Targeting a molecule called Nogo-A, which inhibits the formation of new blood vessels, promotes vascular and neural repair as well as functional recovery after stroke, a mouse study finds. Stroke is a major cause of disability, and the lack of an effective therapy that promotes long-term recovery represents an unmet medical need. Angiogenesis, or the formation of new blood vessels, has been proposed as a therapeutic target, but treatments that promote angiogenesis after cerebral stroke are lacking. Ruslan Rust, Martin Schwab, and colleagues provide evidence in mice that blocking a molecule called Nogo-A, which inhibits angiogenesis and the growth of neuronal projections, promotes vascular and neural repair as well as functional recovery after ischemic stroke, which occurs when an artery that supplies oxygen-rich blood to the brain becomes blocked. Both genetic deletion of Nogo-A and treatment with an antibody that blocks Nogo-A increased the number of newly formed blood vessels and improved behavioral performance on motor tasks assessing stroke-affected limb function 3 weeks after injury. Treatment with the anti-Nogo-A antibody also improved the survival of neurons and connections between neurons, increased levels of the neurotransmitter dopamine, which plays a key role in motor function and recovery, and increased the density of nerve fibers near the damaged tissue 3 weeks after injury. According to the authors, anti-Nogo-A antibodies, including an antibody currently in clinical testing for spinal cord injury, could represent an angiogenesis-promoting therapeutic strategy for ischemic stroke.
Article #19-05309: "Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke," by Ruslan Rust et al.
MEDIA CONTACTS: Ruslan Rust, Swiss Federal Institute of Technology in Zurich, SWITZERLAND; e-mail: rust@irem.uzh.ch; Martin Schwab, ETH and University of Zurich, SWITZERLAND; tel: +41 44 635 33 30; e-mail: schwab@irem.uzh.ch
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Journal
Proceedings of the National Academy of Sciences