MOGGIES miss the point. Right idea..wrong disease?


A couple of weeks ago I did a post asking “Should we be bricking it about taking anti-CD20 antibodies”. I apologise to the non-native English speaking readers…(e.g. Our American friends…:-) at the use of slang. I generally add a link on these things to help you understand and also it expands your knowledge of English. “Bricking it” derives from the idea that you deficate/pooh/Sh1 bricks rather than faeces/pooh because you are so scared…therefore “bricking-it” means you are “very scared”.

When I decided to do blogging, I made a decision to write, more like I speak and not do the “plain-English” stuff that makes things easy to read. We were told to use plain English…but you have to rebel sometimes. I thought it would be more human and likewise it can allow one to add humour, entertainment and light to what are often bleak subjects. Also by entertainment, I mean that it is less boring to do Blog-posts. We could go on fishing trips to catch a DrDrey fish… you get the turgid stuff eleswhere

Todays post is about the Moggies. Now, if you look at what a Moggy is, it is a Britsh slang word for a non-pedigree cat = a mongrel cat.

To my surprise it is evident that a MOGGY mean many thinks in slang English

  1. (Scotland and Northern England regional, obsoleteSynonym of girl: a female child or young woman
  2. (Midlands and Northern England regional, derogatory, rareSynonym of slattern: an unkempt or badlydressed woman
  3. (Midlands and Northern England regional, rareSynonym of scarecrow.
  4. (Midlands regional, rareSynonym of calf.
  5. (Britain) A domestic catespecially (depreciative or derogatory) a non-pedigree or unremarkable cat

However we can add another and this is someone who works on myelin oligodencrocyte glycoprotein (MOG) EAE and thinks that this is MS.

Dr. Love was the first person to show that MOG induced a T cell-mediated disease and remember doing the work for her.

Identification of epitopes of myelin oligodendrocyte glycoprotein for the induction of experimental allergic encephalomyelitis in SJL and Biozzi AB/H mice.Amor S, Groome N, Linington C, Morris MM, Dornmair K, Gardinier MV, Matthieu JM, Baker D.J Immunol. 1994 Nov 15;153(10):4349-56.

This followed from work showing that antibodies to MOG could cause demyelination if the T cells opened the blood-brain barrier to let things in.

When it was found that MOG could induce EAE in transgenic mice this opened a doorway and the Moggy was born. Now if you ask a Moggy to tell you what MS is they tell you what EAE is…Don’t believe me? Read any review on MS and all you get is Th17, Treg stuff.

However, fact is a problem. Neuromyelitis optica (NMO) was once part of MS but is now its own entity. It was found that in NMO many people had antibodies to aquaporin-4. However a subset of these people had antibodies to MOG.

In the current paper

Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study.Takai Y, Misu T, Kaneko K, Chihara N, Narikawa K, Tsuchida S, Nishida H, Komori T, Seki M, Komatsu T, Nakamagoe K, Ikeda T, Yoshida M, Takahashi T, Ono H, Nishiyama S, Kuroda H, Nakashima I, Suzuki H, Bradl M, Lassmann H, Fujihara K, Aoki M; Japan MOG-antibody Disease Consortium. Brain. 2020 May 15. pii: awaa102. doi: 10.1093/brain/awaa102. [Epub ahead of print]

Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis (The Moggies claim otherwise). So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. In this study, we immunohistochemically analysed biopsied (they were alive) brain tissues from 11 patients with MOG antibody-associated disease and other inflammatory demyelinating diseases. Patient median onset age was 29 years (range 9-64), and the median interval from attack to biopsy was 1 month (range 0.5-96). The clinical diagnoses were ADEM (n = 2), MDEM (n = 1), multiple brain lesions without encephalopathy (n = 3), leukoencephalopathy (n = 3) and cortical encephalitis (n = 2). All these cases had multiple/extensive lesions on MRI and were oligoclonal IgG band-negative. Most demyelinating lesions in 10 of 11 cases showed a perivenous demyelinating pattern previously reported in ADEM (153/167 lesions) (and EAE) and a fusion pattern (11/167 lesions) mainly in the cortico-medullary junctions and white matter (Grey/White matter border) , and only three lesions in two cases showed confluent demyelinated plaques (Like mouse EAE where there is limited primary demyelination). In addition, 60 of 167 demyelinating lesions (mainly in the early phase) showed MOG-dominant myelin loss, but relatively preserved oligodendrocytes (Like early EAE), which were distinct from those of AQP4 antibody-positive NMOSD exhibiting myelin-associated glycoprotein-dominant oligodendrogliopathy. In MOG antibody-associated diseases, MOG-laden macrophages were found in the perivascular spaces and demyelinating lesions, and infiltrated cells were abundant surrounding multiple blood vessels in and around the demyelinating lesions, mainly consisting of macrophages (CD68; 1814 ± 1188 cells/mm2), B cells (CD20; 468 ± 817 cells/mm2), and T cells (CD3; 2286 ± 1951 cells/mm2), with CD4-dominance (CD4+ versus CD8+; 1281 ± 1196 cells/mm2 versus 851 ± 762 cells/mm2, P < 0.01) (Just like EAE). Humoral immunity, evidenced by perivascular deposits of activated complements and immunoglobulins, was occasionally observed in some MOG antibody-associated demyelinating lesions (EAE), and the frequency was much lower than that in AQP4 antibody-positive NMOSD. Subpial lesions with perivenous demyelination were observed in both ADEM and cortical encephalitis. Our study suggests that ADEM-like perivenous inflammatory demyelination with MOG-dominant myelin loss is a characteristic finding of MOG antibody-associated disease regardless of whether the diagnostic criteria of ADEM are met. These pathological features are clearly different from those of multiple sclerosis and AQP4 antibody-positive NMOSD, suggesting an independent autoimmune demyelinating disease entity.

So is this EAE-like condition telling the Moggies anything? Are the Moggies purring up the wrong treet? Is a clinical feature of MOG-induced disease…having a disorted world view not based on the clinical reality and feature I wonder.:-)

I know I get critised by you for “doing technobabble “posts. I wonder if they are Moggies?

Barking is a noise of a dog. Purr is a noise of a cat, Moogies are cats, bark is the stuff on the outside of treets, “barking up the wrong tree” is to be wrong about the reason for something or to be wrong in the way to achieve something…Now you know you are dealing

Maybe I’m just bonkers and MS is EAE. Rat, guinea pig EAE has no neutrophils, Mouse EAE has neutrophils. Until now MS has no neutrophils but lets change history and MS has neutrophils therefore mouse EAE=MS

Expansion of Neutrophils and Classical and Nonclassical Monocytes as a Hallmark in Relapsing-Remitting Multiple Sclerosis.Haschka D, Tymoszuk P, Bsteh G, Petzer V, Berek K, Theurl I, Berger T, Weiss GFront Immunol. 2020 Apr 29;11:594. doi: 10.3389/fimmu.2020.00594. eCollection 2020.

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