Key result
Simoa Ptau181/Aβ42 and Lumipulse Ptau181/Aβ42 showed comparable diagnostic accuracy for Alzheimer's disease (AUC 0.739 and 0.733, respectively), though both were weaker than CSF biomarkers.
Why the study?
Recent studies showed plasma biomarkers related to amyloid, tau, and neurodegeneration could potentially identify pathological features of AD, prompting a comparison of clinical and analytical performance across platforms.
Does the Simoa platform provide comparable diagnostic accuracy to the Lumipulse platform for measuring plasma AD biomarkers in patients with cognitive impairment?
Cross-Sectional (n=127)
Does the Simoa platform provide comparable diagnostic accuracy to the Lumipulse platform for measuring plasma AD biomarkers in patients with cognitive impairment?
Effect estimate: AUC 0.739 (95% CI 0.592-0.887)
Both Simoa and Lumipulse platforms show comparable performance for plasma AD biomarkers, particularly Ptau181/Aβ42, which may be useful for screening to reduce lumbar punctures, though they remain inferior to CSF biomarkers.
Plasma p-tau181/Aβ42 ratios perform similarly on both platforms in MCI; leaves open whether plasma assays can supplant CSF testing.
Background Alzheimer’s disease (AD) plasma biomarkers related to amyloid (A), tau (T), and neurodegeneration (N) can potentially be used to identify these pathological features of the disease, as shown in recent studies. Our objective was to compare the clinical and analytical performance of plasma AD biomarkers measured using the single‐molecule array (Simoa) and Lumipulse platforms. Method We quantified ATN and AT plasma biomarkers in 127 patients with mild cognitive impairment (MCI) (n = 81), AD (n = 30), and non‐AD dementia (n = 16) using a Simoa HD‐1/HD‐X analyser (Quanterix) and a Lumipulse G600II automated platform (Fujirebio Europe NV). Result We found a strong correlation between the Simoa and Lumipulse methods, although there were systematic differences between biomarker values measured by each method. Concerning the clinical diagnosis, Simoa Ptau181/Aβ42 (AUC 0.739, 95% CI 0.592–0.887) and Lumipulse Aβ42 and Ptau181/Aβ42 (AUC 0.735, 95% CI 0.589–0.882 and AUC 0.733, 95% CI 0.567‐0.900) had the highest discriminating power. However, their power was significantly lower than that of CSF Aβ42/Aβ40, as measured by Lumipulse (AUC 0.879, 95% CI 0.766–0.992). Similarly, Simoa Ptau181 and Lumipulse Ptau181/Aβ42 were the markers most consistent with the CSF Aβ42/Aβ40 status (AUC 0.801, 95% CI 0.712–0.890 vs. AUC 0.870, 95% CI 0.806–0.934, respectively) at the ≥2.127 and ≥0.084 cut‐offs, respectively. Conclusion The Simoa and Lumipulse plasma AD assays showed comparable clinical and analytical performance. However, the performance of these biomarkers is weaker than that of CSF AD biomarkers. Interestingly, both platforms identify plasma Ptau181/Aβ42 as a promising biomarker for AD. At present, the analysed AD plasma biomarkers may be useful for screening to reduce the number of lumbar punctures in the clinical setting. However, the use of these markers as diagnostic tools requires further investigation.
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Piñol‐Ripoll et al. (2024) conducted a cross-sectional in Mild cognitive impairment, Alzheimer's disease, and non-AD dementia (n=127). Simoa platform for plasma AD biomarkers vs. Lumipulse platform for plasma AD biomarkers was evaluated on Discriminating power for clinical diagnosis (AUC 0.739, 95% CI 0.592-0.887). Simoa Ptau181/Aβ42 and Lumipulse Ptau181/Aβ42 showed comparable diagnostic accuracy for Alzheimer's disease (AUC 0.739 and 0.733, respectively), though both were weaker than CSF biomarkers.
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