🧠 Why Newborns Have Higher Alzheimer’s Biomarker Levels Than Adults
Groundbreaking Study Reveals Unexpected Role of p‑tau217 in Infant Brain Development
A new international study published in Brain Communications has turned conventional wisdom on its head: newborns, especially premature ones, have higher levels of phosphorylated tau217 (p‑tau217) in their blood than even patients with Alzheimer’s disease (AD).
Tau proteins, mainly when phosphorylated at specific sites like threonine-217, are well-known as biomarkers for Alzheimer’s, helping detect the disease even in its early stages. But this new research, involving over 460 participants across four cohorts, shows that p‑tau217 may serve a completely different purpose in healthy babies. The Study Find?
- Newborns had p‑tau217 levels up to 3x higher than Alzheimer’s patients.
- Premature infants (<28 weeks of gestation) had the highest levels.
- These levels declined naturally over the first 3–4 months of life.
- No signs of neurodegeneration were found in these infants, meaning the high p‑tau217 levels are likely physiological, not pathological.
🧪 What Is p‑tau217?
p‑tau217 is a phosphorylated form of tau, a protein critical for stabilizing neurons. In Alzheimer’s, tau becomes abnormally phosphorylated and aggregates into tangles, contributing to neurodegeneration. However, in the developing brain, phosphorylation appears to aid in neural growth and synaptic plasticity.
👶 Why Is It Elevated in Newborns?
The researchers suggest that:
- In the fetal and neonatal brain, p‑tau217 is involved in microtubule dynamics, which are essential for forming connections between neurons.
- The high early-life levels may reflect intense neurodevelopmental activity rather than disease.
- Newborns may have natural protective mechanisms that prevent tau from aggregating into toxic forms — mechanisms that could inspire new Alzheimer’s treatments.
🧩 What Makes This Study Unique?
✅ First study to directly compare p‑tau217 in:
- Healthy newborns (term and preterm)
- Alzheimer’s patients
- Age-stratified healthy controls (teens, adults, elderly)
✅ Multicenter design: Sweden, Australia, Spain, Norway
✅ Longitudinal tracking of premature infants over 133 days
💡 Implications for Alzheimer’s Research
This study provides vital insights into:
- The non-pathological role of tau phosphorylation in early life.
- Why high p‑tau217 doesn’t cause problems in infants.
- How these natural mechanisms might be mimicked in adult therapies to prevent or slow Alzheimer’s progression.

📈 Fast Facts
Group | Mean p‑tau217 (pg/mL) |
---|---|
Healthy newborns (term) | 10.2 |
Premature newborns | Up to 14.0 |
Alzheimer’s patients | 3.7 |
Teenagers | 1.8 |
Young adults | 1.3 |
Older adults (healthy) | 1.8 |
Alzheimer's Disease vs. Infant Brain: p-tau217 |
---|
Aspect | Alzheimer’s Brain (Older Adults) | Newborn/Infant Brain |
---|---|---|
p‑tau217 Level (Blood) | Moderately elevated (avg. ~3.7 pg/mL) | Very high (avg. ~10.2 pg/mL in term infants; even higher in preterm) |
Function of p‑tau217 | Pathological: contributes to tau aggregation, tangle formation, and neurodegeneration | Physiological: supports neurodevelopment, synaptic plasticity, and microtubule dynamics |
Tau Aggregation | Abnormal phosphorylation leads to neurofibrillary tangles and cell death | No aggregation or tangles despite high p‑tau217 |
Clinical Outcome | Cognitive decline, memory loss, dementia | Normal brain development, neuronal growth |
Phosphorylation Role | Abnormal, persistent, amyloid-linked | Transient, developmental regulation |
Protective Mechanisms | Impaired tau clearance, accumulation of toxic tau | Likely robust clearance and protective mechanisms preventing aggregation |
Associated Conditions | Alzheimer’s disease and other tauopathies | Normal neonatal physiology may reflect brain plasticity |
Decline Over Time | No natural decline -levels increase with disease progression | Natural decline to adult levels over the first few months of life |
🧬 Final Thought
Nature may already hold the key to Alzheimer’s prevention - hidden in the biology of our earliest days.
As researchers dive deeper, understanding how infants’ brains handle p‑tau217 could unlock new, safer therapies for neurodegenerative diseases.
🔗 Source: Gonzalez-Ortiz et al., Brain Communications, 2025 DOI: 10.1093/braincomms/fcaf221
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