Dear H4tB -

Good catch re LDN. I was aware of it's anticipated role as a potentiator for opioids, and I certainly swilled enough of the stuff to block opiod receptors the in gut before Hospira, Inc., of Lake Forest IL, the sole RDA licensed produced of Naloxone HCL jacked up the price by 600% within a year, to the point that it was no longer worth the candle.

But never in my wildest imagination did I suspect that it was as versitle as suggested in the website you posted. Of course there weren't all that many published articles, a couple really, the rest of the website being a collection of tantalizing leads that may be fruitful in the near futute.

Thank you again for spotting this.

Mike
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ps Something I stumbled on by chance, really got my attention. I ran down on of the articles alluded to on the website, Microglia-mediated neurotoxicity: uncovering the molecular mechanisms, Block ML, Zecca L, Hong JS, Nat Rev Neurosci. 2007 Jan;8(1):57-69:

Abstract
Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.

PMID: 17180163 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/17180163

This in turn led me to some good stuff having little if anything to do with LDN, but interesting nerverless. See, Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia, Johannes CM Schlachetzki, Bernd L Fiebich, Elisabeth Haake et al, Journal of Neuroinflammation 2010, 7:2, free full text at http://www.ncbi.nlm.nih.gov/pmc/arti...2-2094-7-2.pdf

Abstract
Background: Recent studies suggest an important role for neurotransmitters as modulators of inflammation. Neuroinflammatory mediators such as cytokines and molecules of the arachidonic acid pathway are generated and released by microglia. The monoamine norepinephrine reduces the production of cytokines by activated microglia in vitro. However, little is known about the effects of norepinephrine on prostanoid synthesis. In the present study, we investigate the role of norepinephrine on cyclooxygenase- (COX-)2 expression/synthesis and prostaglandin (PG) E2 production in rat primary microglia.

Results: Interestingly, norepinephrine increased COX-2 mRNA, but not protein expression. Norepinephrine strongly enhanced COX-2 expression and PGE2 production induced by lipopolysaccharide (LPS). This effect is likely to be mediated by b-adrenoreceptors, since b-, but not a-adrenoreceptor agonists produced similar results. Furthermore, b-adrenoreceptor antagonists blocked the enhancement of COX-2 levels induced by norepinephrine and badrenoreceptor agonists.

Conclusions: Considering that PGE2 displays different roles in neuroinflammatory and neurodegenerative disorders, norepinephrine may play an important function in the modulation of these processes in pathophysiological conditions.

PMID: 20064241 [PubMed - in process] PMCID: PMC2819253

http://www.ncbi.nlm.nih.gov/pubmed/20064241