimer’s patients. This suggests the proteins operate independently and that other biological processes – not just amyloid – regulate tau throughout life.

The research aligns with earlier animal studies. Research in mice showed tau levels peak in early development then fall sharply, mirroring the human pattern. Similarly, studies of foetal neurons found naturally high p-tau levels that decline with age.

If p-tau217 is vital for normal brain development, something must switch later in life to make it harmful. Understanding what flips this biological switch – from protective to destructive – could point to entirely new ways of preventing or treating Alzheimer’s.

For decades, Alzheimer’s research has focused almost exclusively on the damage caused by abnormal proteins. This study flips that perspective, showing one of these so-called “toxic” proteins may actually play a vital, healthy role at the start of life.

Babies’ brains might hold the blueprint for keeping tau in check. Learning its secrets could help scientists develop better ways to preserve cognitive function as we age, transforming our approach to one of medicine’s greatest challenges.

Rahul Sidhu does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.