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

Have not read the full text of the article, though the following is part of the synopsis:

"Sudden, uncontrolled movements called dyskinesias—a common side effect of treatment for Parkinson’s disease— are a result of excess serotonin cells in transplanted tissue that trick the brain into releasing dopamine, suggests a new study of two Parkinson's disease patients that received fetal tissue transplants over a decade ago, researchers report in the June 30 issue of Science Translational Medicine"

I guess the question is how do excess serotonin cells "trick" the brain into releasing more dopamine?

from another source:

"...In the new study, using brain imaging, Politis and his colleagues found that the dopamine neurons that decay in Parkinson's disease were restored and functioning in the two patients. But they also found abnormal levels of serotonin neurons within the transplanted tissue.

The serotonin neurons were releasing dopamine, which, when coming from the wrong source, caused the jerking movements.

When patients were given a serotonin receptor agonist, a drug that prevented the serotonin neurons from firing, the involuntary movements ceased..."

http://www.nwpf.org/News.aspx?Item=3397

But is the second reference (where they posit that it is the serotonin neurons themselves releasing the extra dopamine) something they can actually see? Was this already known - that serotonin neurons are capable of producing dopamine?

I wonder....?

It is now known that SSRI drugs (serotonin reuptake inhibitors) over time, downregulate dopamine in the brain. I don't think this is well understood yet, but it appears that the brain senses the excess serotonin and tries to compensate and that involves dopamine. SSRI patients often develop movement disorders of the jaw, face, and tongue that resemble Tardive.
from http://en.wikipedia.org/wiki/Selecti...take_inhibitor

The brain seems to have some internal balancing system regarding neurotransmitters.

This seems analogous to the transplanted cell excess of serotonin in these PD cases.