Neuronal plasticity and functional recovery after ischemic stroke.
Ischemic stroke affects many new patients each year. The sequelae of brain ischemia can include lasting sensorimotor and cognitive deficits, which negatively impact quality of life. Currently, treatment options for improving poststroke deficits are limited, and the development of new clinical alternatives to improve functional recovery after stroke is actively under investigation. Anti-Nogo-A immunotherapy to reduce the central nervous system inhibitory environment, cell transplantation strategies, pharmacological agents, and movement-based therapies represent emerging treatments of poststroke deficits through enhancement of neuroanatomical plasticity.
Cheatwood
Joseph L
JL
Hines VA Hospital, Illinois, USA.
Emerick
April J
AJ
Kartje
Gwendolyn L
GL
D000368:Aged; D000818:Animals; D002545:Brain Ischemia / Q000150:complications*; D006801:Humans; D007167:Immunotherapy; D015915:Motion Therapy, Continuous Passive; D009185:Myelin Proteins / Q000276:immunology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D000070798:Nogo Proteins; D051381:Rats; D020127:Recovery of Function / Q000502:physiology*; D033581:Stem Cell Transplantation; D020521:Stroke / Q000209:etiology / Q000503:physiopathology* / Q000523:psychology / Q000628:therapy*; D000071939:Stroke Rehabilitation
D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603199:RTN4 protein, human; C000603197:Rtn4 protein, rat