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Background <p>We aimed to develop individualized predictions for risk of developing any-cause dementia and Alzheimer’s disease (AD) dementia, in individuals with subjective cognitive decline (SCD) or mild cognitive impairment (MCI), using plasma phosphorylated-tau-181 (pTau181), phosphorylated-tau-217 (pTau217; in a subset), amyloid beta1-42/1–40 (Aβ42/40), glial fibrillary acidic protein (GFAP) and/or neurofilament light (NfL).</p> Methods <p>From the Amsterdam Dementia Cohort we included 314 individuals with SCD (age 61 ± 9&#xa0;years, <i>n</i> = 184 (59%) male, MMSE 29 ± 1) and 253 individuals with MCI (age 65 ± 7&#xa0;years, <i>n</i> = 165 (65%) male, MMSE 27 ± 2), who had annual follow-up (median duration 2.4&#xa0;years). Cox proportional hazards regression models were used to calculate probabilities for progression to dementia and were externally validated in MEMENTO and AIBL cohorts.</p> Results <p>During follow-up 20 SCD and 99 MCI patients developed dementia. For MCI patients who progressed to any form of dementia, plasma GFAP contributed on top of age, sex, and MMSE score in the parsimonious individualized prognostic model (C-index = 0.69 [95%CI = 0.63; 0.76]). With AD-dementia as the outcome, GFAP and pTau181 were selected in the parsimonious model on top of the demographic variables (C-index = 0.71 [95%CI = 0.65; 0.76]). In the subset of 197 MCI individuals with pTau217 measurements, pTau217 was selected in the parsimonious model on top of the demographic variables (C-index = 0.75 [95%CI = 0.69; 0.79]). External validation demonstrated that the models are robust in a memory clinic setting.</p> Conclusions <p>Our prediction models have utility for clinical practice to calculate progression probabilities for development of dementia in individual patients living with MCI over a 1-, 3- and 5-year time period.</p>

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Individualized prediction of clinical progression to dementia using plasma biomarkers in non-demented elderly

  • 期刊论文

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  • 发表日期：

    2025年12月3日

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  • Madison I. J. Honey,
  • Ingrid S. van Maurik,
  • Argonde C. van Harten,
  • Mariam Gouda,
  • Mardou van Leeuwenstijn,
  • Arenda Mank,
  • Calvin Trieu,
  • Vincent Bouteloup,
  • Geneviève Chêne,
  • Isabelle Pellegrin,
  • Carole Dufouil,
  • James D. Doecke,
  • Christopher J. Fowler,
  • Colin L. Masters,
  • Yolande Pijnenburg,
  • David Wilson,
  • Wiesje M. van der Flier,
  • Charlotte E. Teunissen,
  • Inge M. W. Verberk

摘要

Background

We aimed to develop individualized predictions for risk of developing any-cause dementia and Alzheimer’s disease (AD) dementia, in individuals with subjective cognitive decline (SCD) or mild cognitive impairment (MCI), using plasma phosphorylated-tau-181 (pTau181), phosphorylated-tau-217 (pTau217; in a subset), amyloid beta1-42/1–40 (Aβ42/40), glial fibrillary acidic protein (GFAP) and/or neurofilament light (NfL).

Methods

From the Amsterdam Dementia Cohort we included 314 individuals with SCD (age 61 ± 9 years, n = 184 (59%) male, MMSE 29 ± 1) and 253 individuals with MCI (age 65 ± 7 years, n = 165 (65%) male, MMSE 27 ± 2), who had annual follow-up (median duration 2.4 years). Cox proportional hazards regression models were used to calculate probabilities for progression to dementia and were externally validated in MEMENTO and AIBL cohorts.

Results

During follow-up 20 SCD and 99 MCI patients developed dementia. For MCI patients who progressed to any form of dementia, plasma GFAP contributed on top of age, sex, and MMSE score in the parsimonious individualized prognostic model (C-index = 0.69 [95%CI = 0.63; 0.76]). With AD-dementia as the outcome, GFAP and pTau181 were selected in the parsimonious model on top of the demographic variables (C-index = 0.71 [95%CI = 0.65; 0.76]). In the subset of 197 MCI individuals with pTau217 measurements, pTau217 was selected in the parsimonious model on top of the demographic variables (C-index = 0.75 [95%CI = 0.69; 0.79]). External validation demonstrated that the models are robust in a memory clinic setting.

Conclusions

Our prediction models have utility for clinical practice to calculate progression probabilities for development of dementia in individual patients living with MCI over a 1-, 3- and 5-year time period.