This was prominently featured on Google and Reuters news sites, but in case you missed it, there seems to be an interesting new understanding of the role of serotonin in dyskinesia -- and the possible rehabilation and stimulation of dormant dopamine-producing cells with transplants.

Serotonin solves decades-old mystery in Parkinson's disease:
http://www.physorg.com/news197132585.html


Jon

"Administering a drug to block this action almost immediately eliminated the dyskinesias in both patients."

What drug????

Perhaps cyproheptadine:

http://www.ncbi.nlm.nih.gov/pubmed/9696181

buspar

http://en.wikipedia.org/wiki/Buspirone

Here is a more complete listing.

http://www.pharmacorama.com/en/Sections/Serotonin_5.php

Buspar is not a serotonin antagonist that I could find.

Cyproheptadine is an older drug used long ago for itching and has some antihistamine properties. It also stimulates appetite, and is used to actually treat serotonin syndrome.

buspar for "free floating anxiety" ....so can we just start taking it? it can't be that easy. Cal do you know anymore about it?

Buspar is a dopamine agonist. But there are several dopamine transporters and receptors, and I don't know which would be
for PD patients.

I'd ask the doctor on this one.

Because of the mixed effects, and unknowns about Buspar, it may be very variable across the patient population.

http://www.parkinsons-information-ex...rugdb/022.html

Paula:

All I know is that the lead investigator on the study said that they used buspar - that it was very effective but very short term. There was a suggestion that perhaps a "buspar ER" could be helpful long term. The other interesting news out of this study is that the patients they looked at who were transplanted 12-13 years ago or so, still had fully functioning dopamine neurons from the trransplant and did not have to take any Parkinsons meds at all. Their main issue was the dyskinesia. So it sounds like they're trying to reduce the rogue seretonin cells in the lab and then try the transplant technique again.

Forgive me for asking the question, I read the study, and couldn't really get to grips with it, am very tired right now..... Your reply below seems to indicate that there were patients who had transplants years ago, are no longer on ANY pd meds, still have dyskinesias after all that time......... from the rogue overproductive seratonin cells. I am not sure I understand this, surely the reason for having transplants such as these would have been to get rid of dyskinesias anyway, or reduce risk of getting them. So it was experimental........ but the very thing that puts people off taking our gold standard drug, the one that we are told to avoid, and these transplants produce the same things...... the dyskinesias we are told to anticipate and fear, and that we know have given some of the people we know and respect a very hard time.....

It's late here, and I AM tired, but surely there is a difference between the abnormal movement induced by levodopa fluctuation, and those created by these implants.......... they must have different causation, otherwise the whole dyskinesia/l-dopa theory is not what it seems at all.........

perhaps I am just confusing myself....... perhaps someone can come in blazing and put me right and I promise to behave, I do , I do, I do......

Lindy

Maybe dyskinesia has different causations. I remember reading a while back that they originally thought that the presentation of involuntary movement after the implants was a result of the transplanted neurons secreting TOO much dopamine. Now this new study indicates it is rogue seretonin and not dopamine related. At least as far as these individual cases are concerned. I don't think they are positing that buspar will alleviate all dyskinesias - they are merely reporting how it affected these particular study participants.

Cal