MOG-antibody associated demyelinating disease of the CNS: A clinical and pathological study in Chinese Han patients

Zhou, Lei; Huang, Yipeng; Li, Haiqing; Fan, Jia; ZhangBao, Jingzi; Yu, Hai; Li, Yuxin; Lu, Jiahong; Zhao, Chongbo; Lü, Chuan-Zhen; Wang, Min; Quan, Chao

doi:10.1016/j.jneuroim.2017.01.007

Cited by 88 publications

(78 citation statements)

References 39 publications

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“…However this study shows, despite this clinico-radiologic overlap, the pathology of MOGAD is distinct from AQP4-IgG seropositive NMOSD. The presence of hypertrophic reactive astrocytes, preserved to increased AQP4 expression [67,82], occasional Creutzfeldt cells and frequent cortical demyelination in MOGAD, are helpful pathologic discriminators from AQP4-IgG seropositive NMOSD, which is characterized by AQP4 loss, dystrophic astrocytes, and absence of cortical demyelination [58,59]. Our findings support most prior MOGAD pathology cases which similarly reported no AQP4 loss [12].…”

Section: Discussionsupporting

confidence: 82%

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

et al. 2020

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We sought to define the pathological features of myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) in an archival autopsy/biopsy cohort. We histopathologically analyzed 2 autopsies and 22 brain biopsies from patients with CNS inflammatory demyelinating diseases seropositive for MOG-antibody by live-cell-based-assay with full length MOG in its conformational form. MOGAD autopsies (ages 52 and 67) demonstrate the full spectrum of histopathological features observed within the 22 brain biopsies (median age, 10 years; range, 1-66; 56% female). Clinical, radiologic, and laboratory characteristics and course (78% relapsing) are consistent with MOGAD. MOGAD pathology is dominated by coexistence of both perivenous and confluent white matter demyelination, with an over-representation of intracortical demyelinated lesions compared to typical MS. Radially expanding confluent slowly expanding smoldering lesions in the white matter as seen in MS, are not present. A CD4+ T-cell dominated inflammatory reaction with granulocytic infiltration predominates. Complement deposition is present in all active white matter lesions, but a preferential loss of MOG is not observed. AQP4 is preserved, with absence of dystrophic astrocytes, and variable oligodendrocyte and axonal destruction. MOGAD is pathologically distinguished from AQP4-IgG seropositive NMOSD, but shares some overlapping features with both MS and ADEM, suggesting a transitional pathology. Complement deposition in the absence of selective MOG protein loss suggest humoral mechanisms are involved, however argue against endocytic internalization of the MOG antigen. Parallels with MOG-EAE suggest MOG may be an amplification factor that augments CNS demyelination, possibly via complement mediated destruction of myelin or ADCC phagocytosis.

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Section: Discussionsupporting

confidence: 82%

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

et al. 2020

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“…This finding was consistent with previous reports that compared between MOG-ON (32.29±17.1 years old) and AQP4-ON (44.86±14.8 years old),8 MOG-ON (31 years old) and AQP4-ON (38 years old),10 MOG-ON (20±14 years old) and AQP4-ON (23±14 years old) 26. More than half (65%) of our patients with MOG-ON had a juvenile (<18 years) disease onset, which was more than those reported by previous study showing about 12.5%,9 50%10 or 16.7%13 of MOG-Ab-positive patients with demyelinating diseases began during juvenile period. The age at MOG-ON onset ranged from 5 years to 63 years, and the age at AQP4-ON onset ranged from 8 years to 72 years.…”

Section: Discussioncontrasting

confidence: 48%

“…The study of Hacohen et al 12 found that 35% of patients with childhood acquired demyelinating syndrome (ADS) were MOG-Abs-positive and 52% of MOG-Abs-positive patients were ON. One study of Chinese patients with CNS IDD found that ON was the most frequent clinical presentation at onset (75.0%) or during the whole disease course (83.3%) in MOG-Ab-associated IDDs 13. Some previous studies involving patients with NMO spectrum disorders (NMOSD)14 observed retinal neuroaxonal damage in MOG-Ab-positive patients, with or without ON.…”

Section: Introductionmentioning

confidence: 99%

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

et al. 2018

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“…Post‐mortem MS studies have shown myelin and axonal injury within lesions: However, axons appear to be preserved in remyelinated areas (Schultz et al, ): Crucially, if axons are not remyelinated, axonal degeneration occurs (Lee, Biemond, & Petratos, ; Simons, Misgeld, & Kerschensteiner, ; Singh et al, ). Post‐mortem data from MOG lesions demonstrated demyelination with partial axonal preservation (Zhou et al, ). Thus, the differences in WMTI metrics between children and adolescents with MS and MOG versus typically developing children may reflect the impact of the disease on both myelin and axon structure and highlights the role of axonal injury accompanying myelin injury.…”

Section: Discussionmentioning

confidence: 99%

White matter plasticity and maturation in human cognition

Bells

Lefebvre

Longoni

et al. 2019

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White matter plasticity likely plays a critical role in supporting cognitive development. However, few studies have used the imaging methods specific to white matter tissue structure or experimental designs sensitive to change in white matter necessary to elucidate these relations. Here we briefly review novel imaging approaches that provide more specific information regarding white matter microstructure. Furthermore, we highlight recent studies that provide greater clarity regarding the relations between changes in white matter and cognition maturation in both healthy children and adolescents and those with white matter insult. Finally, we examine the hypothesis that white matter is linked to cognitive function via its impact on neural synchronization. We test this hypothesis in a population of children and adolescents with recurrent demyelinating syndromes. Specifically, we evaluate group differences in white matter microstructure within the optic radiation; and neural phase synchrony in visual cortex during a visual task between 25 patients and 28 typically developing age‐matched controls. Children and adolescents with demyelinating syndromes show evidence of myelin and axonal compromise and this compromise predicts reduced phase synchrony during a visual task compared to typically developing controls. We investigate one plausible mechanism at play in this relationship using a computational model of gamma generation in early visual cortical areas. Overall, our findings show a fundamental connection between white matter microstructure and neural synchronization that may be critical for cognitive processing. In the future, longitudinal or interventional studies can build upon our knowledge of these exciting relations between white matter, neural communication, and cognition.

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MOG-antibody associated demyelinating disease of the CNS: A clinical and pathological study in Chinese Han patients

Cited by 88 publications

References 39 publications

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody

Clinical features of demyelinating optic neuritis with seropositive myelin oligodendrocyte glycoprotein antibody in Chinese patients

White matter plasticity and maturation in human cognition

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