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Quantitative thresholds for 18 F‐florbetaben PET for the detection of low amyloid load
Author(s) -
RoéVellvé Núria,
Bullich Santiago,
Marquie Marta,
Barthel Henryk,
Villemagne Victor LL,
Sanabria Angela,
Tartari Juan Pablo,
SotolongoGrau Oscar,
Dore Vincent,
Koglin Norman,
Mueller Andre,
Perrotin Audrey,
Jovalekic Aleksandar,
de Santi Susan,
Tarraga Lluis,
Stephens Andrew W,
Rowe Christopher C,
Sabri Osama,
Seibyl John,
Boada Mercè
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042933
Subject(s) - cutoff , dementia , medicine , cognitive impairment , amyloid β , β amyloid , pathology , nuclear medicine , gastroenterology , alzheimer's disease , disease , physics , quantum mechanics
Background A pathology‐proven cutoff for NeuraCeq ( 18 F‐florbetaben) was previously developed in end‐of‐life cases to discriminate Alzheimer’s disease (AD) patients from elderly Aβ‐negative non‐demented controls (NDC). However, these cutoffs could be of limited use in early stages of AD. Here, we developed and validated 18 F‐florbetaben cutoffs to detect low Aβ deposition and established amyloid pathology. Method The low Aβ deposition threshold was derived from a sample of young healthy controls (YHC) (n=70, 27.6±5.1 y), as 2 standard deviations above the mean. The established pathology cutoff was derived using ROC curve analysis on a sample of visually determined Aβ‐negative NDC (n=62, 67.8±6.8 y) and Aβ‐positive AD dementia patients (n=62, 70.6±8.0 y). Validation was based on longitudinal samples: (1) subjective cognitive decline (SCD) volunteers (n=166; 64.9±7.2 y) and (2) mild cognitively impaired (MCI) subjects (n=45, 72.7 ± 6.5 y). The standard centiloid (CL)methodology was applied for quantification. Result The low Aβ‐deposition detection cutoff was 13.5 CL, and the threshold for established Aβ pathology was 35.7 CL. In the validation samples, the rate of Aβ accumulation in the “low amyloid load” interval (13.5‐35.7 CL) was significantly different from zero (p<0.05), (2.1±2.1 %/year (SCD), 2.6±1.5 %/year (MCI)), which was also observed for “established Aβ deposition” (>35.7 CL) (3.4±3.2 %/y (SCD), 1.4±1.8 %/y (MCI), (p<0.05)). The accumulation rate for Aβ‐negative subjects (<13.5 CL) was not significantly different from zero (‐0.1±1.1 %/year (SCD), 0.1±1.6 %/year (MCI)). Conclusion An interval between 13.5 and 35.7 CL is optimal for the detection of early Aβ deposition and to identify subjects that are likely accumulating Aβ. Further validation tests using additional samples are ongoing.