To answer proudest-mama's question if there is something else out there beside LDN, maybe there is, it's dextromethorphan in the form of cough syrup bought in any drug store over the counter. Some people on this forum take about 5mg nightly (about one teaspoon). According to the work of Dr. Hong's group at the NIH, LDN and DM are opioid receptor antagonists and work in similar ways at low doses (femtomolar or 10 to the -14) to slow or stop neuroinflammatory disease.
Ashley

http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
Femtomolar concentrations of dextromethorphan protect mesencephalic dopaminergic neurons from inflammatory damage.

Li G, Cui G, Tzeng NS, Wei SJ, Wang T, Block ML, Hong JS.

Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA. guorongl@med.unc.edu

Inflammation in the brain has increasingly been recognized to play an important role in the pathogenesis of several neurodegenerative disorders, including Parkinson's disease (PD). Progress in the search for effective therapeutic strategies that can halt this degenerative process remains limited. We previously showed that micromolar concentrations of dextromethorphan (DM), a major ingredient of widely used antitussive remedies, reduced the inflammation-mediated degeneration of dopaminergic neurons through the inhibition of microglial activation. In this study, we report that femto- and micromolar concentrations of DM (both pre- and post-treatment) showed equal efficacy in protecting lipopolysaccharide (LPS) -induced dopaminergic neuron death in midbrain neuron-glia cultures. Both concentrations of DM decreased LPS-induced release of nitric oxide, tumor necrosis factor-alpha, prostaglandin E2 and superoxide from microglia in comparable degrees. The important role of superoxide was demonstrated by DM's failure to show a neuroprotective effect in neuron-glia cultures from NADPH oxidase-deficient mice. These results suggest that the neuroprotective effect elicited by femtomolar concentrations of DM is mediated through the inhibition of LPS-induced proinflammatory factors, especially superoxide. These findings suggest a novel therapeutic concept of using "ultra-low" drug concentrations for the intervention of inflammation-related neurodegenerative diseases.

PMID: 15790998 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract