Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease.

ABSTRACT: This study was designed to test the interaction between amyloid-β and tau proteins as a determinant of metabolic decline in preclinical Alzheimer's disease (AD). We assessed 120 cognitively normal individuals with [¹⁸F]florbetapir positron emission tomography (PET) and cerebrospinal fluid (CSF) measurements at baseline, as well as [¹⁸F]fluorodeoxyglucose ([¹⁸F]FDG) PET at baseline and at 24 months. A voxel-based interaction model was built to test the associations between continuous measurements of CSF biomarkers, [¹⁸F]florbetapir and [¹⁸F]FDG standardized uptake value ratios (SUVR). We found that the synergistic interaction between [¹⁸F]florbetapir SUVR and CSF phosphorylated tau (p-tau) measurements, rather than the sum of

SUBMITTER: Pascoal TA 

PROVIDER: S-EPMC5262471 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature