|
|
||||||||
|
|
|||||||||
|
|
Neurosciences: NeurologyNeurology Posters |
1 Nuclear Medicine; 2 Psychiatry, University Medical Center Hamburg, Hamburg, Germany; 3 Digital Imaging, Philips Research, Hamburg, Germany; 4 Molecular Imaging, Philips Research, Aachen, Germany
934
Objectives: Biomarkers that are useful in the diagnosis of Alzheimers disease (AD) include CSF markers and brain FDG PET. However, their relation is not well understood.
Methods: The correlation between FDG uptake and CSF Aβ1-42, total tau (t-tau), and phosphorylated tau (p-tau181) was investigated in 34 subjects with probable AD. SPM2 was used for this purpose.
Results: Proportionally scaled FDG uptake was reduced in the AD subjects compared to 19 controls bilaterally in precuneus / posterior cingulate, temporo-parietal cortex, and mid frontal cortex (FDR=0.05). Single AD subject analysis at p=0.001 (uncorr) revealed a total volume of significant hypometabolism ranging from 5.3 to 259.4 ml. This hypometabolic volume showed a highly significant negative correlation with MMSE (r=-0.587, p=0.000), but it was not correlated with Aβ1-42 (p=0.540), t-tau (p=0.102), or p-tau181 (p=0.248). Voxel-based correlation analyses at FDR=0.05 showed that the increased local variance of scaled FDG uptake in the AD subjects could be accounted for by a positive correlation with MMSE to a large extent. There was no correlation with any of the CSF markers at this significance level. Explorative correlation analyses (p=0.05 uncorr) revealed a negative correlation of scaled FDG uptake and Aβ1-42 in precuneus / posterior cingulate, temporo-parietal cortex, and mid frontal cortex, predominantly in the left hemisphere. t-tau and p-tau correlated positively with FDG uptake in temporo-parietal cortex, negatively in precuneus.
Conclusions: Although FDG uptake in probable AD was more strongly coupled to cognitive impairment, correlations were also observed with CSF biomarkers.
| ||||||||||||||||||||||||||||||||||||||