Alzheimer’s Marker Found in Newborns: What Does It Mean?
Recent research has revealed surprisingly high levels of the Alzheimer’s disease biomarker pTau217 in newborns, peaking around the fourth to fifth month of pregnancy and decreasing to roughly half its concentration by six months after birth. This finding, while initially concerning, is prompting scientists to re-evaluate our understanding of tau protein function and its role in neurological health.
The study analyzed various proteins in blood samples across different age groups. While pTau217 was elevated in newborns, levels of beta-amyloid were lower in newborns compared to older participants.Another protein, neurofilament light chain (NFL), often associated with brain injury, was also increased in newborns relative to adolescents and adults, though not to the same extent as seen in older individuals. Researchers suggest this elevated NFL in infants might potentially be linked to normal brain development and the physical stress of birth, especially vaginal delivery, wich can cause cranial compression.
The presence of pTau217 is notable given its established connection to both beta-amyloid pathology in Alzheimer’s disease and its elevation in rare neurological conditions like Creutzfeldt-Jakob disease, Niemann-Pick disease type C, and ALS. Certain mutations in the tau gene are also known to increase pTau217 concentration. Previous research has documented extensive tau phosphorylation – a modification of the protein – within the developing brain, though babies do not exhibit the same protein clumps seen in older Alzheimer’s patients, despite the presence of similarly modified tau proteins.
Interestingly,the fetal brain utilizes a unique fetal isoform of tau,differing from the six isoforms typically found in the adult brain. This fetal isoform may play a protective role during development, possibly preventing the protein aggregations that contribute to toxicity in older adults. Further investigation is needed to confirm this hypothesis.
The research also points to the potential for reversibility in tau hyperphosphorylation. Studies on hibernating ground squirrels and black bears demonstrate that increased tau phosphorylation occurs during hibernation and reverses upon awakening, suggesting a protective function during periods of metabolic stress. Similarly, anesthesia in mice can induce tau phosphorylation, a change that is generally reversible unless repeated anesthesia is administered.
The study underscores the complexity of Alzheimer’s disease biology. A positive pTau217 test result in a newborn does not equate to a future Alzheimer’s diagnosis. However, continued research into tau protein dynamics and the mechanisms that reverse its modifications could pave the way for novel therapeutic strategies.
