Hi, this is my first post here but some of you may remember me from the other site. I have been an advocate of Low Dose Naltrexone to stop the progression of Parkinson's. I have been taking 4.5 mg of naltrexone for (low doses of Sinemet and Mirapex too) for about 28 months now and I can't say my PD is worse.
I emailed the MJF site mentioned here with information on LDN and, while a Phd did respond, I believe I got a non-response or no interest at all. It would seem to me that there is reason to believe LDN does stop disease progression, in addition, it is an FDA approved drug, it's cheap and has few side effects. I also included a research paper with work done on naloxone (naltrexone is similar) showing how these opioid (antagonists?) could work in being neuro-protective. LDN is available now, what is the MJF intent? Are they looking to fund research on very expensive treatments which may not be available for many years?
Ashley

A report from the NIH on Naloxone (naltrexone):
The purpose of this study was to identify two neuroprotective compounds with a similar bimodal dose response, to discern whether the neuroprotective characteristics of each compound could converge into a single mechanism, and through this process, to elucidate a common femtomolar site of action.

Parkinson’s disease (PD) is characterized by the specific and progressive death of dopaminergic neurons in the substantia nigra (SN); other neuronal cell types are much less affected. Recent reports have linked inflammation to neurodegenerative disease, where microglia, cells of myeloid lineage responsible for innate immunity in the brain, are considered to be the major cell type underlying the inflammation-mediated neurotoxicity (7 8 9) . The activation of microglia is a complex process involving the release of several soluble proinflammatory factors [tumor necrosis factor {alpha} (TNF-{alpha}), PGE2, IL-1] and free radicals (nitric oxide, superoxide) (7) . Current replacement therapy with L-dopa is able to alleviate disease symptoms, but is unable to alter the disease course. Thus, therapeutic interventions designed to inhibit the microglial inflammatory response offer hope for attenuation of the neurodegenerative disease process. The current anti-inflammatory treatments available, including steroids and nonsteroidal anti-inflammatory drugs, are limited by the ability to influence only a small portion of the microglial response (10) . Thus, identification of compounds acting on novel targets to inhibit the release of a wide range of proinflammatory factors from overactivated microglia is of paramount importance. In the ensuing study, we report that femtomolar concentrations of naloxone and the peptide fragment glycine-glycine-phenylalanine (GGF) attenuate a broad spectrum of the microglia inflammatory response (reactive oxygen species (ROS) and proinflammatory factors) and are neuroprotective with extremely potent efficacy through the inhibition of microglial NADPH oxidase.
http://www.fasebj.org/cgi/content/full/19/6/550
http://www.lowdosenaltrexone.org/index.htm