Abstract
478
Aim: It is assumed that the abnormal amyloid-β deposition is an initiating event in Alzheimer's disease (AD). We evaluated the Pittsburgh compound-B-PET images of very early onset AD (VEOAD), sporadic late onset AD (LOAD) and cognitively normal elder controls (NC) to find whether a different amyloid deposit pattern existed among groups.
Methods: 11C-PIB PET/CT or PET/MRI images of 5 VEOAD patients (Male/Femal:1/4, age range: 36-43 Yr, 39.0 ± 3.4), 15 LOAD patients (Male/Femal:7/8, age range:62-78 Yr, 69.2 ± 4.0) and 12 NC subjects (Male/Femal:7/5, age range:60-74 Yr, 67.4 ± 3.2) with definite clinical diagnosis and complete neuropsychological tests were reviewed. PIB-PET acquisition: All subjects received 11C-PIB injection intravenously (4.44-5.55MBq/kg) 40-min prior to data acquisition, including 2 VEOAD at a PET/CT (Biograph 64, SIEMENS, Germany) and 30 subjects at a PET/MRI scanner (Biograph mMR, SIEMENS, Germany). Data analysis: At first, a PIB template through the 12 normal subjects was made up: the PET data of each subject were registered to the T1 image with a linear transformation. Then, PET image was warped to the standard space using parameters offered by normalization form T1 image to T1 template. Finally, the PIB template was made up by computing the mean value of PET images. Normalization from MNI space to each individual space was made and the parameters were then used to the 90 ROIs of AAL atlas, then 90 ROIs of every subject was obtained. The CGM was chosen as the reference region for standardized uptake value ratio (SUVR) measurement. One way ANOVA analysis was used to assess the differences of ages, MMSE scores and SUVRs of ROIs among 3 groups.
Results: VEOAD patients were younger than LOAD and NC subjects (F=70.02, P<0.05). Both the two AD groups’ MMSE scores were significantly worse than NC (F=43.77, P<0.05). Significant difference was detected on entire 25 ROIs among SUVR of three groups, including bilateral frontal cortex, precuneus, anterior cingulated cortex, and thalamus. Compared with LOAD patients, no significant increased 11C-PIB retention of VEOAD was found on 22 ROIs, but both of the two AD groups showed higher amyloid retention than that of NC. On the other 3 ROIs, including caudate (F=23.96, P < 0.01), putamen (F=12.65, P < 0.01) and amygdala (F=10.35, P < 0.01), 11C-PIB retention of VEOAD was found significantly higher than LOAD and NC.
Conclusions: Extensive higher striatal amyloid deposition as PIB-PET detected in VEOAD, along with diffused cortical deposition, which might associated with their early-onset symptoms. References: 1. Knight WD, Okello AA, Ryan NS,et al., Carbon-11-Pittsburgh compound B positron emission tomography imaging of amyloid deposition in presenilin 1 mutation carriers. Brain. 2011 Jan;134(Pt 1):293-300. 2. Klunk WE, Price JC, Mathis CA, et al., Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees. J Neurosci. 2007 Jun 6;27(23):6174-84.