Fig. 2

Cortical hypometabolism in patients with mild cognitive impairment who converted to Alzheimer’s disease dementia during follow-up (MCI-AD) and patients with mild cognitive impairment with brain amyloidosis (AMY+ MCI) with respect to control subjects. The typical Alzheimer’s disease (AD) group showed a wide area of hypometabolism involving the posterior parietal cortex and the precuneus in both hemispheres as well as the middle and superior occipital gyri, and also involving the posterior cingulate cortex in the left hemisphere (Brodmann areas [BAs] 7, 19, 30, 31, and 40 BA 22), whereas hypometabolism in late converters was limited to the bilateral posterior parietal cortex (BAs 7 and 40). Similarly, in the AMY+ MCI group, those with aggressive AMY+ MCI were characterized by a bilateral extended area of hypometabolism in the left superior temporal gyrus and posterior cingulate cortex, as well as in the posterior parietal cortex, lateral cuneus, and precuneus in both hemispheres (BAs 7, 18, 19, 22, 31, and 40), whereas patients with smoldering mild cognitive impairment (MCI) were characterized by hypometabolism limited to smaller clusters in the bilateral posterior parietal cortex (BA 40). See Table 4 and Additional file 3: Table S1 for details of coordinates and z-scores. Clusters with significant hypometabolism are shown superimposed on a multiple subject averaged magnetic resonance imaging template. The color bars indicate the level of z-scores for significant voxels