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. 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. 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. 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.
