Buster?

[peglem]

I'm confused about Cunningham's anti-neuronal antibodies. Particularly, the anti D1 & D2. Because, it seems to me like "anti" dopamine is something that would lower dopamine levels. But seems like everybody is saying the dopamine levels are higher? So, what is the effect of the anti-dopamines? Are they blocking the receptors? Are they turning on D1 & D2 by activating receptors? Just seems like this would be good to know, especially if one is looking at using psych meds- a kind of clue for what might be more likely to work.

[Buster]

Hi Peglem,

 

As far as I can tell anti-D1 and anti-D2 are about binding to the dopamine 1 and dopamine 2 receptors on neuroblastoma cells. I think there are two D2 receptors (one called short and one called long) where one of them causes signalling and the other one causes inhibition of a signal. To the best that I understand it, when Cunningham says something is anti-lysoganglioside or anti-tubulin or anti-D1 or anti-D2 -- she's saying that the antibody in the blood is interfering with the normal lysoganglioside or tubulin or D1 or D2 bonding at that particular location.

 

So anti-X doesn't mean it attacks X, it means it competes with X -- thereby leaving more X around.

 

Essentially the antibody is mimicing X making it look like you've got more X even though technically you don't. It also seems though that just because the X binds to one of the receptors doesn't seem to mean it causes the same type of signalling. The way it was explained to me was that it's like interference on your car radio -- you still have the base signal but another signal interferes and makes it hard to hear the original signal.

 

Hope that helps, perhaps someone else can add or clarify...

 

Buster

 

 

I'm confused about Cunningham's anti-neuronal antibodies. Particularly, the anti D1 & D2. Because, it seems to me like "anti" dopamine is something that would lower dopamine levels. But seems like everybody is saying the dopamine levels are higher? So, what is the effect of the anti-dopamines? Are they blocking the receptors? Are they turning on D1 & D2 by activating receptors? Just seems like this would be good to know, especially if one is looking at using psych meds- a kind of clue for what might be more likely to work.

[mom md]

I know before we knew it was PANDAS we thought my son had restless leg syndrome because he moved all the time. We tried Mirapex with stimulates dopamine receptors (it is a Parkinsons drug used in RLS) and he got a lot worse. Drugs that antagonize dopamine receptors (like Rispiradol or Haldol ) would help. We were offered rispiradol by a neurologist who beieved we had PANDAS but we never gave it. At the time I was interested in treating the CAUSE and not the symptoms. I think Cunningham is working on a study seeing the effects of Haldol on mice. I heard her say that at one of her lectures.

[peglem]

I know before we knew it was PANDAS we thought my son had restless leg syndrome because he moved all the time. We tried Mirapex with stimulates dopamine receptors (it is a Parkinsons drug used in RLS) and he got a lot worse. Drugs that antagonize dopamine receptors (like Rispiradol or Haldol ) would help. We were offered rispiradol by a neurologist who beieved we had PANDAS but we never gave it. At the time I was interested in treating the CAUSE and not the symptoms. I think Cunningham is working on a study seeing the effects of Haldol on mice. I heard her say that at one of her lectures.

 

We did try risperdal- a couple of times actually. It made her worse, or maybe she just got worse from the PANDAS, and we thought it was the risperdal. But, each time we took her OFF risperdal (3x) we had brief periods of improvement. I just will not use antipsychotics anymore.

[Buster]

The way it was explained to me was that it's like interference on your car radio -- you still have the base signal but another signal interferes and makes it hard to hear the original signal.

 

What I'm trying to say is that it is more like poor regulation (i.e., bad feedback loop) rather than too much or too little. I think that the problem is the randomness of the binding and that the "feedback loop" can't work because there's something other than dopamine binding to the site.

 

It's sort of like trying to figure out your weight by standing on a scale that someone else is randomly putting other things on... The number sort of goes all over the place...

 

That's how I understand it... not as a constant "too much dopamine" or "too little dopamine" but rather that the anti-lyso and anti-D1 and anti-D2 are screwing up the correction factors that figure out how much dopamine to use to cause a signal.

 

Buster