# Plasma p‐tau217 for Alzheimer's disease diagnosis: a memory clinic implementation approach

**Authors:** Giorgia Brodini, Fausto Roveta, Alberto Mario Chiarandon, Silvia Boschi, Lucrezia Bonino, Elisa Maria Piella, Aurora Cermelli, Selene Limoncelli, Giulia Gioiello, Michela Zotta, Adriana Lesca, Giulio Mengozzi, Silvia Morbelli, Innocenzo Rainero, Elisa Rubino

PMC · DOI: 10.1002/dad2.70286 · Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring · 2026-02-24

## TL;DR

This study shows that plasma p-tau217 can accurately detect Alzheimer's disease in memory clinics and could reduce the need for spinal taps.

## Contribution

The paper introduces a practical workflow for integrating plasma p-tau217 into memory clinic diagnostics and validates its clinical utility.

## Key findings

- Plasma p-tau217 distinguished amyloid-positive from amyloid-negative individuals with high accuracy.
- A dual cut-off strategy could reduce lumbar punctures by 65% in clinical practice.
- Neurofilament light chain (NfL) levels were elevated in non-AD neurodegenerative disorders.

## Abstract

Plasma phosphorylated tau at threonine 217 (p‐tau217) has shown excellent diagnostic performance for Alzheimer's disease (AD), yet real‐world validation and implementation pathways remain limited. This study assessed its clinical applicability and proposed a practical workflow for memory clinics.

Plasma p‐tau217, p‐tau181, and neurofilament light chain (NfL) were quantified in consecutive patients referred for cognitive assessment. Cerebrospinal fluid (CSF) amyloid beta (Aβ) 42/40 defined amyloid (A) status, and final etiological diagnoses were reached through multidisciplinary consensus integrating clinical, neuropsychological, and metabolic imaging data.

Among 163 patients (mean age 69.3 ± 7.4 years, 52% female), plasma p‐tau217 distinguished A+ from A− individuals (area under the curve [AUC] 0.90, 81% sensitivity, 91% specificity). AD patients showed the highest p‐tau217 levels, while non‐AD neurodegenerative disorders exhibited elevated NfL (p < 0.001). A dual cut‐off strategy with 95% sensitivity and specificity could have avoided 65% of lumbar punctures.

Plasma p‐tau217 demonstrated robust clinical validity and supports structured integration into routine diagnostic pathways.

Plasma p‐tau217 was evaluated in a real‐world unselected memory‐clinic population.Plasma p‐tau217 accurately identified CSF amyloid pathology.A dual 95% sensitivity/specificity cut‐off strategy could have reduced lumbar punctures by 65%.P‐tau217 supported AD diagnosis, while NfL indicated non‐AD neurodegeneration.A biomarker‐driven workflow was defined for clinical implementation in memory clinics.

Plasma p‐tau217 was evaluated in a real‐world unselected memory‐clinic population.

Plasma p‐tau217 accurately identified CSF amyloid pathology.

A dual 95% sensitivity/specificity cut‐off strategy could have reduced lumbar punctures by 65%.

P‐tau217 supported AD diagnosis, while NfL indicated non‐AD neurodegeneration.

A biomarker‐driven workflow was defined for clinical implementation in memory clinics.

## Linked entities

- **Diseases:** Alzheimer's disease (MONDO:0004975)

## Full-text entities

- **Genes:** APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, NEFL (neurofilament light chain) [NCBI Gene 4747] {aka CMT1F, CMT2E, CMTDIG, NF-L, NF68, NFL}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, CSF2 (colony stimulating factor 2) [NCBI Gene 1437] {aka CSF, GMCSF}
- **Diseases:** parkinsonian syndromes (MESH:D020734), NND (MESH:D019636), RESEARCH (MESH:D014947), primary progressive aphasia (MESH:D018888), corticobasal syndrome (MESH:D000088282), AD (MESH:D000544), MCI (MESH:D060825), dementia with Lewy bodies (MESH:D020961), prion disease (MESH:D017096), obesity (MESH:D009765), neurocognitive disorders (MESH:D019965), FTLD (MESH:D057174), A/T (MESH:D001260), amyloidosis (MESH:D000686), amyloid (MESH:C000718787), Dementia (MESH:D003704), frontotemporal dementia (MESH:D057180), progressive supranuclear palsy (MESH:D013494), axonal damage (MESH:D001480), Cognitive Disorders (MESH:D003072)
- **Chemicals:** EDTA (MESH:D004492), FDG (MESH:D019788)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932973/full.md

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Source: https://tomesphere.com/paper/PMC12932973