Diagnostic accuracy
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
Open access · cc by · source: Europe PMC
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity (mean AUC 0.96) better than p-tau181/231 and similarly to CSF p-tau217 (AUC 0.95).
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
A clinic plasma panel plus genetics can discriminate clinical AD from older controls without being autopsy-confirmed diagnosis.
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
Scope note — PET amyloid/tau positivity in a memory clinic — not clinical-diagnosis AUC vs older controls
Limits the claim's scope: a different population, assay, or outcome.
Plasma p-tau217 can match CSF p-tau217 for PET amyloid/tau status in a memory clinic.
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity with mean AUC 0.96, outperforming plasma p-tau181/231 (AUC 0.76/0.79) and similar to CSF p-tau217 (AUC 0.95). CSF n was only 36.
Evidence for the claim as stated.
Nilvadipine did not slow mild-to-moderate Alzheimer disease over 78 weeks.
In 511 people with mild-to-moderate AD, 8 mg nilvadipine daily for 78 weeks was no better than placebo on ADAS-Cog 12 (p=0.465; 9.41 vs 9.63 point decline). CDR-sb and disability scores were also null; adverse events were more common on drug.
Scope note — biomarker PET accuracy is not a treatment-effect trial
Limits the claim's scope: a different population, assay, or outcome.
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
Evidence for the claim as stated.
Comparing candidates in the same participants is what makes the ranking meaningful.
A head-to-head comparison separated markers that single-marker studies report as similar. Plasma and CSF p-tau217 correlated more strongly with amyloid and tau PET (r = 0.64 to 0.83) than p-tau181 or p-tau231, and plasma p-tau217 reached mean AUC 0.96 against 0.76 and 0.79.
Evidence for the claim as stated.
How much a validation study can claim depends on its sample and its cut-offs, and these differ by an order of magnitude. The p-tau comparison rests on a single memory clinic with cohort-specific thresholds and only 36 CSF samples, while the frailty index draws on a large cohort but reports AUCs around 0.75 that its authors say are not bedside tests.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
How much a validation study can claim depends on its sample and its cut-offs, and these differ by an order of magnitude. The p-tau comparison rests on a single memory clinic with cohort-specific thresholds and only 36 CSF samples, while the frailty index draws on a large cohort but reports AUCs around 0.75 that its authors say are not bedside tests.
History
When this study was placed
Dated entries from the concept change log — when this paper was added or removed as support, challenge, or qualifier on a claim.
Placed as a scope qualifier on Alzheimer’s and MCI markers
In the AD Cardiff Cohort (1,439 clinical AD cases, 508 older controls), plasma Aβ40/42, P-tau181, NfL, and GFAP plus APOE-ε4 and polygenic risk reached AUC 0.81. Aβ-related peptides were lower in cases; P-tau181, NfL, and GFAP were higher. Case-only GWAS linked the Aβ42/Aβ40 ratio to WWOX and COPG2. Authors note ~25% of clinical AD lack AD pathology at autopsy.
Placed as supporting evidence on Alzheimer’s and MCI markers
In 114 Geneva memory-clinic patients, plasma p-tau217 identified amyloid/tau PET positivity with mean AUC 0.96, outperforming plasma p-tau181/231 (AUC 0.76/0.79) and similar to CSF p-tau217 (AUC 0.95). CSF n was only 36.
Placed as a scope qualifier on Alzheimer’s and MCI markers
In 511 people with mild-to-moderate AD, 8 mg nilvadipine daily for 78 weeks was no better than placebo on ADAS-Cog 12 (p=0.465; 9.41 vs 9.63 point decline). CDR-sb and disability scores were also null; adverse events were more common on drug.
Placed as supporting evidence on Alzheimer’s and MCI markers
PET-confirmed p-tau217 accuracy, a null nilvadipine AD RCT, and gabapentinoid dementia incidence answer different questions. A high diagnostic AUC does not imply a drug will slow ADAS-Cog, and claims associations are not trial evidence.
Study at a glance
- Design
- Cross-sectional — Head-to-head diagnostic-accuracy study of plasma and CSF p-tau217 vs p-tau181 and p-tau231 against amyloid- and tau-PET in a Geneva memory-clinic cohort.
- N
- N=114 · 114 participants (CU 33, MCI 67, dementia 14); CSF subset n=36.
- Population
- Memory-clinic patients at Geneva University Hospitals spanning cognitively unimpaired, MCI, and dementia.
- Outcome
- Correlation with A/T-PET, group effect sizes, and ROC AUC for amyloid- and tau-PET positivity.
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Is plasma p-tau217 as useful as CSF for Alzheimer PET positivity?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
114 participants: CU 33, MCI 67, dementia 14.
The study included 114 participants (CU = 33; MCI = 67; Dementia = 14).
Plasma p-tau217 mean AUC for A/T-PET positivity was 0.96 vs 0.76 and 0.79.
ROC curves to identify A-PET and T-PET positivity (AUC average : p -tau217 = 0.96; p -tau181 = 0.76; p -tau231 = 0.79)
Key findings
Plasma/CSF p-tau217 correlated more strongly with A- and T-PET (r 0.64–0.83) than p-tau181 or p-tau231. Plasma p-tau217 had larger group δ (0.55–0.96) and mean AUC 0.96 vs 0.76 (181) and 0.79 (231). CSF p-tau217 AUC 0.95 did not significantly beat CSF 181/231 (0.88/0.89). Authors conclude plasma p-tau217 performed like CSF and could reduce invasive testing.
Methodology
Correlated plasma and CSF p-tau217/181/231 with continuous amyloid- and tau-PET, compared effect sizes across diagnosis and A/T groups, and ran ROC analyses for PET positivity.
Limitations
CSF n=36 is too small for a firm plasma-vs-CSF contest, and cohort-specific cut-offs plus a single memory clinic limit transportability.
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