Follow-up of [11C]PIB uptake and brain volume in patients with Alzheimer disease and controls - PubMed (original) (raw)
. 2009 Oct 13;73(15):1186-92.
doi: 10.1212/WNL.0b013e3181bacf1b. Epub 2009 Sep 2.
Affiliations
- PMID: 19726751
- DOI: 10.1212/WNL.0b013e3181bacf1b
Follow-up of [11C]PIB uptake and brain volume in patients with Alzheimer disease and controls
N M Scheinin et al. Neurology. 2009.
Abstract
Objective: In Alzheimer disease (AD), the accumulation pattern of beta-amyloid over time and its relationship with dementia severity are unclear. We investigated the brain uptake of the amyloid ligand (11)C-labeled Pittsburgh compound B ([(11)C]PIB) and volumetric brain changes over a 2-year follow-up in patients with AD and in aged healthy controls.
Methods: 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 [(11)C]PIB PET, MRI, and neuropsychological assessments. [(11)C]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.
Results: The [(11)C]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 (p < 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 (p = 0.009). Cognitive decline was also evident in other neuropsychological test results. Baseline neocortical [(11)C]PIB uptake ratios predicted subsequent volumetric brain changes in the controls (r = 0.725, p = 0.005).
Conclusions: The results suggest no (or only little) increase in (11)C-labeled Pittsburgh compound B ([(11)C]PIB) uptake during 2 years of Alzheimer disease progression, despite advancing brain atrophy and declining cognitive performance. Nevertheless, changes in [(11)C]PIB uptake during a longer follow-up cannot be excluded. High cortical [(11)C]PIB uptake may predict ongoing brain atrophy in cognitively normal individuals.
Comment in
- Isn't amyloid more than just a marker for Alzheimer disease?
Killiany RJ. Killiany RJ. Neurology. 2009 Oct 13;73(15):1174-5. doi: 10.1212/WNL.0b013e3181be020a. Epub 2009 Sep 9. Neurology. 2009. PMID: 19741212 No abstract available.
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