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OK, I've had about enough of the national health care plan talk. Those that are in favor of it dont' have insurance, or enough insurance, and those that oppose it are concerned about our democracy remaining one and leaving a country worth living in to our descendants (from those I've talked to, this seems to be where the dividing line is). So enough, we just disagree and as witsend said, time will tell.|
So back to PD. I found this news article about rapamycin and thought it worth posting, ask your neuro if he/she might be game to go outside the box and see if it might help your loved one:
First, here's the link: http://stke.sciencemag.org/cgi/conte...ract/2/80/ra36
(oops, the link didnt' work, here's the abstract (you have to subscribe to get the full text):
Inhibition of mTOR Signaling in Parkinson’s Disease Prevents L-DOPA–Induced Dyskinesia
Emanuela Santini1, Myriam Heiman2, Paul Greengard2, Emmanuel Valjent1,3,4,5, and Gilberto Fisone1,2*
1 Department of Neuroscience, Karolinska Institutet, Retzius väg 8, 171 77 Stockholm, Sweden.
2 Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.
3 INSERM, UMR-S839, 75005 Paris, France.
4 Université Pierre et Marie Curie, 75005 Paris, France.
5 Institut du Fer ŕ Moulin, 75005 Paris, France.
Abstract: Parkinson’s disease (PD), a disorder caused by degeneration of the dopaminergic input to the basal ganglia, is commonly treated with L-DOPA. Use of this drug, however, is severely limited by motor side effects, or dyskinesia. We show that administration of L-DOPA in a mouse model of Parkinsonism led to dopamine D1 receptor–mediated activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1), which is implicated in several forms of synaptic plasticity. This response occurred selectively in the GABAergic medium spiny neurons that project directly from the striatum to the output structures of the basal ganglia. The L-DOPA–mediated activation of mTORC1 persisted in mice that developed dyskinesia. Moreover, the mTORC1 inhibitor rapamycin prevented the development of dyskinesia without affecting the therapeutic efficacy of L-DOPA. Thus, the mTORC1 signaling cascade represents a promising target for the design of anti-Parkinsonian therapies.
* To whom correspondence should be addressed. E-mail: email@example.com
Citation: E. Santini, M. Heiman, P. Greengard, E. Valjent, G. Fisone, Inhibition of mTOR Signaling in Parkinson’s Disease Prevents L-DOPA–Induced Dyskinesia. Sci. Signal. 2, ra36 (2009)."
Now what is interesting, is that one of the things I read about rapamycin is that is appears to mimick pathways that are involved when we eat a calorie restricted diet....and I have read several studies showing that rodent PD reverses when fed only every other day...so this is intriguing to me.
If you google rapamycin, particularly on the news button, you will find lots of articles about rapamycin and life-extension. I have also read that rapamycin suppresses the immune system, which leave one exposed to all the bacteria, etc. out there, but if PDers have an over-active immune system to begin with, all this would do is slow it down, a good thing. Another thing: this drug is used extensively for organ transplants, soooooo....it's already approved, and has an estblished safety record. We dont' see our neuro for awhile, but this is on our list of things to ask him about.
There you go again... assuming. You know what happens when you assume?
I'm "in favor" and I have enough insurance and I know many people in the same position and they live in Texas. I think your statement is completely inaccurate and again outdated. I guess you haven't talked to me but of course, Texas is a big state. BTW, I also care about our democracy and also definitely care about leaving our country in good shape for others to enjoy and prosper.
Take care and call me next time you are in No. Texas