Hi,

I don't have Parkinson's Disease, so I hope you don't mind my posting a question here. My sister (bluedahlia) has PD and she posts here. I have narcolepsy.

Anyway, the reason I'm posting is I was recently told that the nerve cell loss (orexin) that causes our disease also seems to happen as PD advances, and I was wondering if anyone here has any theories as to why this might happen. At a recent narcolepsy conference, patients were asked if they had any close relatives with Parkinsons, and half of the room put their hands up, to the astonishment of the researchers there.

The article that I just mentioned is on Medscape -- article 558352. I can't link to it unfortunately as your system doesn't allow URLs for those who have recently joined.

As it turns out, in advanced PD, 50% of these hypocretin neurons are gone. In narcolepsy, 90% are gone. Another thing we found out is that the sleep disorder RBD is a very strong predictor of developing PD in the future.

In case anyone doesn't know, RBD stands for REM Behavior Disorder. With RBD, people physically act out their dreams during REM sleep -- they don't get the normal REM muscle atonia (paralysis) during REM sleep designed to protect us from injuring ourselves. This hasn't been linked to dopamine at all, although periodic limb movement disorder in sleep has.

Another thing I found interesting was that they recently tested an orphan drug used on us in PD. The drug is called Xyrem, and it increases dopamine throughput during the day when used at night.

Finally, I have about Mirapex or Amantadine. Did either of these two drugs feel like a stimulant for any of you (ie. like Adderall) without the side effects of an amphetamine? My doctor was going to prescribe them off label, but then chickened out. That also made me wonder why Adderall isn't used in early PD (it increases dopamine output as well).

Sorry for the long post -- just tossing out whatever came to mind.

Here is a link to the Medscape article; http://www.medscape.com/viewarticle/558352

It has been discussed here; http://brain.oxfordjournals.org/content/131/3/e91.long

Strange, the more I think about it.

Dopamine neurons in the SN and VTA both have receptors for Orexin A and B, with feedback projections.

I'm no expert on Parkinsons, but it involves the SELECTIVE loss of dopamine neurons in the SN only, and dopamine neurons in the VTA don't die off.

To lose that many orexin neurons upstream suggests some kind of disease process that spreads to anything connected to it (ie. through the feedback projections).