Cotcha Yankinov
Bluelight Crew
- Joined
- Jul 21, 2015
- Messages
- 2,952
Sorry I forgot about your vision! It appears this is the study http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324822/ "Methamphetamine Accelerates Cellular Senescence through Stimulation of De Novo Ceramide Biosynthesis", and that the harm is ultimately through NF-KB to some degree, though I still question the role of Tau and amyloid beta in some patient populations.
"We report now that methamphetamine accelerates cellular senescence and activates transcription of genes involved in cell-cycle control and inflammation by stimulating production of the sphingolipid messenger ceramide. This pathogenic cascade is triggered by reactive oxygen species, likely generated through methamphetamine metabolism via cytochrome P450, and involves the recruitment of nuclear factor-κB (NF-κB) to induce expression of enzymes in the de novo pathway of ceramide biosynthesis. Inhibitors of NF-κB signaling and ceramide formation prevent methamphetamine-induced senescence and systemic inflammation in rats self-administering the drug, attenuating their health deterioration. The results suggest new therapeutic strategies to reduce the adverse consequences of methamphetamine abuse and improve effectiveness of abstinence treatments."
Is it curcumin too or just Coenzyme q10 that is a NF-KB inhibitor? I'm not aware of any pharmaceutical NF-KB inhibitors besides minocycline, which I'm not sure of it's potency - I think it's more of a microglial inhibitor but I'm still no sure if I would want to chance it seeing as I believe ALS patients declined faster on it and that if there is a relationship between ceramides and plaques then you would want your microglia up and running.
"We report now that methamphetamine accelerates cellular senescence and activates transcription of genes involved in cell-cycle control and inflammation by stimulating production of the sphingolipid messenger ceramide. This pathogenic cascade is triggered by reactive oxygen species, likely generated through methamphetamine metabolism via cytochrome P450, and involves the recruitment of nuclear factor-κB (NF-κB) to induce expression of enzymes in the de novo pathway of ceramide biosynthesis. Inhibitors of NF-κB signaling and ceramide formation prevent methamphetamine-induced senescence and systemic inflammation in rats self-administering the drug, attenuating their health deterioration. The results suggest new therapeutic strategies to reduce the adverse consequences of methamphetamine abuse and improve effectiveness of abstinence treatments."
Is it curcumin too or just Coenzyme q10 that is a NF-KB inhibitor? I'm not aware of any pharmaceutical NF-KB inhibitors besides minocycline, which I'm not sure of it's potency - I think it's more of a microglial inhibitor but I'm still no sure if I would want to chance it seeing as I believe ALS patients declined faster on it and that if there is a relationship between ceramides and plaques then you would want your microglia up and running.