[Nicknerd]

Hey guys,

Alright...I'm on another MG forum, and someone posted some extremely interesting research.....

This is regarding Ocular MG, but doesn't seem to be limited to the pure ocular form of MG. Basically, it says that a large number for MG patients with the ocular type have antibodies to anticholineriterase (sp.?) which basically means that the sx they experience are due to excess acetylcholine as opposed to too little- so essentially, they are having a cholinergic crisis (this is what i gather from this)...check it out...

This is the published extract from the Journal of Neuroimmunology .


Anti-acetylcholinesterase antibodies associate with ocular myasthenia gravis
Carlo Provenzanoa 1 , Mariapaola Marinoa1, Flavia Scuderia, Amelia Evolib, Emanuela Bartoccionia
Received 4 September 2009; received in revised form 6 November 2009; accepted 6 November 2009. published online 30 November 2009.

Abstract
In MG, anti-AChR or anti-MuSK abs impair neuromuscular transmission. Partial inhibition of AChE can ameliorate symptoms, while a complete block causes a cholinergic blockade. We found anti-AChE abs in 115/240 MG patients, with no correlation with sex, age at onset, thymus pathology, presence of anti-AChR or anti-MuSK antibodies. We found a correlation with the ocular form of the disease, and with milder forms of MG not requiring immunosuppressants; moreover, when we considered only those patients who were off AChEI therapy, we found that ocular patients were positive for anti-AChE abs, while generalized patients were negative. According to an experimental model, we hypothesize that anti-AChE abs could contribute to ptosis through an inhibition of the sympathetic innervation of the tarsal muscle.

This, I think, is applicable to at least a few people here...I think it's pretty profound, and I wonder why our neuros. haven't spoken with us about this possibility...Maybe this is why so many have had negative effects with mestinon?

What do you all think? Did I understand this correctly, or what?

[AnnieB3]

Way cool, Nicky! Super find.

Yeah, so, it looks like an autoimmune process interferes with the ability of the AChE (the enzyme) to "mop up" after acetylcholine, causing too much of acetylcholine. Kind of the opposite of MG.

So MG is to, for example, the Rapsyn CMS mutation where you don't have enough acetylcholine as this new antibody is to Slow Channel Syndrome CMS where there is too much.

I am guessing this article is from Italy or somewhere like that? I haven't been able to find an actual test here except for what has been done in clinical studies on animals. Have you found one?

Well, this just emphasizes what people like Angela Vincent have said. MG AChR and MuSK antibodies are only the tip of the autoimmune iceberg.

Very fascinating indeed. MG may be "the most well-understood autoimmune disease" (which I don't agree with) but the neuromuscular junction is infinitely perplexing.

Annie

http://www.springerlink.com/content/kvhn34021pq76124/

http://www.abcam.com/Acetylcholinest...y-ab35384.html

http://www.williams.edu/imput/synapse/pages/IVA2.html

Susan, This reminds me of how you said you feel better in the sun/heat. Heat increases the enzyme. Hmmmm . . .

[DesertFlower]

Originally Posted by AnnieB3

Susan, This reminds me of how you said you feel better in the sun/heat. Heat increases the enzyme. Hmmmm . . .

Annie, you are right. I do feel better in the heat. And the temperatures went up last week so I am comfortable now temperature-wise...hmmm. So much to learn.


Thanks Nicky.

[jana]

OH MY GOODNESS!!! Nicky, is there a link to the abstract?

[Kathie Glenn]

Originally Posted by Nicknerd

Hey guys,

Alright...I'm on another MG forum, and someone posted some extremely interesting research.....

This is regarding Ocular MG, but doesn't seem to be limited to the pure ocular form of MG. Basically, it says that a large number for MG patients with the ocular type have antibodies to anticholineriterase (sp.?) which basically means that the sx they experience are due to excess acetylcholine as opposed to too little- so essentially, they are having a cholinergic crisis (this is what i gather from this)...check it out...

This is the published extract from the Journal of Neuroimmunology .


Anti-acetylcholinesterase antibodies associate with ocular myasthenia gravis
Carlo Provenzanoa 1 , Mariapaola Marinoa1, Flavia Scuderia, Amelia Evolib, Emanuela Bartoccionia
Received 4 September 2009; received in revised form 6 November 2009; accepted 6 November 2009. published online 30 November 2009.

Abstract
In MG, anti-AChR or anti-MuSK abs impair neuromuscular transmission. Partial inhibition of AChE can ameliorate symptoms, while a complete block causes a cholinergic blockade. We found anti-AChE abs in 115/240 MG patients, with no correlation with sex, age at onset, thymus pathology, presence of anti-AChR or anti-MuSK antibodies. We found a correlation with the ocular form of the disease, and with milder forms of MG not requiring immunosuppressants; moreover, when we considered only those patients who were off AChEI therapy, we found that ocular patients were positive for anti-AChE abs, while generalized patients were negative. According to an experimental model, we hypothesize that anti-AChE abs could contribute to ptosis through an inhibition of the sympathetic innervation of the tarsal muscle.

This, I think, is applicable to at least a few people here...I think it's pretty profound, and I wonder why our neuros. haven't spoken with us about this possibility...Maybe this is why so many have had negative effects with mestinon?

What do you all think? Did I understand this correctly, or what?

Well, this confuses the heck out of me! HA!