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Published online before print September 2, 2009, doi:10.1212/WNL.0b013e3181bacf1b)
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Received February 9, 2009
Accepted July 21, 2009

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

N. M. Scheinin MD*, S. Aalto MSc, J. Koikkalainen DSc, J. Lötjönen DSc, M. Karrasch PhD, N. Kemppainen MD, PhD, M. Viitanen MD, PhD, K. Någren PhD, S. Helin MSc, M. Scheinin MD, PhD, and J. O. Rinne MD, PhD

From the Turku PET Centre (N.M.S., S.A., N.K., K.N., S.H., J.O.R.), University of Turku, Finland; Department of Psychology (S.A., M.K.), Åbo Akademi University, Turku, Finland; VTT Technical Research Centre of Finland (J.K., J.L.), Tampere, Finland; Department of Neurology (N.K.), Turku University Central Hospital, Finland; Turku City Hospital (M.V.), Finland; Clinical Geriatrics (M.V.), Karolinska Institutet, Karolinska University Hospital, Huddinge, Sweden; Department of Clinical Physiology and Nuclear Medicine (K.N.), Rigshospitalet, University of Copenhagen, Denmark; and Clinical Research Services Turku, Institute of Biomedicine (M.S.), University of Turku, Finland.


* To whom correspondence should be addressed. E-mail: noora.scheinin{at}utu.fi.

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 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.

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 [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.

Results: 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 (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 [11C]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 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.


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