For a study, researchers sought to examine the relationship between 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) and postmortem Lewy body disease (LBD) pathology in clinical Alzheimer’s disease (AD). In the Alzheimer’s Disease Neuroimaging Initiative, 62 autopsy-confirmed patients and 110 controls had their FDG-PET scans evaluated. Subjects were grouped into AD(−)/LBD(−), AD(−)/LBD(+), AD(+)/LBD(−), and AD(+)/LBD(+) groups based on neuropathologic assessments of the Braak stage for neurofibrillary tangle, the Consortium to Establish a Registry for AD score for neuritic plaque, and Lewy-related pathology. Investigators studied the relationship between postmortem LBD and AD pathology and antemortem brain metabolism. AD and LBD diseases had substantial interaction effects on decreasing metabolism in the cerebellar vermis, bilateral caudate, putamen, basofrontal cortex, and anterior cingulate cortex. They left the entorhinal cortex and amygdala to increase metabolism in the bilateral parietal and occipital cortices. Corresponding to Lewy body-related hypermetabolic patterns, LBD disease was associated with hypermetabolism in the cerebellar vermis, bilateral putamen, anterior cingulate cortex, and basofrontal cortex. AD pathology was linked with hypometabolism in the bilateral hippocampus, entorhinal cortex, and posterior cingulate cortex regardless of LBD disease. In contrast, LBD pathology was associated with hypermetabolism in the bilateral putamen and anterior cingulate cortex. In clinical AD patients, postmortem LBD and AD diseases had significant interaction effects on antemortem brain metabolism. Identifiable metabolic patterns associated with Alzheimer’s disease and Lewy body dementia (LBD) pathology could be understood by examining both diseases concurrently.