{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:19:19Z","timestamp":1777393159155,"version":"3.51.4"},"reference-count":43,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2024,9,17]],"date-time":"2024-09-17T00:00:00Z","timestamp":1726531200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2024,9,24]]},"abstract":"<jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Tau aggregation demonstrates close associations with hypometabolism in Alzheimer\u2019s disease (AD), although differing pathophysiological processes may underlie their development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To establish whether tau deposition and glucose metabolism have different trajectories in AD progression and evaluate the utility of global measures of these pathological hallmarks in predicting cognitive deficits.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      279 participants with amyloid-\u03b2 (A\u03b2) status, and T1-weighted MRI scans, were selected from the Alzheimer\u2019s Disease Neuroimaging Initiative (\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"http:\/\/adni.loni.usc.edu\">http:\/\/adni.loni.usc.edu<\/jats:ext-link>\n                      ). We created the standard uptake value ratio images using Statistical Parametric Mapping 12 for [\n                      <jats:sup>18<\/jats:sup>\n                      F]AV1451-PET (tau) and [\n                      <jats:sup>18<\/jats:sup>\n                      F]FDG-PET (glucose metabolism) scans. Voxel-wise group and single-subject level SPM analysis evaluated the relationship between global [\n                      <jats:sup>18<\/jats:sup>\n                      F]FDG-PET and [\n                      <jats:sup>18<\/jats:sup>\n                      F]AV1451-PET depending on the A\u03b2 status. Linear models assessed whether tau deposition or glucose metabolism better predicted clinical progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      There was a dissociation between global cerebral glucose hypometabolism and global tau load in amyloid-positive AD and amyloid-negative mild cognitive impairment (MCI) (\n                      <jats:italic>p<\/jats:italic>\n                      \u200a&gt;\u200a0.05). Global hypometabolism was only associated with global cortical tau in amyloid-positive MCI. Voxel-level single subject tau load better predicted neuropsychological performance, Alzheimer\u2019s disease assessment scale-cognitive (ADAS-Cog) 13 score, and one-year change compared with regional and global hypometabolism.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>A dissociation between tau pathology and glucose metabolism at a global level in AD could imply that other pathological processes influence glucose metabolism. Furthermore, as tau is a better predictor of clinical progression, these processes may have independent trajectories and require independent consideration in the context of therapeutic interventions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-240434","type":"journal-article","created":{"date-parts":[[2024,9,24]],"date-time":"2024-09-24T10:42:04Z","timestamp":1727174524000},"page":"987-999","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Do Tau Deposition and Glucose Metabolism Dissociate in Alzheimer\u2019s Disease Trajectory?"],"prefix":"10.1177","volume":"101","author":[{"given":"Joseph","family":"Nowell","sequence":"first","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sanara","family":"Raza","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicholas R.","family":"Livingston","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shayndhan","family":"Sivanathan","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steve","family":"Gentleman","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul","family":"Edison","sequence":"additional","affiliation":[{"name":"Department of Brain Sciences, Division of Neurology, Faculty of Medicine, Imperial College London, London, UK"},{"name":"School of Medicine, Cardiff University, Cardiff, Wales, 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