Newborns exhibit high levels of p-tau217, a protein linked to Alzheimer's disease. This unexpected finding challenges its exclusively toxic role.
An international study reveals that this biomarker, used to diagnose neurodegeneration, may actually contribute to brain development in infants. Researchers suggest its accumulation, harmful in adults, could be beneficial during early life stages.
A biomarker with two faces
P-tau217 is a modified version of the tau protein, essential for neuron stability. In Brain Communications, researchers show its increase in newborns even surpasses levels observed in Alzheimer's patients.
Preterm infants display the highest concentrations, with no signs of pathology. These levels gradually decrease after birth, even though they may reappear later in neurodegenerative diseases. The study thus highlights a dual role, dependent on life stage.
The analyses involve 462 participants, including healthy babies, preterm infants, healthy adults, and adults with Alzheimer's. The mechanisms regulating p-tau217 appear independent of beta-amyloid, another protein involved in Alzheimer's. This distinction opens new avenues for understanding its selective toxicity.
Therapeutic perspectives
Understanding why infant brains tolerate p-tau217 without damage could lead to new treatment approaches. Researchers plan to study newborns' natural protective mechanisms, absent in adults.
Clinical applications are promising, particularly for interpreting diagnostic tests recently approved by the FDA. Authors emphasize the need to distinguish pathological increases from developmental variations.
This research also reignites the debate on Alzheimer's causes by showing p-tau217 accumulation can occur without amyloid. Future studies will focus on factors triggering its toxicity with age.