Methods for Treating and Alleviating Neuropathic Pain Using ApoA-I Binding Protein (AIBP)
Single administration of AIBP can reverse chronic pain as validated in chemotherapy induced peripheral neuropathy. No adverse effects of intrathecal administration have been observed in mouse models; the mice retained normal motor and sensory function.
Delivering therapeutically effective amounts of AIBP (either in the form of AIBP polypeptide or AIBP-expressing nucleic acid) to specifically target inflammatory processes associated with pain. Besides neuropathic pain the technology can also lead to novel treatments for acute respiratory distress syndrome, atherosclerosis and vascular inflammation, Alzheimer’s disease, epilepsy and rheumatoid arthritis.
Researchers at UC San Diego have demonstrated that TLR4 was critical in mediating the transition from acute to persistent pain. TLR4 and other receptors involved in inflammatory signaling localize, constitutively or upon ligand binding, to lipid rafts, which are membrane microdomains characterized by high content of cholesterol and sphingomyelin. AIBP binds to activated TLR4 and facilitates cholesterol removal from "pathologic lipid rafts," which in turn disrupts the raft platform for inflammatory receptors assembly and reduces neuroinflammation. Raising AIBP levels results in selective disruption of lipid rafts in inflamed but not normal cells.
State Of Development The investigators have shown that the intrathecal delivery of an ApoA-I peptide reverses neuropathic pain in several mouse models. Intellectual Property Info A PCT patent PCT/US2016/064938 has been published on June 15, 2017 Tech ID/UC Case 29128/2016-150-0 Related Cases 2016-150-0
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