Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Published online before print September 2, 2009, doi:10.1212/WNL.0b013e3181bacf1b)
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
WNL.0b013e3181bacf1bv1
73/15/1186    most recent
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Scheinin, N. M.
Right arrow Articles by Rinne, J. O.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scheinin, N. M.
Right arrow Articles by Rinne, J. O.
Related Collections
Right arrow PET
Right arrow Volumetric MRI
Right arrow Memory
Right arrow Neuropsychological assessment
Right arrow Alzheimer's disease
Right arrowRelated Article
NEUROLOGY 2009;73:1186-1192
© 2009 American Academy of Neurology

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.

Address correspondence and reprint requests to Dr. Noora Scheinin, Turku PET Centre, PO Box 52, FIN-20521 Turku, Finland noora.scheinin{at}utu.fi

Objective: 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.

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.

Abbreviations: AAL = Automated Anatomic Labeling; Aβ = β-amyloid; AD = Alzheimer disease; [11C]PIB = 11C-labeled Pittsburgh compound B; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, 4th edition; MMSE = Mini-Mental State Examination; MNI = Montreal Neurological Institute; rmANOVA = repeated-measures analysis of variance; ROI = region of interest; SUV = standardized uptake value.

Editorial, page 1174

e-Pub ahead of print on September 2, 2009, at www.neurology.org.

Supported by the Academy of Finland (project 205954), the Sigrid Juselius Foundation, clinical grants (EVO) of Turku University Hospital, the Päivi and Sakari Sohlberg Foundation, and a Niilo Huolma Fellowship, granted by the Medical Faculty of the University of Turku. The MRI analysis work was also partially funded by Tekes–Finnish Funding Agency for Technology and Innovation (www.tekes.fi).

Disclosure: Author disclosures are provided at the end of the article.

Received February 9, 2009. Accepted in final form July 21, 2009.


Related Article

Isn’t amyloid more than just a marker for Alzheimer disease?
Ronald J. Killiany
Neurology 2009 73: 1174-1175. [Full Text] [PDF]



This article has been cited by other articles:


Home page
 NeurologyHome page
R. J. Killiany
Isn't amyloid more than just a marker for Alzheimer disease?
Neurology, October 13, 2009; 73(15): 1174 - 1175.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by AAN Enterprises, Inc.