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<p>We aimed to understand longitudinal associations between Alzheimer’s disease (AD) biomarkers in Autosomal Dominant AD (ADAD) across estimated years to symptom onset (EYO). Forty-five individuals (19 mutation carriers [EYO = −7.9 ± 11.7 years, <i>APP</i> N = 11; <i>PSEN1</i> N = 8]) from Swedish ADAD families participated. All received baseline 18F-Flurodeoxyglucose (FDG) PET and cognitive testing, and a subset (N = 26) plasma glial fibrillary acidic protein (GFAP) measurement. Follow-up data collection (including 106 FDG scans) was performed over 7.4 ± 6.4 years (visits ranged from 1–5, EYO = −25.8 to +10.3 years in mutation carriers). Mixed effects models were applied to determine longitudinal associations. <i>APP</i> and <i>PSEN1</i> mutation carriers showed different FDG uptake profiles from EYO = −20 to −10 years, with a hypermetabolism before hypometabolism in <i>PSEN1</i> mutation carriers. Early increases in plasma GFAP were primarily related to subcortical FDG decreases and cognitive changes in <i>APP</i> mutation carriers compared to non-carriers. We provide evidence for gene-dependent biomarker trajectories in ADAD.</p>

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Early functional changes and plasma GFAP in Swedish families with Autosomal Dominant Alzheimer’s disease mutations

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月27日

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  • Emma S. Luckett,
  • Mariola Zapater-Fajari,
  • Ove Almkvist,
  • Charlotte Johansson,
  • Konstantinos Chiotis,
  • Marco Bucci,
  • Anders Wall,
  • Nicholas J. Ashton,
  • Kaj Blennow,
  • Henrik Zetterberg,
  • Elena Rodriguez-Vieitez,
  • Caroline Graff,
  • Agneta Nordberg

摘要

We aimed to understand longitudinal associations between Alzheimer’s disease (AD) biomarkers in Autosomal Dominant AD (ADAD) across estimated years to symptom onset (EYO). Forty-five individuals (19 mutation carriers [EYO = −7.9 ± 11.7 years, APP N = 11; PSEN1 N = 8]) from Swedish ADAD families participated. All received baseline 18F-Flurodeoxyglucose (FDG) PET and cognitive testing, and a subset (N = 26) plasma glial fibrillary acidic protein (GFAP) measurement. Follow-up data collection (including 106 FDG scans) was performed over 7.4 ± 6.4 years (visits ranged from 1–5, EYO = −25.8 to +10.3 years in mutation carriers). Mixed effects models were applied to determine longitudinal associations. APP and PSEN1 mutation carriers showed different FDG uptake profiles from EYO = −20 to −10 years, with a hypermetabolism before hypometabolism in PSEN1 mutation carriers. Early increases in plasma GFAP were primarily related to subcortical FDG decreases and cognitive changes in APP mutation carriers compared to non-carriers. We provide evidence for gene-dependent biomarker trajectories in ADAD.