(Ivanhoe Newswire)-- There is only one stroke treatment option available today and with such a high rate of individuals suffering from strokes, many would agree that a new solution is necessary.
Now researchers from Stanford University have shown that by removing a matching set of molecules responsible for assisting in regulation of the brain's capacity for forming and breaking connections between nerve cells could greatly increase recovery from a stroke just days after occurring.
Currently the only available stroke treatment is called tissue plasminogen activator, or tPA. The issue with tPA is that it must be administered within a few hours of a stroke to be effective, and patients' brains must first be scanned to determine whether this treatment is appropriate. Furthermore, while tPA limits the initial damage caused by a stroke, it doesn't help the brain restore or replace lost connections between nerve cells, which is necessary for recovery.
For the study, researchers used mice that had been genetically bioengineered to lack certain molecules that a Stanford researcher had previously shown to play a major role in modulating the ease with which important nerve-cell connections are made, strengthened, weakened or destroyed in the brain. The molecules in question include "K" and "D," two of the 50 or so members of the so-called MHC class-1 complex, which plays a key role in the function of the immune system. Alternatively, when a receptor called PirB, which binds to these MHC molecules, is not present, the same improved outcome from stroke happens significant, because receptors make good drug targets.
Carla Shatz, PhD, professor of neurobiology and of biology, and her colleagues surprised the neuroscience and immunology communities a few years back by showing that these molecules "moonlight" in the brain. Here, their job appears to involve inhibiting the readiness of connections among nerve cells (known as synapses) to grow stronger or weaker in response to experience.
In order to re-establish brain functions that have been lost in the massive nerve-cell die-off that follows an extraordinary event such a stroke, it's necessary to restore lost synapses and form new ones at a rapid pace. It's also important to retrain surviving circuits to take over functions formerly served by lost circuits this is the basis of rehabilitation therapy.
"Nobody had ever thought any of these molecules had anything to do with stroke," Shatz, who is the Sapp Family Provostial Professor and also is the director of Bio-X, Stanford's interdisciplinary biosciences research consortium, was quoted as saying. "But our lab had shown in 2009 that mice bioengineered to lack them performed like Olympians on motor-learning tasks."
Not too long ago, Shatz and her colleague, Rona Giffard, MD, PhD, professor of anesthesia and a veteran stroke researcher, began discussing their work, It occurred to them that teaming Shatz's molecules with Giffard's animal-research expertise could provide answers to her question.
The results showed that mice genetically designed to lack both K and D or PirB, a major cell-surface receptor for these molecules, experienced markedly better recovery in their motor performance after a stroke than did normal mice. Giffard and Shatz are the senior authors of the Neuron study.
"This is the very first time anyone has looked for a role of these molecules in stroke, or in recovery from stroke," Giffard was quoted as saying. "Targeting recovery, as opposed to just halting the damage, would have the widest possible chance to help patients after stroke, and could help patients who cannot receive tPA."
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New Stroke Recovery Option