#MSChat
There is no approved therapy to neutralize autoantibodies selectively. Experimental autoimmune encephalomyelitis (EAE) could be a good model to develop such a therapy. The synthetic anti-MOG antibody 8-18C5 can prevent the binding of pathogenic antibodies from EAE mice or people with MOG antibody disease.
Nicotinamide adenine dinucleotide (NAD +) supplementation attenuates demyelination in the experimental autoimmune encephalomyelitis model.
Tregs suppress the pro-inflammatory activity of DCs while promoting the generation of a tolerance-inducing DC phenotype. iTregs exhibit greater efficacy in mitigating brain inflammation in both EAE and EAE provoked by a high-salt diet.
Multiple sclerosis (MS) is an autoimmune condition characterized by myelin destruction and neurodegeneration. Fisetin has a potential neuroprotective effect in CPZ model of MS and can be studied as an adjuvant therapy to enhance remyelination and mitigate disability in MS patients.
Multiple Sclerosis is an inflammatory demyelinating disorder which affects the central nervous system. Treatment has traditionally focused on preventing inflammatory damage
Sappanone A (SA) is a flavonoid compound with anti-inflammatory and antioxidant properties. It significantly improved motor function in SCI mice treated with SA. It reduced the lesion area, increased the residual myelin area, and enhanced neuronal survival. Nrf2 inhibitor ML385 reversed SA's neuroprotective effects.
LPX-TI641 is an orally bioavailable, clinical-stage small-molecule agonist of Tim-3/4. It promotes antigen-independent immune tolerance through Tim receptor agonism and Treg expansion. In EAE models, treatment significantly reduced disease severity, prevented relapses, and maintained clinical benefit after discontinuation.
Neuronal NF-kappa B ablation does not influence neuro-axonal degeneration in experimental autoimmune demyelination. Neuro-ax