Tau-related reduction of glucose metabolism in mild cognitive impairment occurs independently of APOE ε4 genotype and is influenced by Aβ.

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Tác giả: Barry J Bedell, Felix Carbonell, Carolann McNicoll, Alex P Zijdenbos

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: United States : Alzheimer's & dementia : the journal of the Alzheimer's Association , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 655827

INTRODUCTION: Positron emission tomography (PET) imaging studies have shown that amyloid beta (Aβ) is significantly correlated with glucose metabolism in mild cognitive impairment independently of the apolipoprotein E (APOE) ε4 genotype. METHODS: We used a singular value decomposition (SVD) approach to pairwise cross-correlation among tau, Aβ, and fluorodeoxyglucose PET images. The resulting SVD-based tau and Aβ scores as well as the APOE ε4 genotype, were entered as predictors in a voxelwise general linear model for statistical assessment of their effect on FDG. RESULTS: We found cortical regions where a reduced glucose metabolism was maximally correlated with distributed patterns of tau, accounting for the effect of Aβ and APOE ε4 genotype. DISCUSSION: By highlighting the more significant role of tau, rather than Aβ, in the reduction of glucose metabolism, our results provide a better understanding of their combined effect in the development and progression of Alzheimer's disease. HIGHLIGHTS: This study uses a data-driven singular value decomposition approach to the cross-correlation matrix between tau and fluorodeoxyglucose (FDG) images, as well as between FDG and amyloid beta (Aβ) positron emission tomography (PET) images. From a population of mild cognitive impairment subjects, we found that spatially distributed scores of tau PET are associated with an even stronger reduction of glucose metabolism, independent of the apolipoprotein E ε4 genotype and confounded by Aβ. By highlighting the more significant role of tau, rather than Aβ, on the reduction of glucose metabolism, our results provide a better understanding of their combined effects in the development of Alzheimer's disease.
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