Compound aids stroke recovery

Researchers at the Stanford School of Medicine have identified a new molecular compound that could revolutionize the treatment of strokes in humans, for the first time offering the ability to enhance recovery after a stroke has taken place.

Stroke-afflicted mice treated with a molecule called LM22A-4, which helps to stimulate the growth of new neurons, exhibited accelerated and more extensive recovery.

Current stroke-treatment practices focus on limiting initial damage to the brain by breaking up the clots that caused the stroke.

“Since there are about 800,000 strokes each year in the United States and stroke is a leading cause of serious long-term disability, any treatment that improves recovery from stroke would significantly help a large number of people,” wrote Marion Buckwalter, professor of neurology and the paper’s senior author, in an email to The Daily.

Buckwalter and her team tested the compound’s effects by first training a group of mice to perform basic physical tasks, such as walking across a horizontal ladder. After surgically inducing strokes and testing the mice’s speed and agility, researchers treated the equally impaired groups with a placebo or the drug starting three days after the stroke.

“We followed their recovery using tests of gait and speed and found that the drug improved both limb-swing speed (the speed at which they moved the limb weakened by the stroke) and gait accuracy,” Buckwalter wrote.

Buckwalter emphasized the breakthrough’s significance, noting that the compound could have an equivalent effect on human subjects.

LM22A-4 mimics a protein called brain-derived neurotrophic factor (BNDF), which binds with a neural receptor called TrkB to stimulate neuron growth in both humans and mice. Mice treated with LM22A-4 produced twice the number of new nerve cells in stroke-affected areas of the brain compared to mice given the placebo and were able to regain pre-stroke limb-swing speed.

“It was the hoped-for discovery since the drug binds a receptor that is very important for plasticity [adaptability] in neural pathways and very significant because there is currently no drug that we can give to people that works by promoting recovery,” Buckwalter wrote.

In addition to accelerating and enhancing recovery, the treatment also had no detrimental effects on the subject mice, such as inflammation or scar tissue.

Buckwalter noted that the compound’s benefits may be applicable to human stroke victims in the future, offering a substantial leap forward in stroke treatment. She predicted, however, that a time frame of “many years” would be needed before any such drug is approved and available to the general public.

Buckwalter described the current study as “just the first step.”

“The next steps are to find the optimal dosing and time window in which to treat mice and to test for drug toxicity in mice,” Buckwalter wrote, adding that — due to the disparity in size between a human and a mouse brain — further fine-tuning of the molecule itself may be required.