Choroba związana z przeciwciałami białka mieliny oligodendrocytów (mogad)

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (mogad)
Patofizjologia i mechanizm

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) to rzadkie, autoimmunologiczne zapalne zaburzenie demielinizacyjne ośrodkowego układu nerwowego (OUN), charakteryzujące się atakami demielinizacji zależnej od przeciwciał klasy IgG skierowanych przeciwko glikoproteinie mieliny oligodendrocytów (MOG). Patofizjologia MOGAD opiera się na aktywacji limfocytów T CD4+ oraz produkcji przeciwciał anty-MOG (głównie IgG1), które przekraczają barierę krew-mózg, prowadząc do demielinizacji poprzez opsonizację, aktywację dopełniacza i cytotoksyczność komórkową zależną od przeciwciał. W odróżnieniu od stwardnienia rozsianego (SM), w MOGAD dominuje naciek limfocytów T CD4+, a zmiany demielinizacyjne wykazują cechy podobne do wzoru II SM, z zachowaniem oligodendrocytów i obecnością aktywowanego układu dopełniacza, jednak z odmiennym rozkładem topograficznym i charakterem odpowiedzi zapalnej. W badaniach obrazowych nerwów wzrokowych obserwuje się obrzęk i hiperintensywność sygnału T2, głównie w przednich segmentach nerwów wzrokowych, z oszczędzeniem skrzyżowania nerwów wzrokowych.

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) Patogeneza i mechanizm

Charakterystyka białka MOG
Patofizjologia MOGAD
Rola przeciwciał anty-MOG
Badania patologiczne MOGAD
Rola limfocytów T CD4+
Rola układu dopełniacza
Bezpośredni wpływ przeciwciał na oligodendrocyty
Potencjalne czynniki wyzwalające
Układ glimfatyczny w MOGAD
Patogeneza w zapaleniu nerwu wzrokowego
Czynniki ryzyka i otyłość

Wyzwania i przyszłe kierunki

Kolejne rozdziały

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) Patogeneza i mechanizm

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) jest rzadkim, autoimmunologicznym zapalnym zaburzeniem demielinizacyjnym ośrodkowego układu nerwowego (OUN), charakteryzującym się atakami demielinizacji zależnej od układu immunologicznego, która głównie atakuje nerwy wzrokowe, mózg i rdzeń kręgowy.¹² Odkrycie specyficznych przeciwciał klasy IgG w surowicy, które selektywnie wiążą się z glikoproteiną mieliny oligodendrocytów (MOG), przyczyniło się do zwiększenia zrozumienia różnorodnego spektrum zaburzeń, które obecnie określa się jako MOGAD.³ Ogólnie patologiczne cechy wskazują na demielinizacyjną chorobę ośrodkowego układu nerwowego zależną od przeciwciał, która jest odrębna od stwardnienia rozsianego (SM).⁴

Charakterystyka białka MOG

MOG jest niewielkim składnikiem mieliny, wyrażanym na powierzchni oligodendrocytów.⁵ Jako członek nadrodziny immunoglobulin, MOG jest wysoce immunogenny. Funkcja MOG nie została w pełni wyjaśniona, ale może działać jako cząsteczka adhezji komórkowej, regulować stabilność mikrotubul i modulować interakcje immunologiczne mieliny.⁶ Jego lokalizacja na najbardziej zewnętrznej części osłonki mielinowej w OUN czyni go potencjalnym celem dla przeciwciał anty-MOG.⁷⁸ Ta specyficzna lokalizacja na zewnętrznej błonie osłonek mielinowych i na powierzchni błony oligodendrocytów sugeruje, że to białko może być zaangażowane w interakcję z układem immunologicznym i patofizjologię zaburzeń demielinizacyjnych.⁹

Patofizjologia MOGAD

Patofizjologia MOGAD jest napędzana przez ostre ataki, podczas których limfocyty T i przeciwciała MOG przekraczają barierę krew-mózg (BBB).¹⁰¹¹ Początkowa aktywacja limfocytów T na obwodzie jest następnie ponownie aktywowana w przestrzeniach podpajęczynówkowych/okołonaczyniowych przez komórki prezentujące antygen obładowane MOG oraz prozapalne środowisko płynu mózgowo-rdzeniowego, co umożliwia limfocytom T infiltrację miąższu OUN.¹²¹³

W przeciwieństwie do SM, gdzie dominuje infiltracja limfocytów T CD8+, w MOGAD przeważają limfocyty T CD4+, co stwierdzono w badaniach histologicznych zmian chorobowych.¹⁴¹⁵¹⁶ W zmianach tych znajdują się również granulocyty, makrofagi/mikroglej oraz aktywowany układ dopełniacza, które mogą przyczyniać się do demielinizacji podczas ostrych nawrotów.¹⁷¹⁸

Rola przeciwciał anty-MOG

Przeciwciała anty-MOG potencjalnie przyczyniają się do patologii poprzez opsonizację MOG, aktywację dopełniacza i cytotoksyczność komórkową zależną od przeciwciał.¹⁹²⁰ Stymulacja obwodowych limfocytów B specyficznych dla MOG poprzez stymulację receptorów toll-podobnych (TLR) lub przez pomocnicze limfocyty T grudkowe może pomóc limfocytom B różnicować się w komórki plazmatyczne produkujące przeciwciała anty-MOG we krwi obwodowej.²¹

Przeciwciała anty-MOG (IgG1) wiążą się z MOG wyrażonym na powierzchni mieliny i oligodendrocytów, uszkadzając osłonki mielinowe i prowadząc do demielinizacji poprzez cytotoksyczność komórkową zależną od przeciwciał lub aktywację dopełniacza.²² Warto zauważyć, że kiedy ludzkie przeciwciała anty-MOG, które rozpoznają MOG gryzoni, zostały wstrzyknięte dokanałowo gryzoniom z limfocytami T reaktywnymi na mielinę, przeciwciało MOG okazało się być bezpośrednio patogenne, wywołując demielinizację i prowadząc do odkładania dopełniacza.²³

Badania patologiczne MOGAD

Badania patologiczne ludzkiego MOGAD dostarczyły pewnego wglądu w jego patogenezę i skupiały się głównie na zmianach w mózgu podczas biopsji lub autopsji.²⁴ Badania te ujawniły współistniejącą demielinizację okołożylną i zlewną. Demielinizacja korowa jest częsta, a dominują wewnątrzkorowe zmiany demielinizacyjne.²⁵

Typowa jest reakcja zapalna limfocytów T CD4+ z zapaleniem granulocytowym, co różni się od SM, w którym obserwuje się przewagę infiltratu CD8+.²⁶ Zaobserwowano również odkładanie się dopełniacza i odnotowano nakładanie się z patologią SM typu II.²⁷ W przeciwieństwie do zaburzeń ze spektrum neuromyelitis optica seropozytywnych na przeciwciała IgG przeciwko akwaporynie-4, ekspresja akwaporyny-4 jest zachowana w MOGAD, a uszkodzenie astrocytów jest znacznie mniej wyraźne.²⁸²⁹

Zmiany demielinizacyjne w MOGAD bardziej przypominają te obserwowane w stwardnieniu rozsianym niż w NMO. Są podobne do wzoru II stwardnienia rozsianego z limfocytami T i makrofagami otaczającymi naczynia krwionośne, zachowaniem oligodendrocytów i oznakami aktywacji układu dopełniacza.³⁰ Jednak kilka badań przeprowadzonych w 2020 roku wykazało, że zmiany w MOGAD różnią się od tych obserwowanych w SM pod wieloma względami, w tym rozkładem topograficznym w OUN, rodzajem demielinizacji i charakterem odpowiedzi zapalnej.³¹

Rola limfocytów T CD4+

Centralna rola limfocytów T CD4+ specyficznych dla MOG w patogenezie MOGAD została wykazana przez badania, które ujawniają ich obecność w zmianach zapalnych u pacjentów z MOGAD.³² W przeciwieństwie do MS, naciekające limfocyty są głównie typu CD4+ z tylko kilkoma limfocytami B i limfocytami T CD8+.³³

Prozapalne środowisko, które umożliwia otwarcie bariery krew-mózg dla wejścia potencjalnie patogennych przeciwciał, ma kluczowe znaczenie dla patogenezy MOGAD.³⁴ Druga możliwość, zwana hipotezą „outside-in”, zakłada aktywację limfocytów w obwodowych węzłach chłonnych poprzez mimikrę molekularną lub pan-aktywację po systemowym zakażeniu wirusowym.³⁵

Rola układu dopełniacza

Rola aktywacji dopełniacza w MOGAD jest nadal przedmiotem dyskusji i nie została dobrze ustalona.³⁶ Chociaż rola aktywacji dopełniacza jako mechanizmu uszkodzenia została dobrze ustalona w NMOSD, jest to mniej jasne w MOGAD.³⁷ Ścieżki dopełniacza odgrywają rolę zarówno w modelach EAE opartych na MOG, jak i w MOGAD.³⁸

Aktywacja dopełniacza wydaje się odgrywać mniejszą rolę w patogenezie MOGAD niż w przypadku AQP4-NMOSD, co sugeruje, że leczenie ukierunkowane na tę ścieżkę może nie okazać się użyteczne w MOGAD.³⁹

Bezpośredni wpływ przeciwciał na oligodendrocyty

MOG-IgG wykazało bezpośredni patogenny wpływ na oligodendrocyty: zmiana cytoszkieletu, przemieszczanie MOG do tratw lipidowych, zmiana wzoru fosforylacji różnych białek, a ponadto zmiana ekspresji białek aksonalnych.⁴⁰ Przeciwciała pobrane z surowicy pacjentów z MOG-ON, które są głównie izotypu IgG1, indukują demielinizację w modelach zwierzęcych z udziałem szlaku dopełniacza, jeśli reagują krzyżowo z MOG gryzoni w połączeniu z limfocytami T specyficznymi dla zasadowego białka mieliny.⁴¹

Potencjalne czynniki wyzwalające

Rozważano kilka potencjalnych czynników wyzwalających MOGAD. Zaproponowano proces autoimmunologiczny poinfekcyjny jako możliwy mechanizm patofizjologiczny. Inne doniesienia wskazują na mimikrę molekularną między MOG a niektórymi wirusami jako możliwą etiologię.⁴²

Różne czynniki środowiskowe, takie jak infekcje lub szczepienia, mogą wywołać aktywację immunologiczną przeciwko antygenom MOG.⁴³ Stan poinfekcyjny MOGAD może być spowodowany zakażeniem wirusem opryszczki pospolitej, cytomegalowirusem, Borrelia i wirusem Epsteina-Barr.⁴⁴

Ciekawe, że ostatnie dane sugerują rolę COVID-19 w nawrocie MOGAD. Nawrót MOGAD związany z COVID-19 prawdopodobnie wynika z osiągnięcia przez gospodarza progu, prowadzącego do produkcji limfocytów B MOG-IgG1.⁴⁵

Układ glimfatyczny w MOGAD

Niedawne badania wykazały, że układ glimfatyczny może być zaburzony u pacjentów z MOGAD. Średni indeks ALPS (diffusivity along the perivascular space) pacjentów z MOGAD był znacząco niższy niż u zdrowych osób z grupy kontrolnej, co wskazuje na zmniejszoną dynamikę płynu śródmiąższowego i może sugerować zaburzenie funkcji układu glimfatycznego w MOGAD. Dodatkowo wykazano istotną korelację między indeksem ALPS u pacjentów z MOGAD a ich niepełnosprawnością kliniczną.⁴⁶⁴⁷

System oczyszczania odpadów w mózgu może być użyteczny w unikaniu dalszych uszkodzeń tkanek spowodowanych gromadzeniem się neurotoksycznych produktów odpadowych po aktywności zapalnej. Dlatego postawiono hipotezę, że układ glimfatyczny jest zaburzony u pacjentów z MOGAD i przyczynia się do niepełnosprawności klinicznej, pośrednio pogarszając procesy zapalne i neurodegeneracyjne z powodu nieefektywnego usuwania rozpuszczalnych produktów odpadowych, utrzymując prozapalny stan tkanki mózgowej.⁴⁸

Patogeneza w zapaleniu nerwu wzrokowego

Patofizjologia zapalenia nerwu wzrokowego w MOGAD jest szczególnie interesująca, ponieważ MOG nie jest wyrażany w siatkówce.⁴⁹ U pacjentów, którzy przeszli rezonans magnetyczny oczodołów, ujawniono obrzęknięte, powiększone i kręte nerwy wzrokowe, z obustronnymi długimi lub krótkimi segmentami nieprawidłowego sygnału hiperintensywnego T2, który zazwyczaj obejmował przednie części nerwów wzrokowych, oszczędzając skrzyżowanie nerwów wzrokowych i drogi siatkówkowo-pokrywkowe.⁵⁰

Czynniki ryzyka i otyłość

Interesujące jest to, że niedawne badania wykazały związek między otyłością (BMI≥30 kg/m²) a prawdopodobieństwem diagnozy MOGAD u pacjentów z ostrym zapaleniem nerwu wzrokowego. Podczas gdy otyłość w okresie dojrzewania była wcześniej zgłaszana jako związana ze zwiększonym ryzykiem MS, związek między MOGAD a otyłością nie był wcześniej badany. Może to sugerować związek między zapaleniem wywołanym otyłością a wyższym ryzykiem MOGAD.⁵¹

Wyzwania i przyszłe kierunki

Chociaż patogeneza MOGAD jest coraz częściej badana, dokładne mechanizmy pozostają niejasne.⁵² Nie jest jasne, czy przeciwciała anty-MOG są zdolne do bezpośredniej niezależnej patogenności.⁵³ Rola ludzkich przeciwciał MOG-IgG jest mniej jasna i omawiane są różne mechanizmy patogenne. Przyszłe badania, które mają na celu określenie dokładnej patogenezy, są potrzebne do dalszej identyfikacji celów dla skutecznych strategii leczenia.⁵⁴

Ogólnie przewidywanie ryzyka nawrotu w MOGAD pozostaje wyzwaniem i istnieją sprzeczne dane dotyczące związku między serologiczną pozytywnością MOGAD w czasie a ryzykiem przyszłych nawrotów.⁵⁵ Choć poziom miana przeciwciał anty-MOG może wpływać na rokowanie, a rokowanie miana przeciwciał anty-MOG będzie dalej wpływać na nawrót choroby, wiele osób z MOGAD nie będzie miało nawrotu.⁵⁶⁵⁷

Istnieją ograniczone dane dotyczące długoterminowego zarządzania ryzykiem nawrotu w MOGAD, brakuje randomizowanych badań kontrolowanych w tym obszarze.⁵⁸ Wiele osób z MOGAD może skorzystać z długoterminowej immunoterapii, a dalsze zrozumienie dokładnej patofizjologii MOGAD będzie kluczowe w pomaganiu w identyfikacji najbardziej skutecznych metod leczenia w celu zmniejszenia ryzyka przyszłej niepełnosprawności neurologicznej.⁵⁹

Przypadki MOGAD u pacjentów z HIV i znacznie obniżoną odpornością wskazują na możliwość dysregulacji immunologicznej w infekcji HIV. Ponadto zgłaszano nietypowe prezentacje zarówno ADEM, jak i NMOSD u pacjentów zakażonych HIV, a dysregulacja immunologiczna może odgrywać rolę. Obecność przeciwciał anty-MOG i niskie liczby CD4 u pacjentów z zaawansowanym HIV kwestionują niektóre z postulowanych teorii patogenezy MOGAD.⁶⁰

Przyszłe lata będą świadkami znaczącego rozwoju liczby biomarkerów diagnostycznych, prognostycznych i terapeutycznych do odróżnienia MOGAD od NMOSD i MS, otwierając możliwość nowych strategii terapeutycznych.⁶¹

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Materiały źródłowe

#1 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions. Its location on the outermost part of the myelin sheath in the CNS makes it a potential target for MOG antibodies. These induce demyelination in experimental autoimmune encephalomyelitis animal models immunized with MOG. However, most human MOG antibodies do not recognize rodent MOG, which has hampered the application of many rodent studies to human MOGAD. It is notable that when human MOG antibodies that do recognize rodent MOG were injected intrathecally in rodents with myelin-reactive T cells, the MOG antibody was noted to be directly pathogenic, inducing demyelination and leading to complement deposition.
#2 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. […] The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions.
#3 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. […] The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions.
#4 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions. Its location on the outermost part of the myelin sheath in the CNS makes it a potential target for MOG antibodies. These induce demyelination in experimental autoimmune encephalomyelitis animal models immunized with MOG. However, most human MOG antibodies do not recognize rodent MOG, which has hampered the application of many rodent studies to human MOGAD. It is notable that when human MOG antibodies that do recognize rodent MOG were injected intrathecally in rodents with myelin-reactive T cells, the MOG antibody was noted to be directly pathogenic, inducing demyelination and leading to complement deposition.
#5 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions. Its location on the outermost part of the myelin sheath in the CNS makes it a potential target for MOG antibodies. These induce demyelination in experimental autoimmune encephalomyelitis animal models immunized with MOG. However, most human MOG antibodies do not recognize rodent MOG, which has hampered the application of many rodent studies to human MOGAD. It is notable that when human MOG antibodies that do recognize rodent MOG were injected intrathecally in rodents with myelin-reactive T cells, the MOG antibody was noted to be directly pathogenic, inducing demyelination and leading to complement deposition.
#6 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions. Its location on the outermost part of the myelin sheath in the CNS makes it a potential target for MOG antibodies. These induce demyelination in experimental autoimmune encephalomyelitis animal models immunized with MOG. However, most human MOG antibodies do not recognize rodent MOG, which has hampered the application of many rodent studies to human MOGAD. It is notable that when human MOG antibodies that do recognize rodent MOG were injected intrathecally in rodents with myelin-reactive T cells, the MOG antibody was noted to be directly pathogenic, inducing demyelination and leading to complement deposition.
#7 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/
Myelin oligodendrocyte glycoprotein (MOG)-associated disease (MOGAD) is a rare, antibody-mediated inflammatory demyelinating disorder of the central nervous system (CNS) with various phenotypes starting from optic neuritis, via transverse myelitis to acute demyelinating encephalomyelitis (ADEM) and cortical encephalitis. […] MOG is a molecule detected on the outer membrane of myelin sheaths and expressed primarily within the brain, spinal cord and also the optic nerves. […] The specific outmost location of myelin makes it a potential target for autoimmune antibodies and cell-mediated responses in demyelinating processes. […] A critical element of reliable diagnosis is detection of pathogenic serum antibodies MOG with accurate, specific and sensitive methods, preferably with optimized cell-based assay (CBA).
#8 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43
Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed exclusively on the surface of oligodendrocytes in the central nervous system (CNS). […] MOG-antibody associated disease (MOGAD) has evolved into a discrete autoimmune, neuroinflammatory disease entity with a broad clinical spectrum which continues to evolve as our understanding increases. […] The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. […] MOG-specific B cells, plasma cells and their products (MOG Abs) activate MOG-specific effector T cells via CNS resident antigen-presenting cells (APC). […] Anti-MOG antibodies (IgG1) bind MOG expressed on the surface of myelin and oligodendrocytes, damaging myelin sheaths, and leading to demyelination through antibody-dependent cellular cytotoxicity or complement activation. […] The central role of MOG-specific CD4 T cells in the pathogenesis of MOGAD has been demonstrated by studies that reveal their presence in inflammatory lesions of MOGAD patients. […] Although the pathogenesis of MOGAD is increasingly being studied, the precise mechanisms remain unclear.
#9 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/
The substantial progress of MOG-dependent CNS autoimmunity research was made possible by the development of a few models of the diseaseMOG EAE (MOG experimental autoimmune encephalomyelitis) in rodents. […] The localization of MOG at the external lamellae of myelin sheaths and on the surface of oligodendrocytes membrane is not the only hint suggesting this protein may be involved in the interaction with the immune system and pathophysiology of demyelinating disorders. […] Indeed, several clinical trials have found that antibodies against MOG would play a role in MS pathophysiology: they have been shown in active lesions in MS patients, the serum anti-MOG-Ig response has been established in both early and late stage of this disease, patients with higher anti-MOG antibodies had relapses more often and earlier than patients without or low anti-MOG levels.
#10 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). […] Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. […] CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. […] Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses.
#11 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross BBB. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden APCs and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4 T cells, unlike CD8 in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help B cells differentiate into MOG antibody-producing plasma cells in the peripheral blood.
#12 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). […] Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. […] CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. […] Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses.
#13 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross BBB. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden APCs and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4 T cells, unlike CD8 in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help B cells differentiate into MOG antibody-producing plasma cells in the peripheral blood.
#14 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). […] Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. […] CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. […] Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses.
#15 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. […] A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. […] In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#16 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#17 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). […] Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. […] CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. […] Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses.
#18 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross BBB. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden APCs and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4 T cells, unlike CD8 in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help B cells differentiate into MOG antibody-producing plasma cells in the peripheral blood.
#19 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross BBB. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden APCs and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4 T cells, unlike CD8 in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help B cells differentiate into MOG antibody-producing plasma cells in the peripheral blood.
#20 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43
Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed exclusively on the surface of oligodendrocytes in the central nervous system (CNS). […] MOG-antibody associated disease (MOGAD) has evolved into a discrete autoimmune, neuroinflammatory disease entity with a broad clinical spectrum which continues to evolve as our understanding increases. […] The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. […] MOG-specific B cells, plasma cells and their products (MOG Abs) activate MOG-specific effector T cells via CNS resident antigen-presenting cells (APC). […] Anti-MOG antibodies (IgG1) bind MOG expressed on the surface of myelin and oligodendrocytes, damaging myelin sheaths, and leading to demyelination through antibody-dependent cellular cytotoxicity or complement activation. […] The central role of MOG-specific CD4 T cells in the pathogenesis of MOGAD has been demonstrated by studies that reveal their presence in inflammatory lesions of MOGAD patients. […] Although the pathogenesis of MOGAD is increasingly being studied, the precise mechanisms remain unclear.
#21 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/
MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. […] MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross BBB. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden APCs and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4 T cells, unlike CD8 in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help B cells differentiate into MOG antibody-producing plasma cells in the peripheral blood.
#22 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43
Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed exclusively on the surface of oligodendrocytes in the central nervous system (CNS). […] MOG-antibody associated disease (MOGAD) has evolved into a discrete autoimmune, neuroinflammatory disease entity with a broad clinical spectrum which continues to evolve as our understanding increases. […] The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. […] MOG-specific B cells, plasma cells and their products (MOG Abs) activate MOG-specific effector T cells via CNS resident antigen-presenting cells (APC). […] Anti-MOG antibodies (IgG1) bind MOG expressed on the surface of myelin and oligodendrocytes, damaging myelin sheaths, and leading to demyelination through antibody-dependent cellular cytotoxicity or complement activation. […] The central role of MOG-specific CD4 T cells in the pathogenesis of MOGAD has been demonstrated by studies that reveal their presence in inflammatory lesions of MOGAD patients. […] Although the pathogenesis of MOGAD is increasingly being studied, the precise mechanisms remain unclear.
#23 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. The discovery of a disease-specific serum immunoglobulin G (IgG) antibody that selectively binds myelin oligodendrocyte glycoprotein (MOG) has led to increased understanding of a diverse spectrum of disorders, which are now termed MOGAD. Overall, the pathologic features support an antibody-mediated central nervous system (CNS) demyelinating disease distinct from multiple sclerosis (MS). […] MOG is a minor component of myelin and is expressed on the surface of oligodendrocytes. As a member of the immunoglobulin superfamily, MOG is highly immunogenic. The function of MOG has not been fully elucidated, but it may act as a cell adhesion molecule, regulate microtubule stability, and modulate myelin immune interactions. Its location on the outermost part of the myelin sheath in the CNS makes it a potential target for MOG antibodies. These induce demyelination in experimental autoimmune encephalomyelitis animal models immunized with MOG. However, most human MOG antibodies do not recognize rodent MOG, which has hampered the application of many rodent studies to human MOGAD. It is notable that when human MOG antibodies that do recognize rodent MOG were injected intrathecally in rodents with myelin-reactive T cells, the MOG antibody was noted to be directly pathogenic, inducing demyelination and leading to complement deposition.
#24 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#25 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#26 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#27 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#28 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. These studies have revealed coexisting perivenous and confluent demyelination. Cortical demyelination is frequent, and intracortical demyelinating lesions predominate. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. Complement deposition is also noted, and an overlap with pattern II MS pathology has been reported. In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#29 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis
Human pathology studies of MOGAD have provided some insight into its pathogenesis and mostly have focused on the brain lesions during biopsy or at autopsy. […] A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed. […] In contrast to aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent.
#30 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease
MOG (myelin oligodendrocyte glycoprotein) antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica. […] A post-infectious autoimmune process has been proposed as a possible pathophysiologic mechanism. Other reports point to molecular mimicry between MOG and some viruses as a possible etiology. […] Demyelinating lesions of MOG-associated encephalomyelitis resemble more those observed in multiple sclerosis than NMO. They are similar to pattern-II multiple sclerosis with T-cells and macrophages surrounding blood vessels, preservation of oligodendrocytes and signs of complement system activation. […] Several studies performed during 2020 have shown that MOGAD lesions differ from those seen in MS in many aspects, including their topographical distribution in the CNS, the type of demyelination, and the nature of the inflammatory response.
#31 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease
MOG (myelin oligodendrocyte glycoprotein) antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica. […] A post-infectious autoimmune process has been proposed as a possible pathophysiologic mechanism. Other reports point to molecular mimicry between MOG and some viruses as a possible etiology. […] Demyelinating lesions of MOG-associated encephalomyelitis resemble more those observed in multiple sclerosis than NMO. They are similar to pattern-II multiple sclerosis with T-cells and macrophages surrounding blood vessels, preservation of oligodendrocytes and signs of complement system activation. […] Several studies performed during 2020 have shown that MOGAD lesions differ from those seen in MS in many aspects, including their topographical distribution in the CNS, the type of demyelination, and the nature of the inflammatory response.
#32 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43
Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed exclusively on the surface of oligodendrocytes in the central nervous system (CNS). […] MOG-antibody associated disease (MOGAD) has evolved into a discrete autoimmune, neuroinflammatory disease entity with a broad clinical spectrum which continues to evolve as our understanding increases. […] The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. […] MOG-specific B cells, plasma cells and their products (MOG Abs) activate MOG-specific effector T cells via CNS resident antigen-presenting cells (APC). […] Anti-MOG antibodies (IgG1) bind MOG expressed on the surface of myelin and oligodendrocytes, damaging myelin sheaths, and leading to demyelination through antibody-dependent cellular cytotoxicity or complement activation. […] The central role of MOG-specific CD4 T cells in the pathogenesis of MOGAD has been demonstrated by studies that reveal their presence in inflammatory lesions of MOGAD patients. […] Although the pathogenesis of MOGAD is increasingly being studied, the precise mechanisms remain unclear.
#33
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
In contrast to MS, infiltrating lymphocytes were mainly of the CD4+ type with only few B cells and CD8+ T cells. […] Nevertheless, the role of human MOG-IgG is less clear and different pathogenic mechanisms are discussed. Future studies that aim to define the exact pathogenesis, are needed to further identify targets for efficient treatment strategies.
#34
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
Despite the increasing knowledge of clinical MOGAD presentations, the pathophysiology and importantly, the pathogenic role of human MOG-IgG, remains to be fully determined. […] In patients with MOGAD, genetic studies showed no strong correlation between human leukocyte antigen (HLA) genotype and MOGAD development; importantly, no cause for disease pathogenesis has been found. […] A pro-inflammatory environment that enables opening of the blood-brain barrier (BBB) for the entry of potentially pathogenic antibodies is crucial for the pathogenesis of MOGAD. […] The second possibility, called the outside-in hypothesis, posits an activation of lymphocytes in peripheral LN through molecular mimicry or pan-activation after a systemic viral infection. […] A recent study found a protective effect of the HLA-C*03:04 allele, whereas a Dutch study could not find any associations.
#35
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
Despite the increasing knowledge of clinical MOGAD presentations, the pathophysiology and importantly, the pathogenic role of human MOG-IgG, remains to be fully determined. […] In patients with MOGAD, genetic studies showed no strong correlation between human leukocyte antigen (HLA) genotype and MOGAD development; importantly, no cause for disease pathogenesis has been found. […] A pro-inflammatory environment that enables opening of the blood-brain barrier (BBB) for the entry of potentially pathogenic antibodies is crucial for the pathogenesis of MOGAD. […] The second possibility, called the outside-in hypothesis, posits an activation of lymphocytes in peripheral LN through molecular mimicry or pan-activation after a systemic viral infection. […] A recent study found a protective effect of the HLA-C*03:04 allele, whereas a Dutch study could not find any associations.
#36
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
The role of complement activation in MOGAD is still under debate and not well-established. […] MOG-IgG has shown a direct pathogenic effect on oligodendrocytes: changing the cytoskeleton, repartitioning of MOG into lipid rafts, altering the phosphorylation pattern of different proteins, and furthermore, changing the expression of axonal proteins. […] Systematic neuropathological examinations of patients with MOGAD are rare and include several case reports and 2 larger studies. […] The neuropathological examinations of autopsies and biopsies from patients revealed a pattern of perivenous and confluent demyelination present in white matter, the cortex, and in deep gray matter structures. […] Importantly, confluent lesions were the result of fusion of perivenous lesions rather than MS-like radial expanding lesions.
#37 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease
Myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) are a spectrum of idiopathic, inflammatory, demyelinating diseases affecting the central nervous system (CNS). […] The exact pathogenesis of antibody induced injury is not confirmed yet but may possibly include complement activation. […] Although the role of complement activation as a downstream mechanism of injury has been well established in NMOSD, this is less clear in MOGAD. […] Pathologically NMOSD is classified as an astrocytopathy, while MOG IgG associated disorders are classified as oligodendrogliopathies and this difference is reflected in serum and CSF levels of glial fibrillary acidic protein (GFAP), a marker of astrocytic damage which is found less commonly in MOGAD patients compared to NMOSD.
#38 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is now identified routinely owing to the development of widely commercially available cell-based assay (CBA) antibody testing. […] MOG is a minor myelin protein, but anti-MOG antibodies play a critical role in animal models in the induction of both an encephalitogenic T-cell response and humoral, antibody-mediated demyelination. […] Subsequent work demonstrated that only anti-MOG antibodies targeting the native conformation of MOG were pathogenic, whereas anti-MOG antibodies targeting linear epitopes of MOG did not cause disease. […] Complement pathways play a role in both MOG-based EAE models and MOGAD. […] Whether anti-MOG antibodies are capable of direct independent pathogenicity is unclear. […] The risk of relapse in MOGAD is variable, but likely up to 50% of people with MOGAD will not have a relapse. […] Many individuals with MOGAD may benefit from long-term immunotherapy, and further insight into the precise pathophysiology of MOGAD will be critical in helping identify the most effective treatments to reduce the risk of future neurologic disability.
#39 Advancing Expertise in the Understanding of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Masterclass Event Summary – European Medical Journal
https://www.emjreviews.com/neurology/symposium/advancing-expertise-in-the-understanding-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-masterclass-event-summary-s110224/
Recent years have witnessed a significant evolution in the number of diagnostic, prognostic, and therapeutic biomarkers for distinguishing MOGAD from NMOSD and MS, opening up the possibility of novel therapeutic strategies. […] Complement activation appears to play less of a role in MOGAD pathogenesis than in that of AQP4-NMOSD, suggesting that treatments targeting this pathway may not prove useful in MOGAD.
#40
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
The role of complement activation in MOGAD is still under debate and not well-established. […] MOG-IgG has shown a direct pathogenic effect on oligodendrocytes: changing the cytoskeleton, repartitioning of MOG into lipid rafts, altering the phosphorylation pattern of different proteins, and furthermore, changing the expression of axonal proteins. […] Systematic neuropathological examinations of patients with MOGAD are rare and include several case reports and 2 larger studies. […] The neuropathological examinations of autopsies and biopsies from patients revealed a pattern of perivenous and confluent demyelination present in white matter, the cortex, and in deep gray matter structures. […] Importantly, confluent lesions were the result of fusion of perivenous lesions rather than MS-like radial expanding lesions.
#41 MOG antibody-associated optic neuritis | Eye
https://www.nature.com/articles/s41433-024-03108-y
Antibodies taken from the sera of patients with MOG-ON, which are primarily of the IgG1 isotype, induce demyelination in animal models with involvement of the complement pathway if they are cross-reactive with rodent MOG in combination with myelin basic protein-specific T cells. […] The trigger for antibody production in MOGAD is unknown. […] The pathophysiology of ON in MOGAD is particularly interesting as MOG is not expressed in the retina.
#42 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease
MOG (myelin oligodendrocyte glycoprotein) antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica. […] A post-infectious autoimmune process has been proposed as a possible pathophysiologic mechanism. Other reports point to molecular mimicry between MOG and some viruses as a possible etiology. […] Demyelinating lesions of MOG-associated encephalomyelitis resemble more those observed in multiple sclerosis than NMO. They are similar to pattern-II multiple sclerosis with T-cells and macrophages surrounding blood vessels, preservation of oligodendrocytes and signs of complement system activation. […] Several studies performed during 2020 have shown that MOGAD lesions differ from those seen in MS in many aspects, including their topographical distribution in the CNS, the type of demyelination, and the nature of the inflammatory response.
#43 The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children
https://www.explorationpub.com/Journals/ent/Article/100469
Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. […] Diagnosis of MOGAD is mainly made by detecting anti-MOG antibodies in serum using CBAs in the presence of clinical findings compatible with MOGAD, such as multiphasic acute disseminated encephalomyelitis (M-ADEM) in younger children, recurrent optic neuritis (ON) or neuromyelitis optica spectrum disorder (NMOSD) phenotypes in older children and adolescents. […] MOG is a central nervous system (CNS)-specific protein found only on the myelin sheath and on the surface of oligodendrocytes. […] Various environmental factors such as infections or vaccinations can trigger immune activation against MOG antigens. […] The incidence of MOGAD, the only recurrent CNS demyelinating disease that is more common in children than adults, is approximately three times higher than in adults.
#44 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Text
https://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4
The findings specific to MOGAD include seropositive MOG-IgG antibodies, and frequently, CNS demyelination via MRI. […] The post-infectious state of MOGAD may be due to herpes simplex virus, cytomegalovirus, Borrelia, and EpsteinBarr virus infections. […] Several cytokines and inflammatory markers have been implicated to play a role in the post-infectious state and development of MOG-IgG antibodies, including CRP, d-dimer, IL-6, 7, 19, GCSF, IP 10, MCP1.MIP1A and TNF alpha. […] However, the mechanism contributing to the MOG-IgG antibody is unclear. […] Interestingly, the recent data suggest a role for Coronavirus Disease 2019 in Myelin Oligodendrocyte Glycoprotein Antibody Disorder relapse. […] COVID-19-associated MOGAD relapse is likely from the host reaching a threshold, leading to production of MOG-IgG1B-cell. […] More importantly, these findings demonstrate that the SARS-CoV-2 virus may impact disease exacerbation in other relapsing CNS inflammatory disorders.
#45 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Text
https://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4
The findings specific to MOGAD include seropositive MOG-IgG antibodies, and frequently, CNS demyelination via MRI. […] The post-infectious state of MOGAD may be due to herpes simplex virus, cytomegalovirus, Borrelia, and EpsteinBarr virus infections. […] Several cytokines and inflammatory markers have been implicated to play a role in the post-infectious state and development of MOG-IgG antibodies, including CRP, d-dimer, IL-6, 7, 19, GCSF, IP 10, MCP1.MIP1A and TNF alpha. […] However, the mechanism contributing to the MOG-IgG antibody is unclear. […] Interestingly, the recent data suggest a role for Coronavirus Disease 2019 in Myelin Oligodendrocyte Glycoprotein Antibody Disorder relapse. […] COVID-19-associated MOGAD relapse is likely from the host reaching a threshold, leading to production of MOG-IgG1B-cell. […] More importantly, these findings demonstrate that the SARS-CoV-2 virus may impact disease exacerbation in other relapsing CNS inflammatory disorders.
#46 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66
Impaired glymphatic function has been suggested to be implicated in the pathophysiology of MS and aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder. This study aimed to investigate the interstitial fluid dynamics in the brain in patients with myelin oligodendrocyte glycoprotein antibody disorders (MOGAD), another demyelinating disorder, using a noninvasive imaging technique called the diffusivity along the perivascular space (ALPS) index. […] The mean ALPS index of patients with MOGAD was significantly lower than that of healthy controls (Cohen d = 0.93, false discovery rate-corrected P = .02). The lower mean ALPS index was significantly associated with a worse Expanded Disability Status Scale score (Spearman = 0.51; 95% CI, 0.85 to 0.02; P = .03). […] This study suggests that patients with MOGAD may have impaired glymphatic function, as measured by the ALPS index, which is associated with patient disability.
#47 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66
Our results showed that the ALPS index was significantly lower in patients with MOGAD compared with healthy controls, indicating reduced interstitial fluid dynamics, which may suggest impaired glymphatic system function in MOGAD. Additionally, we found a significant correlation between the ALPS index in patients with MOGAD and their clinical disability. […] The causative role of glymphatic dysfunction in patient disability should be investigated through longitudinal studies. Such studies may eventually evaluate the potential of glymphatic function assessment as a predictive marker of relapse and disease progression. […] We demonstrated that patients with MOGAD exhibit impaired glymphatic function and that reduced glymphatic function is linked to patient disability. The findings of this study could potentially enhance our understanding of the pathophysiology of MOGAD and contribute to the development of new therapeutic strategies.
#48 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66
Myelin oligodendrocyte glycoprotein antibody disorders (MOGAD) is a newly recognized entity of demyelinating disorders of the CNS defined by the presence of serum immunoglobulin G (IgG) autoantibodies against myelin oligodendrocyte glycoprotein (MOG). […] The pathologic hallmark of MOGAD is coexisting perivenous and confluent demyelination with relatively preserved oligodendrocytes. […] A waste-clearing system of the brain may be useful in avoiding further tissue damage due to the accumulation of neurotoxic waste products following inflammatory activity. […] Therefore, we hypothesized that the glymphatic system is impaired in patients with MOGAD and contributes to clinical disability by indirectly worsening inflammatory and neurodegenerative processes due to the inefficient removal of soluble waste products, maintaining a proinflammatory state of the brain tissue.
#49 MOG antibody-associated optic neuritis | Eye
https://www.nature.com/articles/s41433-024-03108-y
Antibodies taken from the sera of patients with MOG-ON, which are primarily of the IgG1 isotype, induce demyelination in animal models with involvement of the complement pathway if they are cross-reactive with rodent MOG in combination with myelin basic protein-specific T cells. […] The trigger for antibody production in MOGAD is unknown. […] The pathophysiology of ON in MOGAD is particularly interesting as MOG is not expressed in the retina.
#50 MRI features of myelin oligodendrocyte glycoprotein antibody disease: a descriptive studyâhow it differs from neuromyelitis optica spectrum disorders and multiple sclerosis | Egyptian Journal of Radiology and Nuclear Medicine | Full Text
https://ejrnm.springeropen.com/articles/10.1186/s43055-023-01066-1
Patients with MOGAD who underwent orbital MRI revealed oedematous, enlarged, and tortuous optic nerves, with bilateral long or short segments of abnormal T2 hyperintense signal that typically involved anterior segments of the optic nerves while sparing the optic chiasm and retro-chiasmatic pathways. […] This study has potential limitations. Firstly, the sample size of this study is relatively small as MOGAD is a rare and newly described neuroinflammatory disease. […] We hope our findings help clinicians systematically evaluate and manage patients with suspicious neuroinflammatory diseases.
#51 Obesity is associated with myelin oligodendrocyte glycoprotein antibody-associated disease in acute optic neuritis | Scientific Reports
https://www.nature.com/articles/s41598-022-21592-8
Our study found an association between obesity (BMIâ¥30 kg/m2) and the likelihood of a MOGAD diagnosis in patients with acute ON. […] While obesity during adolescence has been reported to be associated with an increased risk of MS, to our knowledge, the association between MOGAD and obesity has not been explored in the past. […] This may suggest a relationship between obesity-induced inflammation and a higher risk for MOGAD. […] Future prospective investigation of the association between obesity and MOGAD may help shed light on the pathogenic mechanisms of this intriguing disorder.
#52 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43
Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed exclusively on the surface of oligodendrocytes in the central nervous system (CNS). […] MOG-antibody associated disease (MOGAD) has evolved into a discrete autoimmune, neuroinflammatory disease entity with a broad clinical spectrum which continues to evolve as our understanding increases. […] The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. […] MOG-specific B cells, plasma cells and their products (MOG Abs) activate MOG-specific effector T cells via CNS resident antigen-presenting cells (APC). […] Anti-MOG antibodies (IgG1) bind MOG expressed on the surface of myelin and oligodendrocytes, damaging myelin sheaths, and leading to demyelination through antibody-dependent cellular cytotoxicity or complement activation. […] The central role of MOG-specific CD4 T cells in the pathogenesis of MOGAD has been demonstrated by studies that reveal their presence in inflammatory lesions of MOGAD patients. […] Although the pathogenesis of MOGAD is increasingly being studied, the precise mechanisms remain unclear.
#53 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is now identified routinely owing to the development of widely commercially available cell-based assay (CBA) antibody testing. […] MOG is a minor myelin protein, but anti-MOG antibodies play a critical role in animal models in the induction of both an encephalitogenic T-cell response and humoral, antibody-mediated demyelination. […] Subsequent work demonstrated that only anti-MOG antibodies targeting the native conformation of MOG were pathogenic, whereas anti-MOG antibodies targeting linear epitopes of MOG did not cause disease. […] Complement pathways play a role in both MOG-based EAE models and MOGAD. […] Whether anti-MOG antibodies are capable of direct independent pathogenicity is unclear. […] The risk of relapse in MOGAD is variable, but likely up to 50% of people with MOGAD will not have a relapse. […] Many individuals with MOGAD may benefit from long-term immunotherapy, and further insight into the precise pathophysiology of MOGAD will be critical in helping identify the most effective treatments to reduce the risk of future neurologic disability.
#54
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx
In contrast to MS, infiltrating lymphocytes were mainly of the CD4+ type with only few B cells and CD8+ T cells. […] Nevertheless, the role of human MOG-IgG is less clear and different pathogenic mechanisms are discussed. Future studies that aim to define the exact pathogenesis, are needed to further identify targets for efficient treatment strategies.
#55 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease
Overall, prediction of risk of relapse in MOGAD remains challenging and there is conflicting data surrounding relationship between MOGAD seropositivity over time and risk of future relapses. […] There is limited data on long term management of risk of recurrence in MOGAD with randomized controlled trials lacking in this area.
#56 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is now identified routinely owing to the development of widely commercially available cell-based assay (CBA) antibody testing. […] MOG is a minor myelin protein, but anti-MOG antibodies play a critical role in animal models in the induction of both an encephalitogenic T-cell response and humoral, antibody-mediated demyelination. […] Subsequent work demonstrated that only anti-MOG antibodies targeting the native conformation of MOG were pathogenic, whereas anti-MOG antibodies targeting linear epitopes of MOG did not cause disease. […] Complement pathways play a role in both MOG-based EAE models and MOGAD. […] Whether anti-MOG antibodies are capable of direct independent pathogenicity is unclear. […] The risk of relapse in MOGAD is variable, but likely up to 50% of people with MOGAD will not have a relapse. […] Many individuals with MOGAD may benefit from long-term immunotherapy, and further insight into the precise pathophysiology of MOGAD will be critical in helping identify the most effective treatments to reduce the risk of future neurologic disability.
#57 Clinical characteristics and prognosis of pediatric myelin oligodendrocyte glycoprotein antibody-associated diseases in China | BMC Pediatrics | Full Text
https://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-022-03679-3
The positivity rate of MOG-Ab in our study was 33%, which is slightly higher than that reported in studies among children in other countries. […] The initial treatment time was positively correlated with the duration of the disease, and the prognosis may be affected by the disease time course and serum MOG-Ab titer. […] The level of the MOG-Ab titer may affect the MOG-Ab titer prognosis, and the prognosis of the MOG-Ab titer will further affect disease recurrence. […] The choice of treatment after the diagnosis of MOGAD is crucial in determining the prognosis of the disease.
#58 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease
Overall, prediction of risk of relapse in MOGAD remains challenging and there is conflicting data surrounding relationship between MOGAD seropositivity over time and risk of future relapses. […] There is limited data on long term management of risk of recurrence in MOGAD with randomized controlled trials lacking in this area.
#59 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is now identified routinely owing to the development of widely commercially available cell-based assay (CBA) antibody testing. […] MOG is a minor myelin protein, but anti-MOG antibodies play a critical role in animal models in the induction of both an encephalitogenic T-cell response and humoral, antibody-mediated demyelination. […] Subsequent work demonstrated that only anti-MOG antibodies targeting the native conformation of MOG were pathogenic, whereas anti-MOG antibodies targeting linear epitopes of MOG did not cause disease. […] Complement pathways play a role in both MOG-based EAE models and MOGAD. […] Whether anti-MOG antibodies are capable of direct independent pathogenicity is unclear. […] The risk of relapse in MOGAD is variable, but likely up to 50% of people with MOGAD will not have a relapse. […] Many individuals with MOGAD may benefit from long-term immunotherapy, and further insight into the precise pathophysiology of MOGAD will be critical in helping identify the most effective treatments to reduce the risk of future neurologic disability.
#60 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and Human Immunodeficiency virus infection: dilemmas in diagnosis and management: a case series | Journal of Medical Case Reports | Full Text
https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-023-04191-7
There is limited data on the association between MOGAD and HIV infection, with two case reports found in literature. Myelopathy with positive serum MOG antibodies was present in both of these cases, but one had a well-controlled HIV infection while the other was seroconverting at the time of presentation. The three patients reported here had aggressive presentations: the first with an ADEM presentation, the second with LETM extending from the brainstem to conus medullaris with respiratory compromise, and the third with bilateral optic neuritis that did not improve after immunosuppression and plasma exchange. […] These atypical presentations of MOGAD in patients with significant immunocompromise raises the possibility of immune dysregulation from HIV infection. Moreover, atypical presentations of both ADEM and NMOSD in HIV positive patients have been reported and immune dysregulation is thought to play a role. The pathophysiology of MOGAD is not completely understood; however, there are hypotheses that complement activation and CD4-positive T cell inflammation (unlike CD8 T cells in multiple sclerosis) predominate its pathogenesis. The presence of MOG antibodies and low CD4 counts in patients with advanced HIV challenges some of the postulated theories of the MOGAD pathogenesis. Thus, studying MOGAD in HIV infected patients may provide clues as to the type of immune dysregulation occurring in MOGAD patients and hence contribute to further understanding of its pathophysiology.
#61 Advancing Expertise in the Understanding of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Masterclass Event Summary – European Medical Journal
https://www.emjreviews.com/neurology/symposium/advancing-expertise-in-the-understanding-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-masterclass-event-summary-s110224/
Recent years have witnessed a significant evolution in the number of diagnostic, prognostic, and therapeutic biomarkers for distinguishing MOGAD from NMOSD and MS, opening up the possibility of novel therapeutic strategies. […] Complement activation appears to play less of a role in MOGAD pathogenesis than in that of AQP4-NMOSD, suggesting that treatments targeting this pathway may not prove useful in MOGAD.

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (mogad) Patofizjologia i mechanizm

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (MOGAD) Patogeneza i mechanizm

Charakterystyka białka MOG

Patofizjologia MOGAD

Rola przeciwciał anty-MOG

Badania patologiczne MOGAD

Rola limfocytów T CD4+

Rola układu dopełniacza

Bezpośredni wpływ przeciwciał na oligodendrocyty

Potencjalne czynniki wyzwalające

Układ glimfatyczny w MOGAD

Patogeneza w zapaleniu nerwu wzrokowego

Czynniki ryzyka i otyłość

Wyzwania i przyszłe kierunki

Kolejne rozdziały

Materiały źródłowe

#1 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#2 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#3 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#4 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#5 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#6 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#7 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/

#8 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Managementhttps://www.mdpi.com/2073-4468/13/2/43

#9 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/

#10 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#11 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#12 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#13 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#14 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#15 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#16 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#17 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#18 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#19 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#20 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Managementhttps://www.mdpi.com/2073-4468/13/2/43

#21 Pathophysiology of myelin oligodendrocyte glycoprotein antibody diseasehttps://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#22 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Managementhttps://www.mdpi.com/2073-4468/13/2/43

#23 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#24 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#25 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#26 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#27 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#28 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#29 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDatehttps://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#30 MOG antibody disease – Wikipediahttps://en.wikipedia.org/wiki/MOG_antibody_disease

#31 MOG antibody disease – Wikipediahttps://en.wikipedia.org/wiki/MOG_antibody_disease

#32 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Managementhttps://www.mdpi.com/2073-4468/13/2/43

#33https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#34https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#35https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#36https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#37 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinichttps://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#38 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Diseasehttps://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#40https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#41 MOG antibody-associated optic neuritis | Eyehttps://www.nature.com/articles/s41433-024-03108-y

#42 MOG antibody disease – Wikipediahttps://en.wikipedia.org/wiki/MOG_antibody_disease

#43 The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in childrenhttps://www.explorationpub.com/Journals/ent/Article/100469

#44 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Texthttps://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4

#45 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Texthttps://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4

#46 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiologyhttp://www.ajnr.org/content/45/1/66

#47 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiologyhttp://www.ajnr.org/content/45/1/66

#48 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiologyhttp://www.ajnr.org/content/45/1/66

#49 MOG antibody-associated optic neuritis | Eyehttps://www.nature.com/articles/s41433-024-03108-y

#51 Obesity is associated with myelin oligodendrocyte glycoprotein antibody-associated disease in acute optic neuritis | Scientific Reportshttps://www.nature.com/articles/s41598-022-21592-8

#52 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Managementhttps://www.mdpi.com/2073-4468/13/2/43

#53 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Diseasehttps://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#54https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#55 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinichttps://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#56 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Diseasehttps://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#57 Clinical characteristics and prognosis of pediatric myelin oligodendrocyte glycoprotein antibody-associated diseases in China | BMC Pediatrics | Full Texthttps://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-022-03679-3

#58 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinichttps://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#59 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Diseasehttps://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#60 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and Human Immunodeficiency virus infection: dilemmas in diagnosis and management: a case series | Journal of Medical Case Reports | Full Texthttps://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-023-04191-7

Zobacz więcej

Choroba związana z przeciwciałami białka mieliny oligodendrocytów (mogad)
Patofizjologia i mechanizm

#1 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#2 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#3 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#4 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#5 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#6 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#7 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/

#8 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43

#9 Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Current Insights into the Disease Pathophysiology, Diagnosis and Management
https://pmc.ncbi.nlm.nih.gov/articles/PMC7795410/

#10 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#11 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#12 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#13 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#14 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#15 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#16 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#17 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#18 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#19 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#20 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43

#21 Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease
https://pmc.ncbi.nlm.nih.gov/articles/PMC10011114/

#22 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43

#23 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#24 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#25 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#26 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#27 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#28 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis/print

#29 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): Clinical features and diagnosis – UpToDate
https://www.uptodate.com/contents/myelin-oligodendrocyte-glycoprotein-antibody-associated-disease-mogad-clinical-features-and-diagnosis

#30 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease

#31 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease

#32 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43

#33
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#34
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#35
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#36
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#37 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#38 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#40
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#41 MOG antibody-associated optic neuritis | Eye
https://www.nature.com/articles/s41433-024-03108-y

#42 MOG antibody disease – Wikipedia
https://en.wikipedia.org/wiki/MOG_antibody_disease

#43 The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children
https://www.explorationpub.com/Journals/ent/Article/100469

#44 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Text
https://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4

#45 Myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and myelitis in COVID-19: a case report and a review of the literature | The Egyptian Journal of Neurology, Psychiatry and Neurosurgery | Full Text
https://ejnpn.springeropen.com/articles/10.1186/s41983-022-00496-4

#46 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66

#47 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66

#48 Glymphatic System Dysfunction in Myelin Oligodendrocyte Glycoprotein Immunoglobulin G AntibodyâAssociated Disorders: Association with Clinical Disability | American Journal of Neuroradiology
http://www.ajnr.org/content/45/1/66

#49 MOG antibody-associated optic neuritis | Eye
https://www.nature.com/articles/s41433-024-03108-y

#51 Obesity is associated with myelin oligodendrocyte glycoprotein antibody-associated disease in acute optic neuritis | Scientific Reports
https://www.nature.com/articles/s41598-022-21592-8

#52 Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management
https://www.mdpi.com/2073-4468/13/2/43

#53 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#54
https://journals.lww.com/jneuro-ophthalmology/fulltext/2023/03000/the_potential_pathogenicity_of_myelin.2.aspx

#55 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#56 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#57 Clinical characteristics and prognosis of pediatric myelin oligodendrocyte glycoprotein antibody-associated diseases in China | BMC Pediatrics | Full Text
https://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-022-03679-3

#58 Myelin Oligodendrocyte Antibody Disease Fact Sheet | Cleveland Clinic
https://my.clevelandclinic.org/departments/neurological/depts/multiple-sclerosis/ms-approaches/myelin-oligodendrocyte-glycoprotein-antibody-disease

#59 The Evolution of Myelin Oligodendrocyte Glycoprotein AntibodyâAssociated Disease
https://practicalneurology.com/articles/2023-mar/the-evolution-of-myelin-oligodendrocyte-glycoprotein-antibody-associated-disease

#60 Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and Human Immunodeficiency virus infection: dilemmas in diagnosis and management: a case series | Journal of Medical Case Reports | Full Text
https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-023-04191-7