TY - JOUR
T1 - Imaging correlations of tau, amyloid, metabolism, and atrophy in typical and atypical Alzheimer's disease
AU - Whitwell, Jennifer L.
AU - Graff-Radford, Jonathan
AU - Tosakulwong, Nirubol
AU - Weigand, Stephen D.
AU - Machulda, Mary M.
AU - Senjem, Matthew L.
AU - Spychalla, Anthony J.
AU - Vemuri, Prashanthi
AU - Jones, David T.
AU - Drubach, Daniel A.
AU - Knopman, David S.
AU - Boeve, Bradley F.
AU - Ertekin-Taner, Nilüfer
AU - Petersen, Ronald C.
AU - Lowe, Val J.
AU - Jack, Clifford R.
AU - Josephs, Keith A.
N1 - Funding Information:
Disclosures outside the submitted work: M.L.S. owns stocks in Align Technology, Inc., Gilead Sciences, Globus Medical Inc., Inovio Biomedical Corp., Johnson & Johnson, LHC Group, Inc., Medtronic, Inc., Mesa Laboratories, Inc., Natus Medical Incorporated, Oncothyreon, Inc., Parexel International Corporation, and Varex Imaging Corporation. N.E.-T has a patent “Human Monoclonal Antibodies Against Amyloid β Protein” issued and a patent “Their Use as Therapeutic Agents Application” pending. B.F.B. receives grants from Cephalon, Inc., Allon Therapeutics, GE Healthcare, and Mangurian Foundation. D.S.K. receives grants from TauRx, Baxter Pharmaceuticals, Elan Pharmaceuticals, and consults for Lundbeck Pharmaceuticals. R.C.P. consults for Roche, Inc., Merck, Inc., Genetech, Inc., Biogen, Inc., and Eli Lilly and Company. V.J.L. consults for Bayer Schering Pharma, Piramal Life Sciences, and receives grants from GE Healthcare, Siemens Molecular Imaging, and AVID Radiopharmaceuticals. C.R.J. consults for Janssen, Bristol-Meyer-Squibb, GE Healthcare, Johnson & Johnson, and receives grants from Allon and Baxter, Inc, and Pfizer, Inc.
Funding Information:
This work was supported by the National Institutes of Health (grant numbers R01-AG50603 , R21-NS94684 , P50 AG16574 , U01 AG006786 , R01 AG11378 , R01 AG041851 , RF1 AG051504 , U01 AG046139 , and R01 NS080820 ) and the Elsie and Marvin Dekelboum Family Foundation. The sponsors played no role in study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.
Publisher Copyright:
© 2018 the Alzheimer's Association
PY - 2018/8
Y1 - 2018/8
N2 - Introduction: Neuroimaging modalities can measure different aspects of the disease process in Alzheimer's disease, although the relationship between these modalities is unclear. Methods: We assessed subject-level regional correlations between tau on [ 18 F]AV-1451 positron emission tomography (PET), β amyloid on Pittsburgh compound B PET, hypometabolism on [ 18 F] fluorodeoxyglucose PET, and cortical thickness on magnetic resonance imaging in 96 participants with typical and atypical Alzheimer's disease presentations. We also assessed how correlations between modalities varied according to age, presenting syndrome, tau-PET severity, and asymmetry. Results: [ 18 F]AV-1451 uptake showed the strongest regional correlation with hypometabolism. Correlations between [ 18 F]AV-1451 uptake and both hypometabolism and cortical thickness were stronger in participants with greater cortical tau severity. In addition, age, tau asymmetry, and clinical diagnosis influenced the strength of the correlation between [ 18 F]AV-1451 uptake and cortical thickness. Discussion: These findings support a close relationship between tau and hypometabolism in Alzheimer's disease but show that correlations between neuroimaging modalities vary across participants.
AB - Introduction: Neuroimaging modalities can measure different aspects of the disease process in Alzheimer's disease, although the relationship between these modalities is unclear. Methods: We assessed subject-level regional correlations between tau on [ 18 F]AV-1451 positron emission tomography (PET), β amyloid on Pittsburgh compound B PET, hypometabolism on [ 18 F] fluorodeoxyglucose PET, and cortical thickness on magnetic resonance imaging in 96 participants with typical and atypical Alzheimer's disease presentations. We also assessed how correlations between modalities varied according to age, presenting syndrome, tau-PET severity, and asymmetry. Results: [ 18 F]AV-1451 uptake showed the strongest regional correlation with hypometabolism. Correlations between [ 18 F]AV-1451 uptake and both hypometabolism and cortical thickness were stronger in participants with greater cortical tau severity. In addition, age, tau asymmetry, and clinical diagnosis influenced the strength of the correlation between [ 18 F]AV-1451 uptake and cortical thickness. Discussion: These findings support a close relationship between tau and hypometabolism in Alzheimer's disease but show that correlations between neuroimaging modalities vary across participants.
KW - Alzheimer's disease
KW - Cortical thickness
KW - Logopenic aphasia
KW - Magnetic resonance imaging
KW - Positron emission tomography
KW - Posterior cortical atrophy
KW - Tau
KW - β amyloid
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U2 - 10.1016/j.jalz.2018.02.020
DO - 10.1016/j.jalz.2018.02.020
M3 - Article
C2 - 29605222
AN - SCOPUS:85046775618
SN - 1552-5260
VL - 14
SP - 1005
EP - 1014
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
IS - 8
ER -