imtoken冷钱包下载安装|mog
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2024-03-10 23:29:16
FINAL FANTASY XIV: Mog Station
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FINAL FANTASY XIV: Mog Station -ファイナルファンタジーXIV: モグステーション-
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What Does 'Mog' Mean On TikTok? 'Mogging' As 'Lookism' Slang Explained | Know Your Meme
What Does 'Mog' Mean On TikTok? 'Mogging' As 'Lookism' Slang Explained | Know Your Meme
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What Does 'Mog' Mean On TikTok? 'Mogging' As 'Lookism' Slang Explained
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A niche aspect of internet-bred incel culture has leaked onto the teens on TikTok, with young men exchanging lookism chatter about how to best improve their physical appearance with the hope of attracting women. The community has its own lingo, with the term mogging often being evoked to describe the act of simply being more handsome than your peers.
But where did this word come from and what exactly does it mean? Here's a brief recap of the history of the term mog, from 4chan incel forums to slick TikTok propaganda.
Where Does The Word 'Mog' Mean?
The word "mogging" is derived from the acronym AMOG, which stands for "alpha male of the group." To "mog" someone is to assert one's dominance over them, with the hopes of impressing women. The word comes from pickup artist communities that are preoccupied with the urge to attract women, despite having some pretty misogynistic conceptions of them.
Such ideas about "lookism" stem from the belief that attractive people live life on easy mode by earning more respect from their peers and being more appealing to women. But for some people "mogging" isn't just about looks, it can be about being smarter, richer, or better dressed than other men.
Where Did The Term 'Mogging' Originate?
The term "mogging" has been documented online since at least 2016, finding its origins in fitness forums and imageboards. A May 19th, 2016 post on 4chan's /fit/ saw the word being used to describe a 7-foot-tall bodybuilder. Later that year, a British user complained about getting "height-mogged" in a /fit/ thread.
How Did The Term 'Mogging' Become A Meme?
The term mogging spread to fitness-focused meme pages on Instagram in 2021, as seen in posts by @dark_iron_gains and @memes.to.depth from that year.
Jokes about "mogging" or "being mogged" continued after 2021, however, the term also came to be used ironically and jokingly, as seen in a 4chan post where someone talks about how their muscular baby "mogged."
How Did The Term 'Mogging' Grow Popular On TikTok?
The term grew popular on TikTok around the time of the "mog" meme renaissance, as seen in a September 2021 post by @eddyshreds, and a March 2022 post by @7alfredo13, which gathered nearly 2 million plays.
https://www.tiktok.com/embed/v2/6988612378967411974 https://www.tiktok.com/embed/v2/7080984089884413227
For the full history of Mogging, be sure to check out Know Your Meme's encyclopedia entry for more information.
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More Top Image Galleries Biblically Accurate Angels / Be Not Afraid Khyleri Sadako Rooster Teeth Editorial Details Tags mogging, mogged, mog, lookism, mogging tiktok, incel slang, mogger, mog meaning, what does mog mean tiktok, what is a mog, mogging definition, what does mogged mean, what does mogging mean Author Sakshi Rakshale Associate Editor Sakshi Rakshale is a writer and editor at Know Your Meme with a focus on tech, Gen Z and Indian culture. After completing her thesis on futurism and why some people choose to freeze their heads indefinitely, she drew her focus to writing about AI meme culture, internet slang, and deep desi internet lore. Find more of her work on her Substack. Categories Interviews (140) In the Media (167) White Papers (21) Episode Notes (1) Behind the Scenes (12) Meme Review (343) Collections (5232) Poll (113) Guides (1436) Meme Insider (329) Insights (20) More Top Image Galleries Biblically Accurate Angels / Be Not Afraid Khyleri Sadako Rooster Teeth Know Your Meme Like Page 1.8M likes
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难倒大部分神内医生的MOG抗体病，8大临床表型一文掌握 - 知乎
难倒大部分神内医生的MOG抗体病，8大临床表型一文掌握 - 知乎切换模式写文章登录/注册难倒大部分神内医生的MOG抗体病，8大临床表型一文掌握医学界已认证账号髓鞘少突胶质细胞糖蛋白（myelin oligodendrocyte glycoprotein，MOG）是一种只在中枢神经系统（central nervous system，CNS）少突胶质细胞膜上表达的髓鞘蛋白，位于髓鞘最外层表面，在髓鞘构成中所占比例不足0.05%。它由218个氨基酸组成，是免疫球蛋白超家族成员之一。目前研究认为MOG抗体介导的是一种独立的CNS炎性脱髓鞘疾病（即MOG抗体病），不同于多发性硬化和AQP4阳性视神经脊髓炎谱系疾病（neuromyelitis optica spectrum disorder，NMOSD）。近来，随着MOG抗体病的报道逐渐增多，其临床表现及影像学特征也在不断拓宽。MOG抗体病的常见临床表型1.视神经炎（optic neuritis，ON）ON是青少年和成人MOG抗体病最常见的首发临床表现，其在儿童MOG抗体病中也十分常见。近50%MOG抗体相关性ON患者会再发ON。视盘水肿在多发性硬化和视神经脊髓炎谱系疾病（neuromyelitis optica spectrum disorders，NMOSD）中罕见，但在MOG抗体相关性ON中高达86%，严重者出现视乳头周围出血。由于严重视盘水肿，MOG阳性的双侧ON患者可因颅内压升高而被误诊为乳头水肿。急性期眼眶MRI示纵向广泛视神经强化，易累及视神经前部，而视交叉和视束较少受累。视神经周围炎MRI表现为视神经鞘和周围结构炎症，见于50%的MOG相关性ON患者。视神经周围强化有助于鉴别MOG抗体病与NMOSD和多发性硬化。（图源参考文献5）图1：（a,b）T2WI和T1WI增强分别示视神经肿胀和强化。（c,d）纵向广泛性视神经强化。（e）纵向广泛性视神经炎受累范围从视交叉到眶内，左侧为甚。（f-h）冠状位T1WI示眶内视神经和周围视神经鞘强化，部分延伸至周围脂肪组织。（i）轴位T1WI示右侧视神经强化。（j,k）轴位FLAIR示双侧视束病灶。2.横贯性脊髓炎（transverse myelitis，TM）MOG抗体病常以TM为首发表现，可孤立发生或伴发视神经炎及颅内病灶。MOG抗体相关性TM（MOG-TM）在成人中相对常见，也可见于儿童。MOG-TM可累及脊髓任何节段，但较其他中枢神经系统脱髓鞘疾病更易累及脊髓圆锥。MOG-TM影像学通常表现为长节段横贯性脊髓炎，长度跨越3-4个椎体节段，可同时累及脊髓灰质和白质。灰质受累时脊髓MRI可表现为脊髓中央管线样或H型T2加权像高信号。在这点上MOG-TM同AQP4抗体阳性脊髓炎类似。但相比AQP4抗体阳性脊髓炎而言，MOG-TM脊髓强化和水肿发生率低（见下图）。此外，MOG-TM通常激素反应良好，约9%患者预后不良，5%患者出现复发性脊髓炎。（图源参考文献6）图2：MOG-EM患者可见矢状位T2WI线样征，横断位可见H型高信号，脊髓无强化及肿胀效应。AQP4阳性NMOSD患者MRI T2WI示脊髓肿胀明显，伴明显强化。MS患者脊髓多为短节段、斑片状、白质受累为主，部分可伴有强化。3.急性播散性脑脊髓炎（acute disseminated encephalomyelitis，ADEM）儿童MOG抗体病常表现为ADEM或ADEM样综合征（ADEM伴视神经炎、多相性播散性脑脊髓炎）。典型MRI表现为大的、边界不清的双侧病灶，易累及皮层和深部灰质结构，亦可累及皮层下白质和胼胝体，常伴长节段横贯性脊髓炎。此型复发率高，持续存在的MOG抗体与疾病复发和不良预后相关。因此，对于有可能复发的患者建议在发病后半年和1年复查MOG抗体。（作者提供）图3：颅脑MRI示双侧基底节、丘脑斑片状长T1、长T2信号，DWI未见弥散受限。4.脑干炎脑干受累见于30%的MOG抗体病患者，脑干病变常伴视神经、脊髓和小脑受累，亦有孤立性脑干炎报道。脑干任何部位均可受累，以脑桥最为常见，其次是延髓、小脑脚和中脑。极后区综合征是NMOSD的核心临床特征之一，也同样见于MOG抗体病。此外，MOG抗体病还可类似感染性菱脑炎，MRI表现为脑干病灶强化伴软脑膜强化，影像上类似类固醇激素反应性慢性淋巴细胞性炎症伴脑桥血管周围强化症（CLIPPERS）。（图源参考文献7）图4：延髓背侧包括极后区受累（图源参考文献7）图5：MRI增强扫描示脑桥多发点样和线样强化，类似CLIPPERSMOG抗体病的少见临床表型1.皮质脑炎（cerebral cortical encephalitis，CCE）MOG抗体相关性CCE于2017年由Ogawa等首次描述，随后报道逐渐增多。MOG抗体相关性脑炎常累及幕上白质、皮层灰质旁白质、小脑、中脑、延髓和胼胝体，而CCE确十分少见。Budhram等系统性回顾了20例MOG相关性CCE，最常见的症状是癫痫发作（85%），其次是头痛（70%）、发热（65%）和皮层症状（55%）。绝大多数患者至少存在以上两种症状。在这些患者中，CCE常局限于一侧，而少见于双侧。此外，30%患者出现邻近脑沟T2Flair高信号和软脑膜强化。一侧CCE伴癫痫发作被认为是MOG抗体病的特异性临床表型。（作者提供）图6：颅脑MRI示左侧大脑半球皮层T2FLAIR高信号，TIW1和DWI未见信号改变。增强扫描未见强化。PWI示左侧大脑半球皮层灌注较对侧增加。2.无菌性脑膜炎（aseptic meningitis）以往临床和病理研究证实NMOSD患者可出现软脑膜受累，部分伴有皮层病灶，尤其见于MOG抗体阳性患者。此外，动物研究发现CD28缺陷小鼠注入MOG抗体后可诱发无菌性脑膜炎。因此，无菌性脑膜炎可能是MOG抗体病的直接表现。目前，MOG抗体阳性无菌性脑膜炎文献报道少见，它可以是单相或者继发于视神经炎。无菌性脑膜炎患者临床表现为发热、头痛和颈强直，无直接感染证据且对免疫治疗有效。MRI增强扫描可见局灶性或弥漫性软脑膜强化，可伴多发结节样、点状或线样脑实质强化。软脑膜强化预示血脑屏障破坏。有学者推测前驱感染在血脑屏障通透性和功能改变中发挥重要作用。在血脑屏障破坏前提下，MOG抗体进入中枢神经系统。（图源参考文献9）图7：颅脑MRI增强扫描示软脑膜弥漫性强化。3.脱髓鞘假瘤（demyelinating pseudotumor）脱髓鞘假瘤是一种罕见的中枢神经系统炎性脱髓鞘疾病。MOG相关性脱髓鞘假瘤报道罕见。Shu Y等报道了2例右侧额叶和基底节脱髓鞘假瘤的MOG抗体阳性患者。临床表现颅高压症状（头痛、呕吐）、认知障碍和局灶性神经功能缺损。脑组织活检与多发性硬化样病理类似，可见T细胞、巨噬细胞浸润和补体介导的脱髓鞘等病理改变。（图源参考文献10）图8：免疫治疗前后脱髓鞘假瘤的影像学改变。4.颅神经炎目前国外报道了5例表现为颅神经受累的MOG抗体病患者，包括前庭蜗神经和三叉神经。MOG抗体病颅神经受累的病理生理机制目前仍不清楚，共存的脑干病灶可能提示中枢神经系统炎症的延伸。MRI增强扫描可见颅神经根或脑池段强化。其中有2例患者并发脑干病灶，2例患者出现幕上和近皮层白质、小脑脚和脊髓病灶，另1例患者表现为孤立性动眼神经受累。（图源参考文献11）图9：（A,B）患儿左侧动眼神经麻痹（左上睑下垂、左眼内收障碍）；（C,D）颅脑MRI平扫未见幕上和颈髓病灶。（E-G）增强扫描可见左侧动眼神经脑池段强化。T2W CISS序列可见左侧后交通动脉下外侧面动眼神经肿胀。本文首发于医学界，我们坚持并尊重原创版权，未经授权请勿转载，投稿及爆料请联络医学界管理员：wangqiaoli@yxj.org.cn发布于 2021-12-06 20:00抗体医生单克隆抗体赞同 16添加评论分享喜欢收藏申请
EAE（实验性自身免疫性脑脊髓炎）模型建立：MOG (35-55) 髓鞘少突胶质细胞糖蛋白（35-55） - 上海懋康生物科技有限公司
EAE（实验性自身免疫性脑脊髓炎）模型建立：MOG (35-55) 髓鞘少突胶质细胞糖蛋白（35-55） - 上海懋康生物科技有限公司
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>EAE（实验性自身免疫性脑脊髓炎）模型建立：MOG (35-55) 髓鞘少突胶质细胞糖蛋白（35-55）
EAE（实验性自身免疫性脑脊髓炎）模型建立：MOG (35-55) 髓鞘少突胶质细胞糖蛋白（35-55）
时间：2016-09-27
作者：懋康生物
文章来源：懋康原创
产品关键词：
MOG (35-55) 髓鞘少突胶质细胞糖蛋白（35-55）；中枢神经系统（CNS）；Multiple Sclerosis (MS) 多发性硬化症；实验性自身免疫性脑脊髓炎（EAE）；PLP (178-191)；MBP (87-99)；CAS：149635-73-4；
背景描述：
实验性自身免疫性脑脊髓炎（Experimental
Autoimmune Encephalomyelitis，EAE）是最常用的实验性动物模型用来研究人炎症脱髓鞘病，多发性硬化病（Multiple sclerosis，MS）。EAE是一系列免疫病理和神经病理机制交叉作用引发的综合性状况，导致机体出现近似MS的关键性病特征：炎症反应，脱髓鞘，轴突丧失和胶质增生。就减少炎症的反调控机理和髓鞘再生也发生EAE模型中，因此，该模型也可用来研究这些过程。另外，EAE通常用作细胞介导的器官特异性的自身免疫疾病的模型。EAE具有复杂的神经药理学特征，许多目前已用或即将使用的MS治疗药物得以开发、测试或验证，基于EAE研究。
目前主要由三种髓鞘蛋白（或蛋白多肽）用于诱发EAE模型的研究：髓鞘少突胶质细胞糖蛋白（MOG），髓鞘碱性蛋白（MBP）和髓鞘蛋白脂质蛋白（PLP）。
※ MBP是最早用来EAE研究的髓鞘抗原，多以诱发急性EAE（Acute EAE）模型。
※ MOG是目前常用建立EAE模型的髓鞘抗原，多以诱发慢性EAE（Chronic EAE）模型。
※ PLP也是常用建立EAE模型的髓鞘抗原，模型呈现缓解-复发的特点，多用来建立复发-缓解型（Relapse remitting EAE，RR-EAE）模型。
MOG (35-55)基本描述：
MOG，英文全名Myelin oligodendrocyte glycoprotein，中文名髓鞘少突胶质细胞糖蛋白，髓鞘的一种微量成分，属于免疫球蛋白超家族成员之一。也是特定表达于中枢神经系统（CNS）的自身抗原，诱导多发性硬化症的原发性脱髓鞘特征。
MOG (35-55)是髓鞘少突胶质细胞糖蛋白的免疫优势表位，能够诱导强烈的T细胞和B细胞应激反应，具高度致脑炎性，能够诱导啮齿类动物的实验性自身免疫性脑脊髓炎（EAE）模型。EAE是最普遍的MS动物模型，具有MS许多的临床和病理生理学特征。单次注射MOG (35-55)能够产生一种复发-缓解型神经性疾病，表现出大量斑块状脱髓鞘病症。1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的多巴胺神经元损伤模型，免疫接种MOG (35-55)能抑制该神经元的自发再生功能。
MOG (35-55)基本特性：
我司提供两种类型的MOG（35-55），一种是大小鼠MOG（35-55）（货号：MP5413-1MG），一种是人MOG（35-55）（货号：MP5414-1MG），都可诱导建立EAE模型。两者诱导模型方式的差异可见文献描述：Oliver AR.,Rat and human myelin oligodendrocyte
glycoproteins induce experimental autoimmune encephalomyelitis by different
mechanisms in C57BL/6 mice. J Immunol. 2003 Jul 1; 171(1):462-8.
名称
大小鼠MOG（35-55）
人MOG（35-55）
货号
MP5413-1MG
MP5414-1MG
CAS NO：
149635-73-4
[net]
163158-19-8
分子式
C118H177N35O29S
C120H179N35O28S
分子量
2581.97
2591.99
纯度
≥98%（HPLC）
≥98%（HPLC）
单字母序列
MEVGWYRSPFSRVVHLYRNGK
MEVGWYRPPFSRVVHLYRNGK
EAE模型（MOG）诱导方法：
A）常用动物品系（strain）：C57BL/6 mice（有时称为B6）
B）诱导方法：将MOG（35-55）乳化入弗氏完全佐剂佐剂CFA后皮下注射免疫动物。还可添加腹腔注射百日咳毒素，其能促使免疫细胞穿透血脑屏障。常用注射计量是200μg MOG/小鼠。
【详细诱导步骤可参考资料Stefan Bittner et al., Myelin
Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune
Encephalomyelitis (EAE) in C57BL/6 Mice.或者咨询我司021-54736159】。
C）诱导结果：鼠尾肌肉紧张度完全丧失和后肢功能欠缺，约在MOG诱导后第12天发生。加入药物泼尼松龙（prednisone）可预防EAE发生，实验研究中可用作阳性对照【见下图】 。
订购信息：更大包装或产品技术问题，请来电/在线咨询，电话：021-54736159 。网站：www.maokangbio.com。
货号
产品名称
规格
价格（元）
货期
MP5413-1MG
MOG (35-55), Mouse, Rat 大小鼠髓鞘少突胶质细胞糖蛋白（35-55）
1mg
1600
现货
MP5413-5MG
MOG (35-55), Mouse, Rat 大小鼠髓鞘少突胶质细胞糖蛋白（35-55）
5mg
4800
现货
MP5414-1MG
MOG (35-55), Human 人髓鞘少突胶质细胞糖蛋白（35-55）
1mg
1800
现货
相关产品：更大包装或产品技术问题，请来电/在线咨询，电话：021-54736159 。网站：www.maokangbio.com。
货号
产品名称
规格
价格（元）
货期
Sigma F5881
弗氏完全佐剂（CFA）
10ml
180
现货
Sigma F5506
弗氏不完全佐剂（IFA）
10ml
190
现货
Enzo BML-G100-0050
百日咳毒素Pertussis Toxin（PTX）
50μg
咨询
咨询
注意事项
1）我司提供的所有产品仅能用做科研研究，不可用于人身上以及其他治疗性用途。
2）为了您的安全和健康，请穿实验服并戴一次性手套操作。
— —Written/Edited by V.
Shallan【版权归MKBio懋康所有】
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MOG Antibody Disease - Symptoms, Causes, Treatment | NORD
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Home / Rare Diseases / MOG Antibody Disease
Rare Disease Database
Disease Overview
Synonyms
Signs & Symptoms
Causes
Affected Populations
Disorders with Similar Symptoms
Diagnosis
Standard Therapies
Clinical Trials and Studies
References
Programs & Resources
Complete Report
Disease Overview
Synonyms
Signs & Symptoms
Causes
Affected Populations
Disorders with Similar Symptoms
Diagnosis
Standard Therapies
Clinical Trials and Studies
References
Programs & Resources
Complete Report
Rare Disease Database
Disease Overview
Synonyms
Signs & Symptoms
Causes
Affected Populations
Disorders with Similar Symptoms
Diagnosis
Standard Therapies
Clinical Trials and Studies
References
Programs & Resources
Complete Report
Disease Overview
Synonyms
Signs & Symptoms
Causes
Affected Populations
Disorders with Similar Symptoms
Diagnosis
Standard Therapies
Clinical Trials and Studies
References
Programs & Resources
Complete Report
MOG Antibody Disease
Last updated:
December 07, 2021
Years published: 2021
Acknowledgment
NORD gratefully acknowledges Michael Levy, MD, PhD, Neuroimmunologist, Director, NMO Clinic and Research Laboratory, Massachusetts General Hospital and the Siegel Rare Neuroimmune Association for the preparation of this report.
Disease Overview
Summary
MOG antibody disease (MOGAD) is a neurological, immune-mediated disorder in which there is inflammation in the optic nerve, spinal cord and/or brain. Myelin oligodendrocyte glycoprotein (MOG) is a protein that is located on the surface of myelin sheaths in the central nervous system. While the function of this glycoprotein is not exactly known, MOG is a target of the immune system in this disease. The diagnosis is confirmed when MOG antibodies in the blood are found in patients who have repeated inflammatory attacks of the central nervous system. The specific symptoms and severity of MOGAD can vary from one individual to another, but include issues with vision, symptoms associated with damage to the spinal cord, as well as seizures. Treatments are given at onset, and are typically intravenous steroids, plasma exchange (PLEX) or intravenous immunoglobulin (IVIG). Those with MOG antibody disease should consider ongoing treatment with medications that suppress the immune system.
Introduction
Those with MOG antibody disease may previously have been diagnosed with neuromyelitis optica spectrum disorder (NMOSD), transverse myelitis (TM), acute disseminated encephalomyelitis (ADEM), optic neuritis (ON) or multiple sclerosis (MS) because of the pattern of inflammation it causes including brain, spinal cord and optic nerve damage. Patients with persistently positive antibodies to MOG are at risk for recurrent events. Those with MOG antibody disease do not test positive for the NMO antibody called aquaporin 4 (AQP-4). AQP-4 is a water channel protein and those with NMOSD produce autoantibodies against AQP-4. MOG antibody disease and AQP-4 positive NMOSD are thought to have distinct immunological mechanisms. Furthermore, those with MOG antibody disease seem to be less likely to have other autoimmune disorders (such as rheumatoid arthritis, Hashimoto’s thyroiditis, etc.) than those with AQP-4 positive NMOSD.
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Synonyms
MOGAD
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Signs & Symptoms
MOG antibody disease preferentially causes inflammation in the optic nerve, but can also cause inflammation in the spinal cord, brain, and brainstem. Symptoms can include:
Loss or blurring of vision in one or both eyes
Loss of color vision
Paralysis (no motor function) of a limb or limbs
Paraparesis (weakness) of a limb or limbs
Loss of sensation
Loss of bladder or bowel control
Profound bladder retention
Seizures
Those with MOG antibody disease are more likely to have both optic nerves affected at the same time, and if the symptoms are in only one eye, the other optic nerve may show subclinical atrophy.
Children can be found to have the MOG antibody in the setting of ADEM; however, a positive MOG antibody test in the setting of ADEM does not necessarily imply a course of MOGAD. In many children, the MOG antibody disappears within 1 year, and relapses do not occur. In some, the MOG antibody persists, and relapses may occur. When a relapse occurs, the diagnosis of MOGAD is confirmed.
MOG antibody disease can also occur in relation to another condition called anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. NMDA receptor encephalitis is an autoimmune encephalitis that can cause psychosis, issues with memory and language, and seizures.
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Causes
The exact cause of MOGAD is not known. In those with MOGAD, the immune system attacks the MOG protein found on nerves.
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Affected populations
Among patients with AQP-4 seronegative NMOSD, the frequency of a positive MOG antibody test ranges between 7.4% and 39%. Studies have indicated that between 40% and 58% of children diagnosed with ADEM are positive for the anti-MOG antibody. While there is significant overlap between MOGAD, NMOSD, and ADEM, it appears that MOGAD is a unique immunological condition.
Some studies have shown that those with MOG antibody disease are on average younger and are likely to be male compared to those with AQP-4 positive NMOSD, but other studies have shown no age differences and varying gender distributions. One study revealed a higher proportion of those of Caucasian ethnicity among MOG patients, while others have not shown this difference.
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Disorders with Similar Symptoms
Symptoms of the following disorders can be similar to those of MOGAD. Comparisons may be useful for a differential diagnosis. MOGAD can be misdiagnosed as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), transverse myelitis (TM) and acute disseminated encephalomyelitis (ADEM) because of the pattern of inflammation it causes including brain, spinal cord and optic nerve damage.
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Diagnosis
There are blood tests that can test for MOG antibodies. Only cell-based assays are considered reliable for the diagnosis of MOGAD because of the improved specificity over older ELISA tests. CSF analysis from a lumbar puncture may show increased white blood cell counts in some patients during a relapse, and oligoclonal bands are not usually found.
Unlike anti-AQP4 antibodies, anti-MOG antibodies may decrease over time, and may not be detectable early in the disease process or during remission, and this is especially the case for MOG antibody disease associated ADEM. Those with persistent detection of anti-MOG may be more likely to have a relapsing rather than monophasic disease course.
There appears to be no overlap between individuals with anti-MOG positivity and AQP-4 positivity, although there have been some isolated cases reported using the older ELISA assay.
MRI findings are similar to those with MS and NMOSD, but there may be some differences. MOG antibody disease optic neuritis seems to predominantly affect the retrobulbar region, while AQP-4-associated optic neuritis is found intracranially. Furthermore, MOGAD lesions in the brain can look like lesions seen in those with ADEM.
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Standard Therapies
Acute Treatments
Treatment guidelines for MOG antibody disease have not been established. The following are possible treatments in the management of an acute event.
Intravenous Steroids
Although there are no clinical trials that support a unique approach to treat patients with MOG antibody disease, it is well recognized as a standard of care to give high-dose intravenous methylprednisolone for suspected acute myelitis or optic neuritis, generally for 3 to 5 days, unless there are compelling reasons not to. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of 5 days of steroids. Those with MOG antibody disease seem to respond well to steroids. An oral steroid taper may be helpful to prevent steroid-withdrawal relapses.
Plasma Exchange (PLEX)
PLEX is believed to work in autoimmune CNS diseases through the removal of specific or nonspecific soluble factors likely to mediate, be responsible for, or contribute to inflammatory-mediated organ damage. PLEX is often recommended for moderate to aggressive forms of TM and ON, as is very often the case with MOG antibody disease, if there is not much improvement after being treated with intravenous steroids. If presenting symptoms are severe, PLEX may be initiated concurrently with steroids. There have been no prospective clinical trials that prove PLEX’s effectiveness in MOG antibody disease, but retrospective studies of TM treated with IV steroids followed by PLEX have shown a beneficial outcome. PLEX also has been shown to be effective in other autoimmune or inflammatory central nervous system disorders. Early treatment is beneficial – PLEX is typically started within days of administering steroids, very often before the course of steroids has finished. Particular benefit has been shown if started within the acute or sub-acute stage of the myelitis or if there is continued active inflammation on MRI.
Intravenous Immunoglobulin (IVIG)
Another option for treating anti-MOG associated acute inflammation is intravenous immunoglobulin (IVIG). Immunoglobulin comes from pooled blood that is donated from thousands of healthy people. As the name suggests, IVIG is given intravenously. IVIG is generally well-tolerated. Potential adverse reactions are uncommon, but usually occur during or immediately after an infusion and include headache, nausea, muscle pain, fever, chills, chest discomfort, skin and anaphylactic reactions. Reactions after an infusion can be more serious and include migraine headaches, aseptic meningitis, renal impairment and blood clots. Like corticosteroids and PLEX, there are no data confirming the value of IVIG in the setting of acute events. While most studies support the use of corticosteroids and/or PLEX in acute demyelinating syndromes, IVIG can be considered in certain circumstances.
Other Acute Treatments
In cases of no response to either steroids or PLEX therapy and continued presence of active inflammation in the spinal cord, other forms of immune-based interventions may be required. The use of immunosuppressants or immunomodulatory agents may be considered in some patients. Initial presentation with aggressive forms of myelitis, or if particularly refractory to treatment with steroids and/or PLEX, aggressive immunosuppression is considered. Individuals should be monitored carefully as potential complications may arise from immunosuppression. As with all medications, risks versus benefits of aggressive immunosuppression need to be considered and discussed with the clinical care team.
Long-Term Treatments
Initially, the presence of anti-MOG was thought to be associated with fewer relapses and better outcomes than those with AQP-4 positive NMOSD, but studies with longer follow-up times indicate higher relapse rates than previously reported.
A cohort study from 2016 found that 80% of those in the cohort had a multiphasic disease and an annualized relapse rate (AAR) of 0.9. They found that one third of patients with optic neuritis and around half of patients with spinal cord inflammation made a full recovery. In contrast, two other studies showed that the retinal neuro-axonal damage found after an acute attack of optic neuritis was as severe among anti-MOG positive individuals as individuals with AQP-4 positive NMOSD.
Those with MOG antibody disease should consider ongoing treatment with medications that suppress the immune system. There are no FDA-approved medications for maintenance in MOG antibody disease, so anything prescribed is done off-label. The primary therapies used in the U.S. are mycophenolate mofetil (CellCept), rituximab (Rituxan), azathioprine (Imuran) and repeated IVIG infusions or subcutaneous immunoglobulin. Some studies from the United Kingdom have supported the use of IVIG to prevent relapses.
Some patients presenting with optic neuritis or transverse myelitis who also test positive for the MOG antibody may start treatment after the initial event if the attack was severe and the individual does not want to risk a relapse.
All of these medications carry a risk of infections, particularly upper respiratory infections and urinary tract infections (UTIs). Good hygiene and hand washing are important if on immunosuppressants, as is having a good urologist if at risk for UTIs. There is also the risk with any of these medications of the development of a rare brain infection called progressive multifocal leukoencephalopathy, or PML. PML is an infection caused by the reactivation of a virus, called the JC virus, which lives in the kidney. In someone who is immunosuppressed, this virus can escape the kidney, cross the blood-brain barrier, and enter the brain, causing profound inflammation. Although it can be treated, it is very devastating and sometimes fatal. It is important to know that exposure to these medications in MOG antibody disease has not led to a known case of PML. The known rate of incidence of PML if on Rituxan is estimated at 1 in 25,000 and the rate in CellCept is estimated at 1 in 6,000 based on data from use of these medications for immunosuppression for other purposes. The manufacturer of Imuran cautions about a risk of PML with Imuran as well, but the incidence of PML on Imuran is not documented. Clinical diligence and early intervention are important if PML is suspected.
Chronic immunosuppression requires regular skin exams with a dermatologist since the immune system is the best defense against cancer cells developing, and any of these treatments can interfere with its normal functioning.
Mycophenolate mofetil and azathioprine are both twice daily pills which broadly suppress the immune system. Both medications were originally FDA approved for organ transplant rejection prophylaxis, although azathioprine now is indicated in rheumatoid arthritis, and both have been widely used in several autoimmune disorders. These medications require frequent blood draws upfront, then generally twice yearly to monitor for liver toxicity and to ensure optimal immunosuppression (absolute lymphocyte count around 1 and total white blood cell count between 3 and 4).
Azathioprine is the medication that has been around the longest. However, while the AAR seems to be low on azathioprine, one complication with this medication is that some are not able to stay in remission on azathioprine alone and have to also be on steroids (complications of steroids will be discussed below). Additionally, a long-term study of azathioprine found that the risk of lymphatic-proliferative cancers was reported to be 3%. A common side effect includes gastrointestinal upset, and this may manifest as bloating, constipation, nausea, diarrhea, and may vary throughout the course of one’s time on the medication. Azathioprine is contraindicated in pregnancy, so pregnancy planning is very important. It is FDA Category D (which means don’t take this drug during pregnancy unless it’s lifesaving) and is associated with an increased risk of miscarriages, 7% rate of congenital problems, and high rate of bone marrow suppression that recovers after birth. It is the least expensive of the medications. One study among those with MOG antibody disease found that the mean ARR for azathioprine was 0.99, with 41% of the attacks occurring during the first 6 months, and most of these early attacks were in those who were not also being treated with corticosteroids.
Mycophenolate mofetil has a similar effect on the gastrointestinal system, though many report that the symptoms are milder with mycophenolate as compared with azathioprine. Additionally, some patients complain of headaches with mycophenolate, particularly in the beginning; these tend to wane with ongoing use. Lymphoma may be a risk of this medication; however, there have been no cases reported in MOG antibody disease patients while on this medication, so the risk is likely low. Mycophenolate is also contraindicated in pregnancy, so, again, planning is very important. It is also an FDA Category D (don’t take this drug during pregnancy unless it’s lifesaving) and carries a 45% chance of miscarriage. Of those that do not miscarry, 22% have congenital defects mostly in the face (mouth, ears).
Rituximab is an intravascular infusion which works differently from the other two agents listed above. Rather than being a broad immunosuppressant, rituximab completely depletes one particular type of white blood cell called B-cells, which has downstream effects on the rest of the immune system. Though protocols are slightly different, in general, it is given two times twice a year (4 infusions total) and is given in an outpatient infusion center. This is because of a 30% risk of an infusion reaction without pre-medication with some cocktail of methylprednisolone, diphenhydramine and perhaps acetaminophen. The medication is quite well-tolerated. There are generally no side effects to the medication. There is no lymphoma risk with this medication. There is a monthly blood test to monitor the B-cell CD20 expression. Rituximab is safer in pregnancy than the other two previously described, (Category C; may be toxic in animals or no human data) — there are no official FDA reports of birth defects in cases of pregnancy with rituximab, but babies are born with no CD20 cells. It does not appear to increase risk of infection in babies as the cells re-populate within 6-18 months. In monkey studies performed by the manufacturer, there was no toxicity on the fetus, and monkey babies were born with no CD20 cells, again with no infection risks. In the largest case series published in February 2011, out of 153 women who became pregnant on rituximab, there were 4 post-natal infections and two congenital abnormalities (1 club foot, 1 heart defect), but these women were also on other immunosuppressant medications during the pregnancy, including azathioprine and mycophenolate. They concluded that rituximab does not increase the risk of congenital malformations above the natural rate of 1-2%. Planned pregnancy is still recommended. A study looking at rituximab among those with MOG antibody disease found that three out of nine patients experienced a decline in the ARR, and most relapses occurred either soon after an infusion or at the end-of-dose period.
Low-dose prednisone is used as well, more often outside of the U.S. As noted above, some clinicians also use it in combination with azathioprine for those who continue to relapse on azathioprine alone. Its use is oftentimes not favored in the U.S. for maintenance therapy due to the potential complications associated with long-term steroid use, including diabetes, osteoporosis, weight gain, mood instability, hypertension, skin changes, etc.
IVIG has also been used as a maintenance treatment in MOG antibody disease. One retrospective study looked at treatment, AARs, and disability among 59 patients with MOG antibody disease. This study included 7 patients who were using IVIG as a maintenance therapy. Out of these 7 patients, 3 had relapses while on treatment with IVIG, with 3 out of 7 (43%) having treatment failure. Half of the relapses occurred when weaning IVIG doses or increasing dosing intervals. Another prospective study looking at AARs and disability in 102 children with MOG antibody disease found that maintenance treatment with IVIG reduced the median AAR from 2.16 to 0.51. They also found that 4 (33.3%) out of the 12 patients treated with maintenance IVIG relapsed. Some physicians may also prescribe subcutaneous immunoglobulin.
Studies have shown that conventional treatments for MS are not effective and may cause adverse reactions in AQP4-positive NMOSD. Since there is not enough information about their use in MOG antibody disease, and because they may not reduce relapse rates, or they may lead to adverse effects, treatments for MS are not recommended in MOG antibody disease.
Long-Term Care
After the acute phase, rehabilitative care to improve functional skills and prevent secondary complications of immobility involves both psychological and physical accommodations. There is very little written in the medical literature specifically dealing with rehabilitation after MOGAD. However, much has been written regarding recovery from spinal cord injury (SCI), in general, and this literature applies. The physical issues include visual issues, bladder dysfunction, bowel dysfunction, sexual dysfunction, maintenance of skin integrity, spasticity, pain, depression and fatigue. Rehabilitation and learning how to do activities of daily living (i.e., dressing) with mobility issues is an important part of treatment and recovery from MOGAD.
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Clinical Trials and Studies
Controlled, randomized clinical trials evaluating the various therapies for children and adults with MOGAD have not been done. These studies are necessary to determine the optimal therapeutic options for treating individuals with MOGAD.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Tollfree: (800) 411-1222
TTY: (866) 411-1010
Email: prpl@cc.nih.gov
Some current clinical trials also are posted on the following page on the NORD website: https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/
For information about clinical trials sponsored by private sources, contact: www.centerwatch.com
For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/
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References
JOURNAL ARTICLES
Cobo-Calvo A, Ruiz A, Maillart E, et al. Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults: The MOGADOR study. Neurology. 2018 May 22;90(21):e1858-e1869. doi: 10.1212/WNL.0000000000005560. Epub 2018 Apr 25.
Dos Passos GR, Oliveira LM, da Costa BK, et al. MOG-IgG-Associated Optic Neuritis, Encephalitis, and Myelitis: Lessons Learned From Neuromyelitis Optica Spectrum Disorder. Front Neurol. 2018 Apr 4;9:217. doi: 10.3389/fneur.2018.00217. eCollection 2018.
Fan S, Xu Y, Ren H, et al. Comparison of myelin oligodendrocyte glycoprotein (MOG)-antibody disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) when they co-exist with anti-NMDA (N-methyl-D-aspartate) receptor encephalitis. Mult Scler Relat Disord. 2018 Feb;20:144-152. doi: 10.1016/j.msard.2018.01.007. Epub 2018 Jan 31.
Guo Y, Tian X, Wang X, Xiao Z. Adverse Effects of Immunoglobulin Therapy. Front Immunol. 2018 Jun 8;9:1299. doi: 10.3389/fimmu.2018.01299. eCollection 2018.
Gutman JM, Kupersmith M, Galetta S, Kister I. Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with optic neuritis and seizures. J Neurol Sci. 2018 Apr 15;387:170-173. doi: 10.1016/j.jns.2018.01.042. Epub 2018 Feb 2.
Hacohen Y, Rossor T, Mankad K, et al. ‘Leukodystrophy-like’ phenotype in children with myelin oligodendrocyte glycoprotein antibody-associated disease. Dev Med Child Neurol. 2018 Apr;60(4):417-423. doi: 10.1111/dmcn.13649. Epub 2017 Dec 30.
Hacohen Y, Wong YY, Lechner C, et al. Disease Course and Treatment Responses in Children With Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease. JAMA Neurol. 2018 Apr 1;75(4):478-487. doi: 10.1001/jamaneurol.2017.4601.
Kezuka T, Ishikawa H. Diagnosis and treatment of anti-myelin oligodendrocyte glycoprotein antibody positive optic neuritis. Jpn J Ophthalmol. 2018 Mar;62(2):101-108. doi: 10.1007/s10384-018-0561-1. Epub 2018 Feb 14.
Ramanathan S, Mohammad S, Tantsis E, et al. Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination. J Neurol Neurosurg Psychiatry. 2018 Feb;89(2):127-137. doi: 10.1136/jnnp-2017-316880. Epub 2017 Nov 15.
Weber MS, Derfuss T, Metz I, Brück W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. Ther Adv Neurol Disord. 2018 Mar 29;11:1756286418762083. doi: 10.1177/1756286418762083. eCollection 2018.
Cherin P, Marie I, Michallet M, et al. Management of adverse events in the treatment of patients with immunoglobulin therapy: A review of evidence. Autoimmun Rev. 2016 Jan;15(1):71-81. doi: 10.1016/j.autrev.2015.09.002. Epub 2015.
Jarius S, Ruprecht K, Kleiter I, et al. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome. J Neuroinflammation. 2016; 13: 280.
Lechner C, Baumann M, Hennes EM, et al. Antibodies to MOG and AQP4 in children with neuromyelitis optica and limited forms of the disease. J Neurol Neurosurg Psychiatry. 2016 Aug;87(8):897-905. doi: 10.1136/jnnp-2015-311743. Epub 2015 Dec 8.
Baumann M, Sahin K, Lechner C, et al. Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. J Neurol Neurosurg Psychiatry. 2015;86(3):265-272.
Brilot F, Dale RC, Selter RC, et al. Antibodies to native myelin oligodendrocyte glycoprotein in children with inflammatory demyelinating central nervous system disease. Ann Neurol. 2009 Dec;66(6):833-42. doi: 10.1002/ana.21916.
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