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Updated: Dec 5, 2025
Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Brain structural and functional alterations in MOG antibody disease
Zhizheng Zhuo1, Yunyun Duan1, Decai Tian2
1Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China/Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing, P.R. China.
Background:
The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function is unknown.
Objectives:
The aim of this study was to study the multimodal brain MRI alterations in MOGAD and to investigate their clinical significance.
Methods:
A total of 17 MOGAD, 20 aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4 + NMOSD), and 28 healthy controls (HC) were prospectively recruited. Voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) were compared between groups. Clinical associations and differential diagnosis were determined using partial correlation and stepwise logistic regression.
Results:
In comparison with HC, MOGAD had GM atrophy in frontal and temporal lobe, insula, thalamus, and hippocampus, and WM fiber disruption in optic radiation and anterior/posterior corona radiata; DC decreased in cerebellum and increased in temporal lobe. Compared to AQP4 + NMOSD, MOGAD presented lower GM volume in postcentral gyrus and decreased DC in cerebellum. Hippocampus/parahippocampus atrophy associated with Expanded Disability Status Scale (R = -0.55, p = 0.04) and California Verbal Learning Test (R = 0.62, p = 0.031). The differentiation of MOGAD from AQP4 + NMOSD achieved an accuracy of 95% using FA in splenium of corpus callosum and DC in occipital gyrus.
Conclusion:
Distinct structural and functional alterations were identified in MOGAD. Hippocampus/parahippocampus atrophy associated with clinical disability and cognitive impairment.
Insights
Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) causes brain structure and function changes, including hippocampus atrophy linked to disability. This study reveals distinct MRI alterations in MOGAD patients.
Area of Science:
- Neuroscience
- Immunology
- Radiology
Background:
- The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function remains largely unknown.
- Understanding these changes is crucial for diagnosis and management.
Purpose of the Study:
- To investigate multimodal brain MRI alterations in MOGAD.
- To explore the clinical significance of these MRI findings.
- To differentiate MOGAD from aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4+NMOSD).
Main Methods:
- Recruited 17 MOGAD, 20 AQP4+NMOSD, and 28 healthy controls (HC).
- Utilized voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) analyses.
- Employed partial correlation and stepwise logistic regression for clinical associations and differential diagnosis.
Main Results:
- MOGAD patients showed GM atrophy and white matter (WM) fiber disruption compared to HC.
- Distinct patterns of GM volume and DC alterations were observed in MOGAD compared to AQP4+NMOSD.
- Hippocampus/parahippocampus atrophy correlated with disability and cognitive impairment.
Conclusions:
- MOGAD is associated with unique structural and functional brain alterations.
- Hippocampal atrophy is a key finding linked to clinical disability and cognitive deficits in MOGAD.
- Multimodal MRI, particularly FA and DC, can accurately differentiate MOGAD from AQP4+NMOSD.
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