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IC‐P‐169: BDNF, Aβ, and cortical atrophy in preclinical Alzheimer's disease
Author(s) -
Doré Vincent,
Laws Simon M.,
Bourgeat Pierrick,
Fripp Jurgen,
Martins Ralph N.,
Ellis Kathryn A.,
Masters Colin L.,
Ames David,
Macaulay Lance,
Maruff Paul,
Salvado Olivier,
Rowe Christopher C.,
Villemagne Victor L.
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.2015.06.192
Subject(s) - atrophy , precuneus , hippocampus , medicine , alzheimer's disease , hippocampal formation , biomarker , neuroscience , pathology , oncology , endocrinology , psychology , disease , cognition , biology , psychiatry , biochemistry
Methods:18 cognitively normal elders (78.86 4.9 y) received 18FAV-1451 and 11C-PiB PET (mean 154 d apart). AV-1451 SUVR images (80-100 min post-injection, cerebellar gray reference) were transformed into MNI152 2mm space and smoothed (4mm FWHM). Elders were stratified by age (e.g. n 1⁄4 9 “Old-old”, >1⁄4 78 y; n 1⁄4 9 “Young-Old”) or PiB (Ab) status (n 1⁄4 7 PiB+ [DVR >1⁄4 1.08]; n1⁄4 11 PiB-). For visualization of peaks (Figure 1; highest 10% of voxels), intensities of all subjects’ gray and white matter voxels (SPM12 tissue probability masks at p > .3; cerebellar gray excluded, to create mask) were plotted; a threshold at 90% (1.40) was used to visualize spatial distributions, based on averaging sub-