|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From MRC Clinical Sciences Centre and Division of Neuroscience (P.E., A.H., N.P., Y.F.T., G.H., A.K., M.R., D.J.B.), Hammersmith Hospital, Imperial College London; Dementia Research Centre (H.A.A., D.C., N.F., M.R.), UCL, Institute of Neurology; and Hammersmith Imanet (R.H., D.J.B.), GE Healthcare, UK.
Address correspondence and reprint requests to Dr. David J Brooks, Hartnett Professor of Neurology, Cyclotron Building, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK; e-mail: david.brooks{at}csc.mrc.ac.uk
Objective: To investigate the association between brain amyloid load in Alzheimer disease (AD) measured by [11C]PIB-PET, regional cerebral glucose metabolism (rCMRGlc) measured by [18F]FDG-PET, and cognition.
Methods: Nineteen subjects with AD and 14 controls had [11C]PIB-PET and underwent a battery of psychometric tests. Twelve of those subjects with AD and eight controls had [18F]FDG-PET. Parametric images of [11C]PIB binding and rCMRGlc were interrogated with a region-of-interest atlas and statistical parametric mapping. [11C]PIB binding and rCMRGlc were correlated with scores on psychometric tests.
Results: AD subjects showed twofold increases in mean [11C]PIB binding in cingulate, frontal, temporal, parietal, and occipital cortical areas. Higher cortical amyloid load correlated with lower scores on facial and word recognition tests. Two patients fulfilling the clinical criteria for AD had normal [11C]PIB at baseline. Over 20 months this remained normal in one but increased in the cingulate of the other. Mean levels of temporal and parietal rCMRGlc were reduced by 20% in AD and these correlated with mini mental scores, immediate recall, and recognition memory test for words. Higher [11C]PIB uptake correlated with lower rCMRGlc in temporal and parietal cortices.
Conclusion: [11C]PIB-PET detected an increased amyloid plaque load in 89% of patients with clinically probable Alzheimer disease (AD). The high frontal amyloid load detected by [11C]PIB-PET in AD in the face of spared glucose metabolism is of interest and suggests that amyloid plaque formation may not be directly responsible for neuronal dysfunction in this disorder.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the February 13 issue to find the title link for this article.
Editorial, see page 482
This article was previously published in electronic format as an Expedited E-Pub on October 25, 2006, at www.neurology.org.
Disclosure: David Brooks is Chief Medical Officer of Imanet, GE Healthcare.
Received March 6, 2006. Accepted in final form August 7, 2006.
Related articles in Neurology:
This article has been cited by other articles:
![]() |
J. Koivunen, A. Verkkoniemi, S. Aalto, A. Paetau, J.-P. Ahonen, M. Viitanen, K. Nagren, J. Rokka, M. Haaparanta, H. Kalimo, et al. PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease Brain, July 1, 2008; 131(7): 1845 - 1853. [Abstract] [Full Text] [PDF] |
||||
![]() |
A.M. Fjell, K.B. Walhovd, I. Amlien, A. Bjornerud, I. Reinvang, L. Gjerstad, T. Cappelen, F. Willoch, P. Due-Tonnessen, R. Grambaite, et al. Morphometric Changes in the Episodic Memory Network and Tau Pathologic Features Correlate with Memory Performance in Patients with Mild Cognitive Impairment AJNR Am. J. Neuroradiol., June 1, 2008; 29(6): 1183 - 1189. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. E. Carlson, M. M. Moore, A. Dame, D. Howieson, L. C. Silbert, J. F. Quinn, and J. A. Kaye Trajectories of brain loss in aging and the development of cognitive impairment Neurology, March 11, 2008; 70(11): 828 - 833. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. R. Jack Jr, V. J. Lowe, M. L. Senjem, S. D. Weigand, B. J. Kemp, M. M. Shiung, D. S. Knopman, B. F. Boeve, W. E. Klunk, C. A. Mathis, et al. 11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment Brain, March 1, 2008; 131(3): 665 - 680. [Abstract] [Full Text] [PDF] |
||||
![]() |
G.D. Rabinovici, W.W. Seeley, E.J. Kim, M.L. Gorno-Tempini, K. Rascovsky, T.A. Pagliaro, S.C. Allison, C. Halabi, J.H. Kramer, J.K. Johnson, et al. Distinct MRI Atrophy Patterns in Autopsy-Proven Alzheimer's Disease and Frontotemporal Lobar Degeneration American Journal of Alzheimer's Disease and Other Dementias, January 1, 2008; 22(6): 474 - 488. [Abstract] [PDF] |
||||
![]() |
K HERHOLZ, S F CARTER, and M JONES Positron emission tomography imaging in dementia Br. J. Radiol., December 1, 2007; 80(Special_Issue_2): S160 - S167. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. E. Pike, G. Savage, V. L. Villemagne, S. Ng, S. A. Moss, P. Maruff, C. A. Mathis, W. E. Klunk, C. L. Masters, and C. C. Rowe {beta}-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease Brain, November 1, 2007; 130(11): 2837 - 2844. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Lockhart, J.R. Lamb, T. Osredkar, L.I. Sue, J.N. Joyce, L. Ye, V. Libri, D. Leppert, and T.G. Beach PIB is a non-specific imaging marker of amyloid-beta (A{beta}) peptide-related cerebral amyloidosis Brain, October 1, 2007; 130(10): 2607 - 2615. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Nelissen, M. Vandenbulcke, K. Fannes, A. Verbruggen, R. Peeters, P. Dupont, K. Van Laere, G. Bormans, and R. Vandenberghe A{beta} amyloid deposition in the language system and how the brain responds Brain, August 1, 2007; 130(8): 2055 - 2069. [Abstract] [Full Text] [PDF] |
||||
![]() |
Imaging Amyloid and Regional Cerebral Glucose Metabolism in Alzheimer Disease Journal Watch Neurology, June 19, 2007; 2007(619): 1 - 1. [Full Text] |
||||
![]() |
R. J. Bateman and D. Eidelberg Testing a test for Alzheimer disease Neurology, February 13, 2007; 68(7): 482 - 483. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |