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

被引:103
作者
Scheinin, N. M. [1 ]
Aalto, S. [1 ,2 ]
Koikkalainen, J. [3 ]
Lotjonen, J. [3 ]
Karrasch, M. [2 ]
Kemppainen, N. [1 ,4 ]
Viitanen, M. [5 ,6 ]
Nagren, K. [1 ,7 ]
Helin, S. [1 ]
Scheinin, M. [8 ]
Rinne, J. O. [1 ]
机构
[1] Univ Turku, Turku PET Ctr, FIN-20521 Turku, Finland
[2] Abo Akad Univ, Dept Psychol, Turku, Finland
[3] VTT Tech Res Ctr Finland, Tampere, Finland
[4] Turku Univ, Cent Hosp, Dept Neurol, Turku, Finland
[5] Turku City Hosp, Turku, Finland
[6] Karolinska Univ Hosp, Karolinska Inst, Huddinge, Sweden
[7] Univ Copenhagen, Dept Clin Physiol & Nucl Med, Rigshosp, DK-1168 Copenhagen, Denmark
[8] Univ Turku, Clin Res Serv Turku, Inst Biomed, FIN-20521 Turku, Finland
基金
芬兰科学院;
关键词
MILD COGNITIVE IMPAIRMENT; PITTSBURGH COMPOUND-B; POSITRON-EMISSION-TOMOGRAPHY; PET AMYLOID LIGAND; HYPOTHESIS; DEPOSITION; ATROPHY; PIB;
D O I
10.1212/WNL.0b013e3181bacf1b
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
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 C-11-labeled Pittsburgh compound B ([C-11]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 [C-11]PIB PET, MRI, and neuropsychological assessments. [C-11]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 [C-11]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 [C-11]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 C-11-labeled Pittsburgh compound B ([C-11]PIB) uptake during 2 years of Alzheimer disease progression, despite advancing brain atrophy and declining cognitive performance. Nevertheless, changes in [C-11]PIB uptake during a longer follow-up cannot be excluded. High cortical [C-11]PIB uptake may predict ongoing brain atrophy in cognitively normal individuals. Neurology (R) 2009; 73: 1186-1192
引用
收藏
页码:1186 / 1192
页数:7
相关论文
共 24 条
[1]
AALTO S, 2009, EUR J NUCL MED 0604
[2]
Frequent Amyloid Deposition Without Significant Cognitive Impairment Among the Elderly [J].
Aizenstein, Howard Jay ;
Nebes, Robert D. ;
Saxton, Judith A. ;
Price, Julie C. ;
Mathis, Chester A. ;
Tsopelas, Nicholas D. ;
Ziolko, Scott K. ;
James, Jeffrey A. ;
Snitz, Beth E. ;
Houck, Patricia R. ;
Bi, Wenzhu ;
Cohen, Ann D. ;
Lopresti, Brian J. ;
DeKosky, Steven T. ;
Halligan, Edythe M. ;
Klunk, William E. .
ARCHIVES OF NEUROLOGY, 2008, 65 (11) :1509-1517
[3]
Amyloid load and cerebral atrophy in Alzheimer's disease:: An 11C-PIB positron emission tomography study [J].
Archer, Hilary A. ;
Edison, Paul ;
Brooks, David J. ;
Barnes, Jo ;
Frost, Chris ;
Yeatman, Toni ;
Fox, Nick C. ;
Rossor, Martin N. .
ANNALS OF NEUROLOGY, 2006, 60 (01) :145-147
[4]
The neuropsychology of preclinical Alzheimer's disease and mild cognitive impairment [J].
Collie, A ;
Maruff, P .
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 2000, 24 (03) :365-374
[5]
Two-year follow-up of amyloid deposition in patients with Alzheimer's disease [J].
Engler, Henry ;
Forsberg, Anton ;
Almkvist, Ove ;
Blomquist, Gunnar ;
Larsson, Emma ;
Savitcheva, Irina ;
Wall, Anders ;
Ringheim, Anna ;
Langstrom, Bengt ;
Nordberg, Agneta .
BRAIN, 2006, 129 :2856-2866
[6]
In vivo mapping of amyloid toxicity in Alzheimer disease [J].
Frisoni, G. B. ;
Lorenzi, M. ;
Caroli, A. ;
Kemppainen, N. ;
Nagren, K. ;
Rinne, J. O. .
NEUROLOGY, 2009, 72 (17) :1504-1511
[7]
Friston K., 1995, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402
[8]
Medicine - The amyloid hypothesis of Alzheimer's disease: Progress and problems on the road to therapeutics [J].
Hardy, J ;
Selkoe, DJ .
SCIENCE, 2002, 297 (5580) :353-356
[9]
Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease [J].
Ikonomovic, Milos D. ;
Klunk, William E. ;
Abrahamson, Eric E. ;
Mathis, Chester A. ;
Price, Julie C. ;
Tsopelas, Nicholas D. ;
Lopresti, Brian J. ;
Ziolko, Scott ;
Bi, Wenzhu ;
Paljug, William R. ;
Debnath, Manik L. ;
Hope, Caroline E. ;
Isanski, Barbara A. ;
Hamilton, Ronald L. ;
DeKosky, Steven T. .
BRAIN, 2008, 131 :1630-1645
[10]
IIC PiB and structural MRI provide complementary information in imaging of Alzheimers disease and amnestic mild cognitive impairment [J].
Jack, Clifford R., Jr. ;
Lowe, Val J. ;
Senjem, Matthew L. ;
Weigand, Stephen D. ;
Kemp, Bradley J. ;
Shiung, Maria M. ;
Knopman, David S. ;
Boeve, Bradley F. ;
Klunk, William E. ;
Mathis, Chester A. ;
Petersen, Ronald C. .
BRAIN, 2008, 131 :665-680