title: Disease Modifying Potential of Glatiramer Acetate in Huntington's Disease.
abstract: BACKGROUND
  Deficiencies in brain-derived-neurotrophic-factor have been implicated in the pathogenesis of Huntington's disease (HD).
  
  
  OBJECTIVE
  Glatiramer acetate, an FDA- approved drug used for the treatment of multiple sclerosis, has been shown to increase brain-derived-neurotrophic-factor levels in immune cells; hence, we investigated whether it could have similar effects in striatal cells.
  
  
  METHODS
  Wild-type and HD striatal cells were treated with glatiramer acetate for 48 hrs. HD transgenic and wild-type mice were injected with glatiramer acetate (1.5 to 1.7 mg/mouse) for five days. These treatments were followed by protein measurements for brain-derived-neurotrophic-factor.
  
  
  RESULTS
  Glatiramer acetate elicited concentration-dependent increases in brain-derived-neurotrophic-factor protein levels in wild-type and HD striatal cells and in striatal tissue from N171-82Q transgenic mice. Glatiramer acetate also improved metabolic activity of HD striatal cells, and significantly reduced the early hyperactivity phenotype exhibited by N171-82Q transgenic mice.
  
  
  CONCLUSIONS
  These findings suggest that glatiramer acetate may represent a useful therapeutic approach for HD. The excellent safety and tolerability record of this compound makes it an ideal candidate for drug repurposing efforts.
authors.affiliation: Department of Neurosciences, University of California, San Diego, CA, USA.
authors.forename: Jody
authors.initials: J
authors.lastname: Corey-Bloom
authors.affiliation: Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, CA, USA.
authors.forename: Haiqun
authors.initials: H
authors.lastname: Jia
authors.affiliation: Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, CA, USA.
authors.forename: Alaina M
authors.initials: AM
authors.lastname: Aikin
authors.affiliation: Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, CA, USA.
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Thomas
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000503:physiopathology*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005240:Feasibility Studies; D000068717:Glatiramer Acetate / Q000008:administration & dosage*; D006801:Humans; D006816:Huntington Disease / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009043:Motor Activity / Q000187:drug effects*; D016896:Treatment Outcome
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D007166:Immunosuppressive Agents; D000068717:Glatiramer Acetate
keywords: BDNF; Glatiramer acetate; copaxone; jumping; neurodegenerative; striatum