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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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I plan to add Inosine/DMAE to my methylprednisolone treatment, did you already open a thread where we can document Inosine/DMAE trials?
This might be misleading, I have cavitations (diagnosed with a Cone Beam) but I have zero pain locally, I could apply pressure everywhere on my jawbone and don't find anything suspicious.
Hi!A cone beam is a new one for me. Is that a new method of detecting jawbone cavitations? Should I include it in the roadmap?
Don't know if that is only me, but already much much less inosine shoot my uric acid above normal. Guess the DMAE could be substituted with other forms of choline.
I think you would need to substitute it with another amino alcohol. DMAE is an amino alcohol, and this is what is required to make Imunovir.
As a natural antioxidant, UA provides up to 60% of the antioxidant capacity in human blood . UA preserves the peroxidase activity of both cytosolic Superoxide Dismutase 1 (SOD and extracellular SOD3, which defend against the formation of superoxide (O2−) and peroxynitrite . UA can also effectively prevent cytoskeleton from the insults caused by peroxynitrite-induced inactivation of cellular enzymes . In addition, UA is capable of binding iron and inhibits iron-dependent ascorbate oxidation, thus preventing against oxidative stress-induced injuries. As such, a reduced UA concentration may adversely lead to increased oxidative stress and damage to neural cells. However, recent studies indicate that UA’s antioxidant property couldn’t explain all of its beneficial effects in the CNS. One study found that astroglia are required for UA to exert its protective effects on the spinal cord against injury . UA stimulates expression of a glutamate transporter in astroglia, by which it protects neurons from glutamate-induced toxicity. Besides its capability of scavenging reactive oxygen species, UA can also indirectly confer neuronal protection via activation of astroglia. On the other hand, lower UA levels may be generated during CNS inflammation due to overconsumption of UA in scavenging excessive oxidative stress . Notably, administration of UA to an experimental autoimmune/allergic encephalomyelitis mouse model, given either before or after the appearance of symptoms, promoted the survival rate of these mice . Administration of UA effectively decreased oxidative stress and neuronal deaths in animal models of PD . Interestingly, treatment of patients with a UA precursor, inosine, prevented progression of MS in all 11 patients tested and even improved the symptoms of some patients . Thus, it is highly likely that a reduced serum UA level is a predictor rather than a consequence of neurodegeneration. Therefore, it is plausible to speculate that the neurodegenerative processes in patients with the neurological disorders may be exacerbated by the compromised neuroprotective effects due to the decreased UA levels.