RT Journal Article SR Electronic T1 FDG and amyloid PET reflect the neuropathological staging schemes of Braak and Thal JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 281 OP 281 VO 61 IS supplement 1 A1 Ganna Blazhenets A1 Lars Frings A1 Arnd Sorensen A1 Philipp Meyer YR 2020 UL http://jnm.snmjournals.org/content/61/supplement_1/281.abstract AB 281Introduction: We recently applied principal components analyses to amyloid and FDG PET data to identify so-called Alzheimer’s dementia conversion-related covariance patterns of amyloid load (Aβ-ADCRP) and regional glucose metabolism (FDG-ADCRP) which significantly predict conversion to Alzheimer’s disease (AD) dementia in patients with mild cognitive impairment (MCI) (1,2). Here, we validate these patterns against neuropathological data as expressed by Thal and Braak staging schemes of amyloid-beta plaques and neurofibrillary tau tangles (probably driving regional degeneration and hypometabolism), respectively. Methods: We included a group of ADNI patients who underwent autopsy examination (as of October 2019) and for whom amyloid PET with AV45 (n = 22) and FDG PET (n = 38) scans were available. We compared the pathologic findings as reported in the ADNI database according to Thal and Braak stages to the pattern expression scores (PES) of the Aβ-ADCRP and FDG-ADCRP, respectively. The relationship between neuroimaging biomarkers and neuropathological schemes (Thal phase vs. amyloid PET and Braak stage vs. FDG PET) was assessed by constructing a generalized linear model controlled for the time span between PET examination and death, age at PET, and years of education. Results: The most frequent primary pathologic diagnoses were AD neuropathological change (n = 31.82 %). We observed a highly significant association between PES of Aβ-ADCRP and Thal amyloid phase (R2 = 0.59; t value [PES of Aβ-ADCRP] = 5.44, p =2×10-5) that was even stronger when adjusted for time span between amyloid PET acquisition date and death (R2 = 0.69; t value [PES of Aβ-ADCRP] = 5.92, p = 1×10-5). The PES of FDG-ADCRP showed a significant correlation to Braak stage of neurofibrillary tangles (R2 = 0.27; t value [PES of FDG-ADCRP] = 3.61, p = 9×10-4) that was considerably strengthened (R2 = 0.46; t value [PES of FDG-ADCRP] = 4.57, p = 6×10-5) by taking into account the time to death and influence of individuals’ education [Years of education, age at PET, years of education × age at PET]. Conclusions: This study shows that the PES of Aβ-ADCRP is a valid biomarker of underlying amyloid pathology, as demonstrated by its strong correlation with the Thal amyloid phase. The PES of FDG-ADCRP showed good correspondence with the Braak tangle stage and, therefore, the coherence between neurodegeneration and the distribution of tau pathology. References: 1. Blazhenets G, Ma Y, Sorensen A, et al. Principal Components Analysis of Brain Metabolism Predicts Development of Alzheimer Dementia. J Nucl Med. 2019;60:837-843. 2. Blazhenets G, Ma Y, Sorensen A, et al. Predictive Value of (18)F-Florbetapir and (18)F-FDG PET for Conversion from Mild Cognitive Impairment to Alzheimer Dementia. J Nucl Med. 2019.