Background <p>Plasma p-tau217 is a promising biomarker for detecting incipient AD pathology, but direct comparison of different p-tau217 assays in community-based cohorts are limited.</p> Methods <p>We evaluated two cohorts from southwestern Pennsylvania, USA; the MYHAT-NI study, which included two-year longitudinal follow-up neuroimaging assessments of Aβ, tau, and cortical thickness; and the Human Connectome Project/CoBRA cohort, targeting a 50:50 split of self-identified Black and non-Hispanic White individuals. Plasma p-tau217 was measured using four different assays: Lumipulse, Johnson &amp; Johnson, ALZpath, and NULISA. Aβ and tau pathologies were assessed with [<sup>11</sup>C]PiB PET and [<sup>18</sup>F]Flortaucipir PET, respectively. Clinical Dementia Rating and Montreal Cognitive Assessment were used to assess cognitive performance.</p> Results <p>We included 344 participants (MYHAT-NI: <i>n</i> = 111, median age 76 [IQR: 72–80], 54% female; HCP/CoBRA: <i>n</i> = 234, median age 62 [IQR: 52–70], 65% female). All four p-tau217 assays exhibited moderate to strong cross-platform correlations (Spearman correlations of 0.40–0.86), and statistically equivalent AUCs (of 0.84–0.90) for determining Aβ positivity.</p> Conclusions <p>Our findings show strong equivalent performances of plasma p-tau217 assays to identify amyloid positivity across two highly diverse cohorts of community-dwelling older adults.</p>

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Head-to-head comparison of plasma p-tau217 immunoassays for incipient Alzheimer’s disease in community cohorts

  • Rebecca A. Deek,
  • Wasiu G. Balogun,
  • Xuemei Zeng,
  • Gallen Triana-Baltzer,
  • Tharick A. Pascoal,
  • Hartmuth C. Kolb,
  • Beth Snitz,
  • Ann D. Cohen,
  • Thomas K. Karikari

摘要

Background

Plasma p-tau217 is a promising biomarker for detecting incipient AD pathology, but direct comparison of different p-tau217 assays in community-based cohorts are limited.

Methods

We evaluated two cohorts from southwestern Pennsylvania, USA; the MYHAT-NI study, which included two-year longitudinal follow-up neuroimaging assessments of Aβ, tau, and cortical thickness; and the Human Connectome Project/CoBRA cohort, targeting a 50:50 split of self-identified Black and non-Hispanic White individuals. Plasma p-tau217 was measured using four different assays: Lumipulse, Johnson & Johnson, ALZpath, and NULISA. Aβ and tau pathologies were assessed with [11C]PiB PET and [18F]Flortaucipir PET, respectively. Clinical Dementia Rating and Montreal Cognitive Assessment were used to assess cognitive performance.

Results

We included 344 participants (MYHAT-NI: n = 111, median age 76 [IQR: 72–80], 54% female; HCP/CoBRA: n = 234, median age 62 [IQR: 52–70], 65% female). All four p-tau217 assays exhibited moderate to strong cross-platform correlations (Spearman correlations of 0.40–0.86), and statistically equivalent AUCs (of 0.84–0.90) for determining Aβ positivity.

Conclusions

Our findings show strong equivalent performances of plasma p-tau217 assays to identify amyloid positivity across two highly diverse cohorts of community-dwelling older adults.