18F-Florbetapir PET in Patients with Frontotemporal Dementia and Alzheimer Disease

被引:32
作者
Kobylecki, Christopher [1 ,2 ]
Langheinrich, Tobias [1 ,2 ]
Hinz, Rainer [1 ]
Vardy, Emma R. L. C. [1 ,3 ,4 ,5 ]
Brown, Gavin [1 ]
Martino, Mara-Elena [1 ,6 ]
Haense, Cathleen [7 ]
Richardson, Anna M. [2 ,8 ]
Gerhard, Alexander [1 ,2 ]
Anton-Rodriguez, Jose M. [1 ]
Snowden, Julie S. [1 ,2 ]
Neary, David [1 ,2 ]
Pontecorvo, Michael J. [9 ]
Herholz, Karl [1 ]
机构
[1] Univ Manchester, Inst Brain Behav & Mental Hlth, Manchester, Lancs, England
[2] Salford Royal NHS Fdn Trust, Cerebral Funct Unit, Greater Manchester Neurosci Ctr, Salford, Lancs, England
[3] Newcastle Univ, Inst Neurosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England
[4] Newcastle Univ, Inst Ageing, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England
[5] Newcastle Upon Tyne Hosp NHS Fdn Trust, Dept Older Peoples Med, Newcastle Upon Tyne, Tyne & Wear, England
[6] Inst Invest Sanitaria Gregorio Maranon, Unidad Med & Cirugia Expt, Madrid, Spain
[7] Hannover Med Sch, Dept Nucl Med, Hannover, Germany
[8] Univ Manchester, Manchester Med Sch, Manchester, Lancs, England
[9] Avid Radiopharmaceut, Philadelphia, PA USA
关键词
amyloid; PET; Alzheimer's disease; frontotemporal dementia; diagnosis; POSITRON-EMISSION-TOMOGRAPHY; LOBAR DEGENERATION; CLINICAL-DIAGNOSIS; FLORBETAPIR-PET; FDG-PET; F; 18; BRAIN; PRESENTATIONS; DEPOSITION; PATHOLOGY;
D O I
10.2967/jnumed.114.147454
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Pathologic deposition of amyloid beta (A beta) protein is a key component in the pathogenesis of Alzheimer disease (AD) but not a feature of frontotemporal dementia (FTD). PET ligands for A beta protein are increasingly used in diagnosis and research of dementia syndromes. Here, we report a PET study using F-18-florbetapir in healthy controls and patients with AD and FTD. Methods: Ten healthy controls (mean age +/- SD, 62.5 +/- 5.2 y), 10 AD patients (mean age +/- SD, 62.6 +/- 4.5), and 8 FTD patients (mean age +/- SD, 62.5 +/- 9.6) were recruited to the study. All patients underwent detailed clinical and neuropsychologic assessment and T1-weighted MR imaging and were genotyped for apolipoprotein E status. All participants underwent dynamic F-18-florbetapir PET on a high-resolution research tomograph, and FTD patients also underwent F-18-FDG PET scans. Standardized uptake value ratios (SUVRs) were extracted for pre-defined gray and white matter regions of interest using cerebellar gray matter as a reference region. Static PET images were evaluated by trained raters masked to clinical status and regional analysis. Results: Total cortical gray matter F-18-florbetapir uptake values were significantly higher in AD patients (median SUVR, 1.73) than FTD patients (SUVR, 1.13, P = 0.002) and controls (SUVR, 1.26, P = 0.04). F-18-Florbetapir uptake was also higher in AD patients than FTD patients and controls in the frontal, parietal, occipital, and cingulate cortices and in the central subcortical regions. Only 1 FTD patient (homozygous for apolipoprotein E e4) displayed high cortical F-18-florbetapir retention, whereas F-18-FDG PET demonstrated mesiofrontal hypometabolism consistent with the clinical diagnosis of FTD. Most visual raters classified 1 control (10%) and 8 AD (80%) and 2 FTD (25%) patients as amyloid-positive, whereas ratings were tied in another 2 FTD patients and 1 healthy control. Conclusion: Cortical F-18-florbetapir uptake is low in most FTD patients, providing good discrimination from AD. However, visual rating of FTD scans was challenging, with a higher rate of discordance between interpreters than in AD and control subjects.
引用
收藏
页码:386 / 391
页数:6
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