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[P4–239]: FDG‐PET POWER TO PREDICT MEMORY DECLINE IN ALZHEIMER's DISEASE DEPENDS ON DISEASE PHASE AND AMYLOID AND TAU STATUS
Author(s) -
Struyfs Hanne,
Pascoal Tharick A.,
Ng Kok Pin,
Mathotaarachchi Sulantha S.,
Shin Monica,
Kang Min Su,
Therriault Joseph,
Smeets Dirk,
Ribbens Annemie,
Gauthier Serge,
Bjerke Maria,
Engelborghs Sebastiaan,
RosaNeto Pedro
Publication year - 2017
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.2017.06.2107
Subject(s) - neurodegeneration , pittsburgh compound b , neuroscience , alzheimer's disease , pathophysiology , psychology , medicine , amyloid (mycology) , disease , pathology
temporal progression of disease is unclear. We used a novel MRI phasing algorithm, based on pathological staging studies, to test the hypothesis that non-amnestic AD has disease originating and spreading in neocortex.Methods:We inferred the anatomical origin and progression of disease in each AD variant based on the frequency of regional atrophy patterns in cross-sectional MRI from 131 patients with AD, confirmed through autopsy or CSF results. Disease progression models were computed separately for typical amnestic AD (aAD, 38 scans), logopenic variant primary progressive aphasia (lvPPA, 97 scans), posterior cortical atrophy (PCA, 54 scans), corticobasal syndrome (CBS, 31 scans), and behavioural/ dysexecutive-variant AD (bvAD, 39 scans). For each AD variant, 4 phases of atrophy were defined in 120 anatomical regions-of-interest (ROIs) using a grey matter volume threshold of Z< -1.0 relative to elderly controls. The origin of disease (Phase 1) was inferred from the most frequently atrophied 10% of ROIs; similarly, Phases 2, 3, and 4 comprised ROIs in the 2nd, 3rd, and 4th deciles of atrophy frequency. Results:We observed a unique distribution of atrophy for each phenotype. Phase 1 ROIs in our model represent the anatomical origin of disease, including: MTL for the aAD group (relatively spared in other phenotypes), left lateral temporal lobe for lvPPA, occipito-parietal cortex for PCA, temporo-parietal cortex for CBS, and fronto-temporal cortex for bvAD. Disease phase was significantly correlated with MMSE score and disease duration, independently of age. Conclusions: Our neuroimaging data showed unique maps of progressive atrophy for each AD variant. The classification of patients into phases was validated by correlations with disease duration and neuropsychological performance. We propose these results represent maps of distinct anatomic progression, with non-amnestic phenotypes showing neocortical origin and spread of disease.