p-tau217

check icon Optimal Result: 0 - 0.18 pg/mL.

p-tau217 is a form of the tau protein that’s phosphorylated at threonine 217. Rising levels in blood (plasma) or cerebrospinal fluid (CSF) reflect Alzheimer’s-type biology—in particular, the presence of amyloid plaques and tau changes in the brain. In head-to-head research, p-tau217 generally performs as well as or better than older phospho-tau markers (e.g., p-tau181) for identifying AD-type pathology.

Why it matters

  • Earlier, less-invasive insight: A blood test can help flag Alzheimer’s-consistent changes before or alongside imaging/CSF studies.

  • Better triage in memory workups: Results help determine who should proceed to confirmatory testing (e.g., amyloid PET, CSF biomarkers).

  • Clearer differential diagnosis: Elevated p-tau217 favors Alzheimer’s disease (AD) over many non-AD dementias when the clinical picture is mixed.

  • Therapy decisions: As disease-modifying treatments evolve, p-tau217 (often alongside Aβ42) supports eligibility decisions and baseline characterization.

When this test is useful

  • New or progressive memory and thinking changes under evaluation

  • Atypical presentations where AD vs. non-AD dementia is unclear

  • Establishing baseline biology prior to therapy discussions

  • Reducing the need for PET or lumbar puncture when pre-test probability is moderate to high

How to interpret your result

Always use the reference range and cutoffs on your own lab report. Assays and platforms are not interchangeable.

  • High p-tau217 (or high p-tau217/Aβ42 ratio): Increases the likelihood of AD-type amyloid/tau pathology. Your clinician may recommend confirmatory testing (amyloid PET or CSF) if results would change management.

  • Low p-tau217 (or low ratio): Makes AD-type pathology less likely at the time of testing. Your clinician may explore alternative causes of symptoms.

  • Borderline/indeterminate: Some labs use two cutoffs (“rule-in” / “rule-out”) with a gray zone. Borderline results often prompt repeat testing or confirmatory studies based on clinical judgment.

What can influence the number?

  • Assay & platform: Methods differ (immunoassay vs. mass spec), and cutoffs are assay-specific.

  • Clinical context: Acute illness, kidney/liver disease, or mixed neurodegenerative processes can complicate interpretation.

  • Preanalytical factors: Follow your lab’s guidance on collection and handling.

Related biomarkers often ordered together

  • Aβ42 (± Aβ40) and the p-tau217/Aβ42 ratio (improves discrimination)

  • p-tau181, p-tau231 (additional phospho-tau markers)

  • NfL (neurofilament light) (general neurodegeneration marker; not AD-specific)

  • Total tau, Aβ42/40 ratio, basic labs and imaging as clinically indicated

Limitations & caveats

  • Not a diagnosis by itself. p-tau217 indicates likelihood of AD-type pathology and must be interpreted with history, exam, cognitive testing, and—when needed—PET or CSF results.

  • Population/setting matter. Performance is strongest in symptomatic adults evaluated in specialty settings; routine screening of people without symptoms isn’t established.

  • Gray-zone results happen. A minority of tests are indeterminate and require follow-up.

FAQs

Is there a “normal range” for p-tau217?
Ranges and cutoffs are lab- and assay-specific. Always rely on the interval printed on your report rather than a generic value from another source.

How does p-tau217 compare with p-tau181?
Both track AD biology, but p-tau217 often shows higher diagnostic accuracy. Many centers now prefer p-tau217 when available.

Do I still need an amyloid PET or lumbar puncture?
Sometimes. p-tau217 can rule in or rule out AD-type pathology for many patients, but confirmatory testing may still be recommended when results are borderline, conflicting, or when confirmation would alter treatment.


What to do next

  1. Review your report’s reference interval/cutoff. Note the assay name if listed.

  2. Put your number in context. Combine p-tau217 with symptoms, cognitive testing, and other labs (Aβ42, p-tau217/Aβ42 ratio, NfL).

  3. Discuss follow-up. Ask your clinician whether results justify repeat testing, amyloid PET, or CSF biomarkers.

  4. Track over time. Re-testing may be useful if symptoms evolve or if initial results were borderline.

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