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IC‐P‐182: Association Between TAU Deposition and Retrospective Amyloid Accumulation Rates in Early Symptomatic Stages of Alzheimer's Disease
Author(s) -
Tosun Duygu,
Weiner Michael W.
Publication year - 2016
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.2016.06.213
Subject(s) - tauopathy , pittsburgh compound b , voxel , psychology , neurodegeneration , amyloid (mycology) , neuroscience , cognitive decline , medicine , nuclear medicine , cognition , disease , pathology , dementia , cognitive impairment , radiology
scores) using the control group as reference (Figure-1). To identify spatial patterns of abnormal AV-1451 and FDG voxels, we made binary maps of W-scores>1.65 (95 percentile in controls). We then compared mean W-scores, the spatial extent of abnormal voxels, and the overlap between AV-1451 and FDG in global gray matter and 6 cortical regions-of-interest (Mann-Whitney U-test for significance). To assess whether AV-1451W-scores were greater in hypometabolic regions, we performed a two-sample t-test comparing mean AV-1451W-scores (>1.65) inside versus outside of abnormal FDG voxels for each patient. Results:AV-1451 and FDG patterns showed striking overlap across AD patients, with highest W-scores in lateral temporoparietal and medial parietal cortices (Figure-2). Globally, mean W-scores were greater for AV-1451 (8.1963.31) than FDG (1.6360.37, p<0.001; Figure-3A), and the spatial extent of abnormal AV-1451 voxels (78.8613.4%) exceeded FDG (34.2614.3%, p<0.001; Figure-3B). Most voxels with reduced FDG also had elevated AV-1451 (89.7612.6%), while only a minority of elevated AV-1451 voxels had reduced FDG (39.1616.2%, p<0.001; Figure-3C). These results were mirrored across regions-of-interest (Table-2). Among voxels with increased AV-1451, mean AV-1451 W-scores were greater inside (12.9065.02) versus outside (7.0562.79) of hypometabolic regions in 22/22 patients (t1⁄44.78, p<0.001). Conclusions:Our results support a model in which tau pathology precedes neurodegeneration. The widespread extent of elevated AV-1451 suggests the presence of tau pathology throughout cortex in AD patients, whereas hypometabolism was more constrained to temporoparietal regions with especially high AV-1451 uptake. These regions may be vulnerable to early development or converging spread of tau pathology across the AD clinical spectrum.