title: Plasticity and remodeling of brain.
abstract: The injured brain can be stimulated to amplify its intrinsic restorative processes to improve neurological function. Thus, after stroke, both cell and pharmacological neurorestorative treatments, amplify the induction of brain neurogenesis and angiogenesis, and thereby reduce neurological deficits. In this manuscript, we describe the use of bone marrow mesenchymal cells (MSCs) and erythropoietin (EPO) as examples of cell-based and pharmacological neurorestorative treatments, respectively, for both stroke and a mouse model of experimental autoimmune encephalomyelitis (EAE). We demonstrate that these therapies significantly improve neurological function with treatment initiated after the onset of injury and concomitantly promote brain plasticity. The application of MRI to monitor changes in the injured brain associated with reduction of neurological deficit is also described.
authors.affiliation: Department of Neurology, Henry Ford Health System, 2799 West Grand Bouleverd, Detroit, MI 48202, USA. chopp@neuro.hfh.edu
authors.forename: Michael
authors.initials: M
authors.lastname: Chopp
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000628:therapy*; D004195:Disease Models, Animal; D004921:Erythropoietin / Q000627:therapeutic use; D018380:Hematopoietic Stem Cell Transplantation / Q000379:methods; D006801:Humans; D051379:Mice; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D011994:Recombinant Proteins
chemical_list: D011994:Recombinant Proteins; D004921:Erythropoietin