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.
Similar articles
- Amyloid PET imaging in patients with mild cognitive impairment: a 2-year follow-up study.
Koivunen J, Scheinin N, Virta JR, Aalto S, Vahlberg T, Någren K, Helin S, Parkkola R, Viitanen M, Rinne JO. Koivunen J, et al. Neurology. 2011 Mar 22;76(12):1085-90. doi: 10.1212/WNL.0b013e318212015e. Epub 2011 Feb 16. Neurology. 2011. PMID: 21325653 - Quantitative longitudinal interrelationships between brain metabolism and amyloid deposition during a 2-year follow-up in patients with early Alzheimer's disease.
Förster S, Yousefi BH, Wester HJ, Klupp E, Rominger A, Förstl H, Kurz A, Grimmer T, Drzezga A. Förster S, et al. Eur J Nucl Med Mol Imaging. 2012 Dec;39(12):1927-36. doi: 10.1007/s00259-012-2230-9. Epub 2012 Aug 28. Eur J Nucl Med Mol Imaging. 2012. PMID: 22926714 - Two-year follow-up of amyloid deposition in patients with Alzheimer's disease.
Engler H, Forsberg A, Almkvist O, Blomquist G, Larsson E, Savitcheva I, Wall A, Ringheim A, Långström B, Nordberg A. Engler H, et al. Brain. 2006 Nov;129(Pt 11):2856-66. doi: 10.1093/brain/awl178. Epub 2006 Jul 19. Brain. 2006. PMID: 16854944 - PET imaging of brain amyloid in dementia: a review.
Quigley H, Colloby SJ, O'Brien JT. Quigley H, et al. Int J Geriatr Psychiatry. 2011 Oct;26(10):991-9. doi: 10.1002/gps.2640. Epub 2010 Dec 28. Int J Geriatr Psychiatry. 2011. PMID: 21905095 Review. - Pittsburgh compound B retention and progression of cognitive status--a meta-analysis.
Chen X, Li M, Wang S, Zhu H, Xiong Y, Liu X. Chen X, et al. Eur J Neurol. 2014 Aug;21(8):1060-1067. doi: 10.1111/ene.12398. Epub 2014 Feb 24. Eur J Neurol. 2014. PMID: 24612390 Review.
Cited by
- Negative 11C-PIB PET Predicts Lack of Alzheimer's Disease Pathology in Postmortem Examination.
Scheinin NM, Gardberg M, Röyttä M, Rinne JO. Scheinin NM, et al. J Alzheimers Dis. 2018;63(1):79-85. doi: 10.3233/JAD-170569. J Alzheimers Dis. 2018. PMID: 29614642 Free PMC article. - Divergent network connectivity changes in behavioural variant frontotemporal dementia and Alzheimer's disease.
Zhou J, Greicius MD, Gennatas ED, Growdon ME, Jang JY, Rabinovici GD, Kramer JH, Weiner M, Miller BL, Seeley WW. Zhou J, et al. Brain. 2010 May;133(Pt 5):1352-67. doi: 10.1093/brain/awq075. Epub 2010 Apr 21. Brain. 2010. PMID: 20410145 Free PMC article. - The biochemical aftermath of anti-amyloid immunotherapy.
Maarouf CL, Daugs ID, Kokjohn TA, Kalback WM, Patton RL, Luehrs DC, Masliah E, Nicoll JA, Sabbagh MN, Beach TG, Castaño EM, Roher AE. Maarouf CL, et al. Mol Neurodegener. 2010 Oct 7;5:39. doi: 10.1186/1750-1326-5-39. Mol Neurodegener. 2010. PMID: 20929585 Free PMC article. - The use of PET in Alzheimer disease.
Nordberg A, Rinne JO, Kadir A, Långström B. Nordberg A, et al. Nat Rev Neurol. 2010 Feb;6(2):78-87. doi: 10.1038/nrneurol.2009.217. Nat Rev Neurol. 2010. PMID: 20139997 Review. - Impact of apolipoprotein E4-cerebrospinal fluid β-amyloid interaction on hippocampal volume loss over 1 year in mild cognitive impairment.
Chiang GC, Insel PS, Tosun D, Schuff N, Truran-Sacrey D, Raptentsetsang ST, Thompson PM, Reiman EM, Jack CR Jr, Fox NC, Jagust WJ, Harvey DJ, Beckett LA, Gamst A, Aisen PS, Petersen RC, Weiner MW; Alzheimer's Disease Neuroimaging Initiative. Chiang GC, et al. Alzheimers Dement. 2011 Sep;7(5):514-20. doi: 10.1016/j.jalz.2010.12.010. Alzheimers Dement. 2011. PMID: 21889115 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical