title: Neurorepair versus neuroprotection in stroke.
abstract: Stroke is the second to third leading cause of death and the main cause of severe, long-term disability in adults. However, treatment is almost reduced to fibrinolysis, a therapy useful in a low percentage of patients. Given that the immediate treatment for stroke is often unfeasible in the clinical setting, the need for new therapy strategies is imperative. After stroke, the remaining impairment in functions essential for routine activities, such as movement programming and execution, sensorimotor integration, language and other cognitive functions have a deep and life-long impact on the quality of life. An interesting point is that a slow but consistent recovery can be observed in the clinical practice over a period of weeks and months. Whereas the recovery in the first few days likely results from edema resolution and/or from reperfusion of the ischemic penumbra, a large part of the recovery afterwards is due mainly to brain plasticity, by which some regions of the brain assume the functions previously performed by the damaged areas. Neurogenesis and angiogenesis are other possible mechanisms of recovery after stroke. An understanding of the mechanisms underlying functional recovery may shed light on strategies for neurorepair, an alternative with a wide therapeutic window when compared with neuroprotective strategies.
authors.affiliation: Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, Spain.
authors.forename: Olivia
authors.initials: O
authors.lastname: Hurtado
authors.forename: Jesus M
authors.initials: JM
authors.lastname: Pradillo
authors.forename: David
authors.initials: D
authors.lastname: Alonso-Escolano
authors.forename: Pedro
authors.initials: P
authors.lastname: Lorenzo
authors.forename: Tomás
authors.initials: T
authors.lastname: Sobrino
authors.forename: José
authors.initials: J
authors.lastname: Castillo
authors.forename: Ignacio
authors.initials: I
authors.lastname: Lizasoain
authors.forename: María Angeles
authors.initials: MA
authors.lastname: Moro
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002454:Cell Differentiation; D002465:Cell Movement; D049109:Cell Proliferation; D002986:Clinical Trials as Topic; D003131:Combined Modality Therapy; D003566:Cytidine Diphosphate Choline / Q000494:pharmacology / Q000627:therapeutic use; D015259:Dopamine Agents / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009473:Neuronal Plasticity; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D044968:Regenerative Medicine / Q000639:trends; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000166:cytology* / Q000187:drug effects; D020521:Stroke / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D000071939:Stroke Rehabilitation
chemical_list: D003566:Cytidine Diphosphate Choline; D015259:Dopamine Agents; D018696:Neuroprotective Agents; D017367:Selective Serotonin Reuptake Inhibitors