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Purpose <p>Amyloid positron emission tomography (PET) is central to the biological diagnosis and staging of Alzheimer’s disease (AD), yet longitudinal data for [¹⁸F]Florapronol remain limited. We evaluated whether baseline [¹⁸F]Florapronol amyloid burden is associated with 4-year [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG) metabolic neurodegeneration in amnestic mild cognitive impairment (MCI).</p> Methods <p>Twenty-nine patients with amnestic MCI were enrolled; 16 (55.2%) completed 4-year follow-up (amyloid-positive [Aβ+]: <i>n</i> = 7; amyloid-negative [Aβ–]: <i>n</i> = 9). All underwent baseline [¹⁸F]Florapronol PET, [¹⁸F]FDG PET, and cognitive testing; [¹⁸F]FDG PET and the Korean Mini-Mental State Examination (K-MMSE) were repeated at 2 and 4 years. Associations were assessed with correlation analyses and age-adjusted regression; conversion analyses were exploratory.</p> Results <p>All 7 Aβ + completers were A + N+ (amyloid- and neurodegeneration-positive) at baseline. Over 4 years, Aβ + completers showed greater decline in [¹⁸F]FDG standardized uptake value ratio (SUVR) than Aβ– completers (median − 0.170 SUVR; <i>p</i> = 0.016) and greater K-MMSE decline (median − 5.0; <i>p</i> = 0.031). Higher baseline [¹⁸F]Florapronol SUVR was associated with lower 4-year [¹⁸F]FDG SUVR after age adjustment (partial <i>r</i> = − 0.909, <i>p</i> &lt; 0.001) and with faster annualized [¹⁸F]FDG decline after adjustment for baseline [¹⁸F]FDG (partial <i>r</i> = − 0.734, <i>p</i> = 0.001). All 5 converters to AD dementia were Aβ + .</p> Conclusion <p>In this A + N+-enriched amnestic MCI cohort, baseline [¹⁸F]Florapronol amyloid burden was associated with 4-year [¹⁸F]FDG metabolic decline and showed descriptively higher specificity for AD dementia conversion than [¹⁸F]FDG visual positivity. Multicenter validation with tau biomarkers, apolipoprotein E genotyping, and Centiloid calibration is required before clinical use.</p>

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[18F]Florapronol (Alzavue®) Amyloid Burden and 4-Year [18F]FDG Metabolic Neurodegeneration in Amnestic Mild Cognitive Impairment

  • 期刊论文

  • 发表日期：

    2026年7月31日

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  • Su Yeon Park,
  • Inki Lee,
  • Ilhan Lim,
  • Byung Il Kim,
  • Dae Yoon Chi,
  • Byeong Hyeon Byeon,
  • Jeong Ho Ha

摘要

Purpose

Amyloid positron emission tomography (PET) is central to the biological diagnosis and staging of Alzheimer’s disease (AD), yet longitudinal data for [¹⁸F]Florapronol remain limited. We evaluated whether baseline [¹⁸F]Florapronol amyloid burden is associated with 4-year [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG) metabolic neurodegeneration in amnestic mild cognitive impairment (MCI).

Methods

Twenty-nine patients with amnestic MCI were enrolled; 16 (55.2%) completed 4-year follow-up (amyloid-positive [Aβ+]: n = 7; amyloid-negative [Aβ–]: n = 9). All underwent baseline [¹⁸F]Florapronol PET, [¹⁸F]FDG PET, and cognitive testing; [¹⁸F]FDG PET and the Korean Mini-Mental State Examination (K-MMSE) were repeated at 2 and 4 years. Associations were assessed with correlation analyses and age-adjusted regression; conversion analyses were exploratory.

Results

All 7 Aβ + completers were A + N+ (amyloid- and neurodegeneration-positive) at baseline. Over 4 years, Aβ + completers showed greater decline in [¹⁸F]FDG standardized uptake value ratio (SUVR) than Aβ– completers (median − 0.170 SUVR; p = 0.016) and greater K-MMSE decline (median − 5.0; p = 0.031). Higher baseline [¹⁸F]Florapronol SUVR was associated with lower 4-year [¹⁸F]FDG SUVR after age adjustment (partial r = − 0.909, p < 0.001) and with faster annualized [¹⁸F]FDG decline after adjustment for baseline [¹⁸F]FDG (partial r = − 0.734, p = 0.001). All 5 converters to AD dementia were Aβ + .

Conclusion

In this A + N+-enriched amnestic MCI cohort, baseline [¹⁸F]Florapronol amyloid burden was associated with 4-year [¹⁸F]FDG metabolic decline and showed descriptively higher specificity for AD dementia conversion than [¹⁸F]FDG visual positivity. Multicenter validation with tau biomarkers, apolipoprotein E genotyping, and Centiloid calibration is required before clinical use.