title: Rapamycin reduces clinical signs and neuropathic pain in a chronic model of experimental autoimmune encephalomyelitis.
abstract: Current treatments used in Multiple Sclerosis (MS) are partly effective in the early stages of the disease but display very limited benefits in patients affected by progressive MS. One possible explanation is that these therapies are unable to target the inflammatory component most active during the progressive phase of the disease, and compartmentalized behind the blood-brain barrier. Our findings show that Rapamycin ameliorates clinical and histological signs of chronic EAE when administered during ongoing disease. Moreover, Rapamycin significantly reduced the hyperalgesia observed before clinical development of EAE which, in turn, is completely abolished by the administration of the drug.
authors.affiliation: Institute of Pharmacology, Catholic University Medical School, Rome, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Lisi
authors.forename: P
authors.initials: P
authors.lastname: Navarra
authors.forename: R
authors.initials: R
authors.lastname: Cirocchi
authors.forename: A
authors.initials: A
authors.lastname: Sharp
authors.forename: E
authors.initials: E
authors.lastname: Stigliano
authors.forename: D L
authors.initials: DL
authors.lastname: Feinstein
authors.forename: C
authors.initials: C
authors.lastname: Dello Russo
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy / Q000276:immunology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006023:Glycoproteins / Q000633:toxicity; D006930:Hyperalgesia / Q000188:drug therapy; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D051379:Mice; D008810:Mice, Inbred C57BL; D004676:Myelin Basic Protein / Q000235:genetics / Q000378:metabolism; D009186:Myelin Sheath / Q000378:metabolism; D063308:Myelin-Oligodendrocyte Glycoprotein; D009437:Neuralgia / Q000188:drug therapy* / Q000473:pathology; D017288:Pain Threshold / Q000187:drug effects; D010446:Peptide Fragments / Q000633:toxicity; D037342:Pertussis Toxin / Q000633:toxicity; D012333:RNA, Messenger / Q000378:metabolism; D020123:Sirolimus / Q000627:therapeutic use*; D013601:T-Lymphocytes / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
chemical_list: D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D006023:Glycoproteins; D007166:Immunosuppressive Agents; D004676:Myelin Basic Protein; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; D012333:RNA, Messenger; C445081:myelin oligodendrocyte glycoprotein (35-55); D037342:Pertussis Toxin; D020123:Sirolimus