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Published on: February 28, 2021
Multi-tracer PET and MR imaging visualize distinct metabolic and inflammatory profiles in the white matter of NMOSD
Shuwei Bai1, Hongda Shao2, Hong Yang3
1Department of Neurology, Punan Branch of Renji Hospital, Shanghai Jiao Tong University School of Medicine (Punan Hospital in Pudong New District, Shanghai), Shanghai, 200125, China.
Abstract:
This study investigates distinct neuroinflammatory patterns in neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) using multi-tracer PET and MR imaging. Eight NMOSD (5F/3M; median age 36.5) and six MOGAD patients (2F/4M; median age 34.0) underwent PET scans with [18F]FDG (glucose metabolism), the translocator protein (TSPO) ligand [18F]PBR06 (glial activation), and [11C]acetate (astrocyte metabolism), integrated with synchronous 3T MRI sequences. Standardized uptake value ratios (SUVRs) referenced to contralateral white matter (WM) or whole brain were statistically compared across specific anatomic regions: active lesions, normal-appearing WM (NAWM), and periventricular zones. Both groups exhibited elevated [18F]PBR06 SUVR within lesions compared to contralateral WM, marking microgliosis. Crucially, NMOSD lesions showed significantly lower [18F]FDG SUVR (p = 0.01; metabolic impairment) and [11C]acetate SUVR (astrocyte dysfunction) than MOGAD lesions. Lesional [18F]PBR06 uptake correlated significantly with [18F]FDG uptake. Beyond lesions, NMOSD patients had higher [18F]FDG SUVR in cerebellar WM (p < 0.01) and periventricular regions near the fourth ventricle (p = 0.01), and higher [18F]PBR06 SUVR in cerebral WM (p = 0.03), contrasted with MOGAD. With lesions in both disorders demonstrating microgliosis, NMOSD exhibited more severe lesion-specific metabolic suppression and astrocyte dysfunction, reflected in reduced [11C]acetate uptake, coupled with regional inflammation (microgliosis) and hypermetabolism. These differential multi-tracer PET patterns, especially the combined reduction in lesional astrocytic ([11C]acetate) and metabolic ([18F]FDG) markers in NMOSD versus MOGAD, highlight multimodal PET/MRI as a powerful tool for differentiating NMOSD and MOGAD pathophysiology.
Insights
Neuromyelitis optica spectrum disorder (NMOSD) and MOGAD show distinct neuroinflammation patterns. NMOSD lesions have reduced glucose metabolism and astrocyte dysfunction compared to MOGAD, indicating different disease pathophysiology.
Area of Science:
- Neuroimmunology
- Neuroimaging
- Neurology
Background:
- Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOGAD) are distinct autoimmune inflammatory demyelinating diseases of the central nervous system.
- Differentiating NMOSD and MOGAD is crucial for appropriate treatment and prognosis, but overlapping clinical and radiological features can pose challenges.
Purpose of the Study:
- To investigate and compare distinct neuroinflammatory patterns in NMOSD and MOGAD using multi-tracer positron emission tomography (PET) and magnetic resonance (MR) imaging.
- To identify specific PET imaging biomarkers that can help differentiate the pathophysiology of NMOSD and MOGAD.
Main Methods:
- Eight NMOSD and six MOGAD patients underwent PET scans with [18F]FDG (glucose metabolism), [18F]PBR06 (glial activation), and [11C]acetate (astrocyte metabolism), integrated with 3T MRI.
- Standardized uptake value ratios (SUVRs) were statistically compared across active lesions, normal-appearing white matter (NAWM), and periventricular regions.
Main Results:
- Both NMOSD and MOGAD lesions showed microgliosis (elevated [18F]PBR06 SUVR).
- NMOSD lesions exhibited significantly lower [18F]FDG SUVR (metabolic impairment) and [11C]acetate SUVR (astrocyte dysfunction) compared to MOGAD lesions.
- NMOSD patients displayed distinct patterns of regional hypermetabolism and microgliosis in normal-appearing white matter and periventricular areas compared to MOGAD.
Conclusions:
- Multi-tracer PET/MRI reveals differential neuroinflammatory and metabolic profiles between NMOSD and MOGAD.
- NMOSD is characterized by more severe lesion-specific metabolic suppression and astrocyte dysfunction, alongside distinct regional inflammatory patterns.
- These findings underscore the utility of multimodal PET/MRI in distinguishing NMOSD and MOGAD pathophysiology.
