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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

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Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy.

Annalise E Miner¹, Henrik Zetterberg^{2,3,4,5,6,7,8}, Kaj Blennow^2,4,8,9

¹Boston University CTE Center and Alzheimer's Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts.

JAMA Network Open

|July 13, 2026

Summary

Plasma phosphorylated tau 217 (p-tau217) is not ideal for detecting chronic traumatic encephalopathy (CTE) in individuals with repetitive head impacts (RHI). However, it can help rule out beta-amyloid (Aβ) pathology in those at risk for CTE.

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Nuclear Magnetic Resonance Spectroscopy for the Identification of Multiple Phosphorylations of Intrinsically Disordered Proteins

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Published on: December 27, 2016

Area of Science:

Neuroscience
Biomarker Discovery
Neuropathology

Background:

Repetitive head impacts (RHI) pose a risk for developing chronic traumatic encephalopathy (CTE).
In vivo biomarkers are needed for early detection of neuropathologies associated with RHI and CTE.
Current diagnostic methods for CTE are limited, necessitating the exploration of novel biomarkers.

Purpose of the Study:

To evaluate plasma phosphorylated tau 217 (p-tau217) as a potential biomarker for CTE.
To assess p-tau217's performance in detecting beta-amyloid (Aβ) pathology in individuals exposed to RHI.
To explore the concordance of plasma p-tau217 levels with postmortem CTE neuropathology.

Main Methods:

A longitudinal, multicenter, case-control study involving former American football players (cases) and unexposed asymptomatic men (controls).
Plasma p-tau217 levels were measured and classified as positive, intermediate, or negative.
Aβ-positron emission tomography (PET) and tau-PET imaging were utilized, alongside postmortem brain analyses in a subsample.

Main Results:

Plasma p-tau217 levels were higher in former football players compared to controls, correlating with Aβ-PET positivity.
Plasma p-tau217 showed similar performance to CSF biomarkers in predicting Aβ-PET positivity.
In postmortem analyses, p-tau217 showed concordance with Aβ-PET, but two cases with stage III CTE had normal p-tau217 levels.

Conclusions:

Plasma p-tau217 is unlikely to be a reliable biomarker for detecting CTE in individuals with RHI exposure.
Plasma p-tau217 demonstrates utility in ruling out Aβ pathology in individuals at risk for CTE.
Further research is needed to identify definitive in vivo biomarkers for CTE detection.