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O5‐02‐01: Brain and cognitive correlates of subjective cognitive decline differ between healthy elderly with and without β‐amyloid pathology
Author(s) -
Vogel Jacob W.,
Doležalová Monika Varga,
Joie Renaud,
Marks Shawn,
Fero Allison,
Landau Susan M.,
Schwimmer Henry,
Schreiber Stefanie,
Jagust William J.
Publication year - 2015
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 - 10.1016/j.jalz.2015.07.451
Subject(s) - pittsburgh compound b , cognitive decline , episodic memory , cognition , psychology , neuroimaging , medicine , positron emission tomography , effects of sleep deprivation on cognitive performance , alzheimer's disease neuroimaging initiative , alzheimer's disease , magnetic resonance imaging , dementia , neuroscience , disease , radiology
Figure 1. bined measures of amyloid and tau pathology predict subsequent hypometabolism in cognitively normal subjects.Methods: CN individuals (n1⁄4108) who had CSF total tau (t-tau), phospho-tau181p (p-tau), Ab1–42, [18F]FDG and [18F]Florbetapir measurements in baseline and 24 month follow-up were analyzed. Subjects were dichotomized using CSFAb1–42, t-tau and p-tau published cutoffs, and further divided in [18F]Florbetapir positive and negative. [18F] FDG and [18F]Florbetapir PET SUVRs were computed using the pons and cerebellum as reference regions, respectively. We tested our hypothesis using voxel-based linear model, which included 24 month [18F]FDG PET SUVR changes as a response variable and global [18F]Florbetapir PET SUVR, CSF Ab1–42, t-tau, ptau status as factors; model was corrected for age, gender and APOE4 status. Results:Were FDR corrected (p < 0.001). Table 1 summarizes the study demographics. Figure 1 shows areas in which metabolic declines in [F]FDG were predicted by the interaction of baseline p-tau and [F]Florbetapir PET status. [F]FDG SUVRs did not differ between the groups composed by the dichotomization of CSF p-tau and Global [F]Florbetapir PET. In contrast, the group with abnormal CSF p-tau and [F]Florbetapir PET status had 20-30% lower follow-up [F]FDG SUVRs mean in the mesial temporal structures. Voxel-based factorial using CSF Ab1–42 or t-tau values showed no significant results. Conclusions: The present results support the conceptual framework in which pathological levels of brain amyloidosis and hyperphosphorylated tau precedes metabolic declines in preclinical stages of AD. In fact, the regions displaying the highest rate of hypometabolism are confined to brain circuits vulnerable to early stages of tau pathology as described by Braak. The present data also support previous research indicating the coexistence of amyloid and ptau pathology as determinants of disease progression.