In a surprising new discovery, scientists have found that newborn babies and patients with Alzheimer’s disease both have high levels of a protein long linked to brain degeneration—yet in babies, it appears to support healthy brain growth.
The study, led by researchers at the University of Gothenburg and published in Brain Communications, reveals how the same molecule, p-tau217, can play two opposite roles in the brain depending on a person’s age and health.
The protein, known as phosphorylated tau (specifically the p-tau217 form), has recently gained attention as a key blood marker for diagnosing Alzheimer’s disease.
In older adults, elevated levels of p-tau217 typically signal the presence of harmful brain changes, such as amyloid plaques and tau tangles—clumps that damage and kill brain cells over time, leading to memory loss and confusion.
But this new research shows that newborns—especially premature ones—have even higher levels of p-tau217 in their blood than people with Alzheimer’s. Importantly, these infants do not have any signs of disease. In fact, in babies, high p-tau217 appears to be part of a healthy, natural process that helps the brain develop.
The study analyzed blood samples from over 400 individuals, ranging from premature and full-term newborns to young adults, older adults, and those with Alzheimer’s.
It found that p-tau217 levels are highest just after birth and gradually decline over the first few months of life, eventually reaching stable adult levels. This is the first time p-tau217 has been measured in the blood of human newborns, giving researchers a valuable look into its role in early brain development.
What makes this finding so remarkable is how differently the same protein behaves in different stages of life. In Alzheimer’s patients, p-tau217 is linked to brain cell breakdown. But in babies, it likely helps neurons grow, connect, and shape the young brain. Researchers believe this dual nature could reveal new ways to protect the brain against aging-related damage.
Dr. Fernando Gonzalez-Ortiz, the study’s lead author, explained that the newborn brain might have a natural way of managing or neutralizing tau, allowing it to function safely during rapid development. This protective system could be lost with age, which may explain why tau becomes harmful in older brains.
“If we can understand how newborns manage high tau levels without any damage, we may be able to recreate that protection later in life,” Gonzalez-Ortiz said. “That could lead to new treatments for Alzheimer’s disease.”
The study also found that the earlier a baby is born, the higher their p-tau217 levels tend to be. This suggests that the protein may play a role in helping the brain catch up in development when it’s under pressure, such as after a premature birth.
These findings challenge the idea that amyloid plaques are the main cause of p-tau217 increases. While plaques may drive p-tau217 in Alzheimer’s, that clearly isn’t the case in babies—pointing to the possibility that multiple pathways, not just amyloid, influence how tau behaves in the brain.
Given that p-tau217 has now been approved by the U.S. FDA as a tool for diagnosing Alzheimer’s, understanding what causes its rise—and what it truly means—is more important than ever. This study suggests doctors and researchers may need to consider age and context more carefully when interpreting high p-tau217 levels.
Ultimately, the research opens up an intriguing possibility: by learning from how the infant brain safely uses p-tau217 to grow, scientists might discover ways to protect the aging brain from the same protein’s damaging effects. In this case, one molecule tells two very different stories—one about the beginning of life, and one about its later challenges.
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The research findings can be found in Brain Communications.
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