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My views on the Cunningham test


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I'm not saying this is the case with your brother, but it does make you wonder since you now know that their is autoimmune disorder in the family. The article explained how 20% of schizophrenia is caused by prenatal infections. I can't remember the post-natal number. So, for some the infection occurs early in life, but the schizophrenia doesn't surface until adulthood.

 

A stunning number was that children who were born to mothers exposed to the german measles (rubella) during the 1964 US epidemic were 10 times more likely than other children to develop schizophrenia!

 

Did you or any of your family ever wonder if it was caused by an autoimmune reaction?

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Looks like I'm a bit late to the party here.

 

The science is:

Cunningham and Kirvan isolated 3 antibodies 24.3.1, 31.1.1 and 37.2.1 that interacted or inhibited binding of Monosialoganglioside GM1. These antibodies also had epitype for N-acetyl-beta-D-glucosamine. Finally, 24.3.1 was found to cause activation of Cam Kinase II when presented to neuroblastoma cells. N-acetyl-beta-D-glucosamine is the dominant carbohydrate on GABHS.

 

Now translating:

Cunningham and Kirvan found 3 antibodies that interfered with neurotransmitters in the brain. These antibodies target a particular molecular sequence which happens to be a part of the Group A Beta Hemolytic cell wall structure. In neuro-blastoma cells Cam Kinase II activation regulates the amount of dopamine released.

 

So what Cunningham was studying was the disregulation of dopamine due to the introduction of antibodies.

 

While CaM Kinase II can occur elsewhere in the body (i.e., muscles etc), Cunningham was testing the level of Cam Kinase II activation with neuro-blastoma cells and the interaction with dopamine.

 

Now to the question about Strep:

 

What was unusual about 24.3.1 was that it was targeting a particular carbohydrate (GlcNAC). This carbohydrate is the predominantcomponent of the GABHS cell wall; however, this carbohydrate does exist elsewhere in the body (in particular in joints) and thus it's possible for some other event to cause the activation of the B-cell for the production of the anti-GlcNAC antibody. Kirvan and Cunningham are not yet able to discuss causality but only correspondence -- i.e., that the antibodies exist in more quantity in children with certain symptoms and if exposed to neuroblastoma cells cause CaM Kinase II activation.

 

So, no they do not know whether the antibody is produced only in response to Strep -- but can show that the antibody is produced in a group of children in response to GABHS.

 

 

 

I don't think it was ever said that her findings were unique to strep. I believe what she has studied over the last years focused on strep. Am I right with this? Also, because this is PANDAS forum and for a long time dealt with strep was the main trigger perhaps some inferred it was strep only? But I don't think that was actually ever said.
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Better late then never... thanks again for simplifying the science!

 

-Wendy

 

Looks like I'm a bit late to the party here.

 

The science is:

Cunningham and Kirvan isolated 3 antibodies 24.3.1, 31.1.1 and 37.2.1 that interacted or inhibited binding of Monosialoganglioside GM1. These antibodies also had epitype for N-acetyl-beta-D-glucosamine. Finally, 24.3.1 was found to cause activation of Cam Kinase II when presented to neuroblastoma cells. N-acetyl-beta-D-glucosamine is the dominant carbohydrate on GABHS.

 

Now translating:

Cunningham and Kirvan found 3 antibodies that interfered with neurotransmitters in the brain. These antibodies target a particular molecular sequence which happens to be a part of the Group A Beta Hemolytic cell wall structure. In neuro-blastoma cells Cam Kinase II activation regulates the amount of dopamine released.

 

So what Cunningham was studying was the disregulation of dopamine due to the introduction of antibodies.

 

While CaM Kinase II can occur elsewhere in the body (i.e., muscles etc), Cunningham was testing the level of Cam Kinase II activation with neuro-blastoma cells and the interaction with dopamine.

 

Now to the question about Strep:

 

What was unusual about 24.3.1 was that it was targeting a particular carbohydrate (GlcNAC). This carbohydrate is the predominantcomponent of the GABHS cell wall; however, this carbohydrate does exist elsewhere in the body (in particular in joints) and thus it's possible for some other event to cause the activation of the B-cell for the production of the anti-GlcNAC antibody. Kirvan and Cunningham are not yet able to discuss causality but only correspondence -- i.e., that the antibodies exist in more quantity in children with certain symptoms and if exposed to neuroblastoma cells cause CaM Kinase II activation.

 

So, no they do not know whether the antibody is produced only in response to Strep -- but can show that the antibody is produced in a group of children in response to GABHS.

 

 

 

I don't think it was ever said that her findings were unique to strep. I believe what she has studied over the last years focused on strep. Am I right with this? Also, because this is PANDAS forum and for a long time dealt with strep was the main trigger perhaps some inferred it was strep only? But I don't think that was actually ever said.

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Perhaps she has not focused on strep, but the acronym PANDAS really focuse on strep, and that is what most people hear. I think this is making it difficult for general docs to think of the PANDAS/PITAND coninuum. Why do we not include PITAND when we talk about PANDAS?

 

I could not agree more! IT is amazing how many specialists defined Sandra as a spectrum of mental conditions of all sorts and walks just because they read the PANDAS acronym and did not even bother to figure the entire picture. Best was a neuropsychiatrist who told us in end of 2008 that she had anxiety disorder (with a history of very positive reaction to Clarithromycin, Prednisone and IVIG) because her older suster was school bullied way back in elementary and junior high , and that PANDAS was all about Strep. No Strep meant for him a mental condition. As simple as that. Yes, and I will never forget the long que to neuurologists who thought I was only a bother with the insistance on this infection (Influenza A followed by Mycoplasma Pneomonia) she had just before it all started at the age of 15.

 

I have tried to ask that PITAND or ITAND or whatever the name needs to be to reflect the actual condition be included, but got replies (also on this forum) that research funding is meagre for PANDAS and that any such change will cause confusion. In fact I think that PITAND or whatever that should be, no being spoken of poses a threat to the quality of treatment and future of my 20 years old daughter. Those doctors here who bother to read about the condition see the main stream, or worse, the anti PANDAS politics some doctors drive, and are afraid to diagnose or treat the already diagnosed elsewhere. I had to go twice abroad to have Sandra diagnosed correctly, tested and treated by proxy. For the past 5 years my life is an on going war against the medical establishment to accept that this is a real condition and a treatable one. That she may have a chronic condition but that need not be a debilitating one as it has been for so many years.

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Perhaps she has not focused on strep, but the acronym PANDAS really focuse on strep, and that is what most people hear. I think this is making it difficult for general docs to think of the PANDAS/PITAND coninuum. Why do we not include PITAND when we talk about PANDAS?

 

I could not agree more! IT is amazing how many specialists defined Sandra as a spectrum of mental conditions of all sorts and walks just because they read the PANDAS acronym and did not even bother to figure the entire picture. Best was a neuropsychiatrist who told us in end of 2008 that she had anxiety disorder (with a history of very positive reaction to Clarithromycin, Prednisone and IVIG) because her older suster was school bullied way back in elementary and junior high , and that PANDAS was all about Strep. No Strep meant for him a mental condition. As simple as that. Yes, and I will never forget the long que to neuurologists who thought I was only a bother with the insistance on this infection (Influenza A followed by Mycoplasma Pneomonia) she had just before it all started at the age of 15.

 

I have tried to ask that PITAND or ITAND or whatever the name needs to be to reflect the actual condition be included, but got replies (also on this forum) that research funding is meagre for PANDAS and that any such change will cause confusion. In fact I think that PITAND or whatever that should be, no being spoken of poses a threat to the quality of treatment and future of my 20 years old daughter. Those doctors here who bother to read about the condition see the main stream, or worse, the anti PANDAS politics some doctors drive, and are afraid to diagnose or treat the already diagnosed elsewhere. I had to go twice abroad to have Sandra diagnosed correctly, tested and treated by proxy. For the past 5 years my life is an on going war against the medical establishment to accept that this is a real condition and a treatable one. That she may have a chronic condition but that need not be a debilitating one as it has been for so many years.

 

AMEN!!! and God Bless Bat-shev!!!!

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