MS Speaks
Multiple Sclerosis => TREATMENTS => COPAXONE (glatiramer acetate) => Topic started by: agate on April 02, 2015, 04:02:49 pm
-
Copaxone was given to rats after acute ischemic stroke, and the researchers found it promoted neurogenesis and improved recovery. Any implications for MS treatment aren't mentioned here but it's an interesting finding.
From PubMed, March 31, 2015:
PLoS One. 2015 Mar 30;10(3):e0121854. doi: 10.1371/journal.pone.0121854. eCollection 2015.
Copolymer-1 promotes neurogenesis and improves functional recovery after acute ischemic stroke in rats
Cruz Y1, Lorea J1, Mestre H1, Kim-Lee JH1, Herrera J1, Mellado R1, Gálvez V1, Cuellar L1, Musri C1, Ibarra A2.
Author information
1Facultad de Ciencias de la Salud, Universidad Anáhuac México Norte, Huixquilucan, Estado de México, México.
2Facultad de Ciencias de la Salud, Universidad Anáhuac México Norte, Huixquilucan, Estado de México, México; Centro de Investigación del Proyecto CAMINA A.C. Distrito Federal, México.
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.
The abstract can be seen here (http://www.ncbi.nlm.nih.gov/pubmed/25821957).