Contributions
Abstract: EP1556
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: PET imaging with tracers such as [18F]Florbetaben (FBB) allows the in vivo visualization of cortical β amyloid (Aβ) depositions as occurring in Alzheimer's disease. FBB also - independently from Aβ - binds to brain white matter (WM) myelin, suggesting a potential value in imaging multiple sclerosis (MS). After promising preliminary results, further studies employing this tracer in other WM diseases are currently missing.
Objectives: To assess in vivo quantification of FBB uptake in patients with different WM diseases in comparison to non-WM diseased controls. We hypothesized a decreased WM tracer accumulation in the patient group as a surrogate of myelin loss.
Methods: We examined 13 patients with pathophysiologically distinguishable WM diseases (MS [n=4]; progressive multifocal leukoencephalopathy [PML, n=3]; adult-onset leukodystrophy [genetically determined, n=3]; cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL, n=3]) and concurrent mild cognitive impairment using FBB-PET/MRI. 13 age- and gender-matched patients with cognitive impairment but without WM disease served as controls. PET data were acquired 90-110min after injection of FBB using a simultaneous PET/MR System (Biograph mMR, Siemens). Segmentation of WM and generation of standard volumes of interests (Automated Anatomical Labeling atlas) was performed in PMOD 3.5. WM lesions were segmented by the lesion prediction algorithm as implemented in the LST toolbox for SPM. We determined the WM standardized uptake value (SUV) ratio (SUVRWM) using the cerebellar cortex as reference region. For WM diseases, the WM lesion SUV Ratio (SUVRWML) was calculated using the same reference.
Results: SUVRsWM were significantly lower in patients than controls (1.78±0.32 vs.1.90±0.14, p=0.04). Within the patient group, WM lesions showed an even lower tracer retention than normally appearing WM (SUVRWML vs. SUVRWM: 0.98±0.22 vs. 1.78±0.32, p< 0.001). These findings were independent of the cortical tracer uptake. An additional subgroup analysis regarding WM uptake degree and distribution between the different WM diseases is planned after recruitment of a larger cohort.
Conclusion: Patients with pathophysiologically different WM diseases show decreased FBB WM binding, especially in WM lesions, compared to non-WM-diseased controls. Further research in larger cohorts is justified to investigate the potential of FBB PET/MRI in evaluating demyelinating diseases.
Disclosure:
SH has no conflicts of interest with respect to the contents of this abstract. Within the past year before abstract submission, she has received support to attend a scientific meeting from Merck-Serono and Actelion.
PW, RS, JO, ST, MP, DL and K-TH have nothing to disclose.
MR received travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he has nothing to disclose.
OS received research support, consultant honoraria, and travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he received consulting honoraria and travel expenses also from Siemens Healthcare.
FTB has no conflicts of interest with respect to the contents of this abstract. Within the past year before abstract submission, he received funding from the DFG; received, through his institution, research support for investigator-initiated studies from Actelion and Novartis; has served on scientific advisory boards for Novartis, Sanofi/Genzyme and Roche; has received support to attend a scientific meeting from Biogen; and has received personal honoraria for speaking from Bayer Schering, Biogen, Roche and Sanofi/Genzyme.
HB received research support, consultant honoraria, and travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he received consulting honoraria and travel expenses also from Siemens Healthcare.
Abstract: EP1556
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: PET imaging with tracers such as [18F]Florbetaben (FBB) allows the in vivo visualization of cortical β amyloid (Aβ) depositions as occurring in Alzheimer's disease. FBB also - independently from Aβ - binds to brain white matter (WM) myelin, suggesting a potential value in imaging multiple sclerosis (MS). After promising preliminary results, further studies employing this tracer in other WM diseases are currently missing.
Objectives: To assess in vivo quantification of FBB uptake in patients with different WM diseases in comparison to non-WM diseased controls. We hypothesized a decreased WM tracer accumulation in the patient group as a surrogate of myelin loss.
Methods: We examined 13 patients with pathophysiologically distinguishable WM diseases (MS [n=4]; progressive multifocal leukoencephalopathy [PML, n=3]; adult-onset leukodystrophy [genetically determined, n=3]; cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL, n=3]) and concurrent mild cognitive impairment using FBB-PET/MRI. 13 age- and gender-matched patients with cognitive impairment but without WM disease served as controls. PET data were acquired 90-110min after injection of FBB using a simultaneous PET/MR System (Biograph mMR, Siemens). Segmentation of WM and generation of standard volumes of interests (Automated Anatomical Labeling atlas) was performed in PMOD 3.5. WM lesions were segmented by the lesion prediction algorithm as implemented in the LST toolbox for SPM. We determined the WM standardized uptake value (SUV) ratio (SUVRWM) using the cerebellar cortex as reference region. For WM diseases, the WM lesion SUV Ratio (SUVRWML) was calculated using the same reference.
Results: SUVRsWM were significantly lower in patients than controls (1.78±0.32 vs.1.90±0.14, p=0.04). Within the patient group, WM lesions showed an even lower tracer retention than normally appearing WM (SUVRWML vs. SUVRWM: 0.98±0.22 vs. 1.78±0.32, p< 0.001). These findings were independent of the cortical tracer uptake. An additional subgroup analysis regarding WM uptake degree and distribution between the different WM diseases is planned after recruitment of a larger cohort.
Conclusion: Patients with pathophysiologically different WM diseases show decreased FBB WM binding, especially in WM lesions, compared to non-WM-diseased controls. Further research in larger cohorts is justified to investigate the potential of FBB PET/MRI in evaluating demyelinating diseases.
Disclosure:
SH has no conflicts of interest with respect to the contents of this abstract. Within the past year before abstract submission, she has received support to attend a scientific meeting from Merck-Serono and Actelion.
PW, RS, JO, ST, MP, DL and K-TH have nothing to disclose.
MR received travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he has nothing to disclose.
OS received research support, consultant honoraria, and travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he received consulting honoraria and travel expenses also from Siemens Healthcare.
FTB has no conflicts of interest with respect to the contents of this abstract. Within the past year before abstract submission, he received funding from the DFG; received, through his institution, research support for investigator-initiated studies from Actelion and Novartis; has served on scientific advisory boards for Novartis, Sanofi/Genzyme and Roche; has received support to attend a scientific meeting from Biogen; and has received personal honoraria for speaking from Bayer Schering, Biogen, Roche and Sanofi/Genzyme.
HB received research support, consultant honoraria, and travel expenses from Piramal Imaging related to this abstract. Within the past year before abstract submission, he received consulting honoraria and travel expenses also from Siemens Healthcare.