Follow-up of [ ¹¹ C]PIB uptake and brain volume in patients with Alzheimer disease and controls

Abstract

<b>Objective:</b> In Alzheimer disease (AD), the accumulation pattern of β-amyloid over time and its relationship with dementia severity are unclear. We investigated the brain uptake of the amyloid ligand ¹¹C-labeled Pittsburgh compound B ([¹¹C]PIB) and volumetric brain changes over a 2-year follow-up in patients with AD and in aged healthy controls. <b>Methods:</b> Fourteen patients with AD (mean age 72 years, SD 6.6) and 13 healthy controls (mean age 68 years, SD 5.4) were examined at baseline and after 2 years (patients with AD: mean 2.0 years, SD 0.2; controls: mean 2.1 years, SD 0.6) with [¹¹C]PIB PET, MRI, and neuropsychological assessments. [¹¹C]PIB uptake was analyzed with a voxel-based statistical method (SPM), and quantitative data were obtained with automated region-of-interest analysis. MRI data were analyzed with voxel-wise tensor-based morphometry. <b>Results:</b> The [¹¹C]PIB uptake of the patients with AD did not increase significantly during follow-up when compared with that of the controls. MRI showed progressive brain volume change in the patients with AD, e.g., in the hippocampal region, temporal cortex, and precuneus (<i>p</i> &lt; 0.05). The mean Mini-Mental State Examination score of the patients with AD declined from 24.3 (SD 3.1) at baseline to 21.6 (SD 3.9) at follow-up (<i>p</i> = 0.009). Cognitive decline was also evident in other neuropsychological test results. Baseline neocortical [¹¹C]PIB uptake ratios predicted subsequent volumetric brain changes in the controls (<i>r</i> = 0.725, <i>p</i> = 0.005). <b>Conclusions:</b> The results suggest no (or only little) increase in ¹¹C-labeled Pittsburgh compound B ([¹¹C]PIB) uptake during 2 years of Alzheimer disease progression, despite advancing brain atrophy and declining cognitive performance. Nevertheless, changes in [¹¹C]PIB uptake during a longer follow-up cannot be excluded. High cortical [¹¹C]PIB uptake may predict ongoing brain atrophy in cognitively normal individuals.