Abstract
Stroke triggers a systemic inflammatory response that exacerbates the initial injury. Immunizing with peptides derived from CNS proteins can stimulate protective autoimmunity (PA). The most renowned of these peptides is copolymer-1 (Cop-1) also known as glatiramer acetate. This peptide has been approved for use in the treatment of multiple sclerosis. Cop-1-specific T cells cross the blood-brain barrier and secrete neurotrophins and anti-inflammatory cytokines that could stimulate proliferation of neural precursor cells and recruit them to the injury site; making it an ideal therapy for acute ischemic stroke. The aim of this work was to evaluate the effect of Cop-1 on neurogenesis and neurological recovery during the acute phase (7 days) and the chronic phase of stroke (60 days) in a rat model of transient middle cerebral artery occlusion (tMCAo). BDNF and NT-3 were quantified and infarct volumes were measured. We demonstrated that Cop-1 improves neurological deficit, enhances neurogenesis (at 7 and 60 days) in the SVZ, SGZ, and cerebral cortex through an increase in NT-3 production. It also decreased infarct volume even at the chronic phase of tMCAo. The present manuscript fortifies the support for the use of Cop-1 in acute ischemic stroke.
Highlights
Acute ischemic stroke is a leading cause of serious long-term disability in adults [1]
The day before the surgical procedure all animals (n = 70) were tested for neurological deficit, baseline data demonstrates that all subjects had a score of 0
This study demonstrates that immunization with Cop-1 significantly improves neurological deficit and infarct volume after 60 days in a transient middle cerebral artery occlusion (tMCAo) rat model
Summary
Acute ischemic stroke is a leading cause of serious long-term disability in adults [1]. Central nervous system (CNS) damage is known to trigger a systemic inflammatory response that may exacerbate brain injury [2]. Several studies have demonstrated that the modulation of this inflammatory response results in protective autoimmunity (PA)[3,4,5]. PA has shown to improve functional recovery in animal models of stroke, spinal cord injury, Parkinson, and Alzheimer disease[6,7,8,9]. Immunizing with peptides derived from proteins found in the CNS can stimulate PA. Perhaps the most renown of these peptides is copolymer-1 (Cop-1) known as glatiramer acetate
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