Researchers have identified a major component of brain recovery after a stroke

Well fuck, this was identified already in Oct. 2015, so rather than do the research that actually creates a translational intervention they tell us more followup is needed. NO ONE wants to take ANY RESPONSIBILITY to actually solve stroke. Fucking lazy assholes. 3 years from now someone is going to write a similar article exclaiming about this new stroke recovery breakthrough. We get writeups but NO action.

Discovery Could Lead to Better Recovery After Stroke  Oct. 2015

Researchers have identified a major component of brain recovery after a stroke 

 Mar 22, 2018 12:21 pm by Chris Dunkan



By examining brain tissue from mice, monkeys and humans, researchers have found that a molecule known as growth and differentiation factor 10 (GDF10) is a key factor in the repair mechanism after a stroke. The findings of the study published in the Scientific Review of Nature Neuroscience suggest that GDF10 may be a potential treatment for post-stroke recovery.
“Research findings help identify the post-stroke repair mechanisms. Detecting this protein further promotes our knowledge of how the brain itself is cured by the catastrophic effects of the stroke, and can help develop new therapeutic strategies to promote recovery, “says Francesca Bosetti, Ph .D, director of the NINDS (National Institute of Neurological Disorders and Stroke) stroke program and co-author of the study.

The stroke can occur when a blood vessel in the brain is obstructed, preventing nearby tissues from getting the necessary nutrients. When brain tissues lack oxygen and nutrients begin to die. Once this happens, repair mechanisms such as axial tagging are activated as the brain attempts to overcome the damage. During the axonal tagging, healthy neurons create new connections by restoring some of the connections lost or destroyed during the stroke, resulting in partial recovery. Before this study, it was not known what caused the axonal outburst.
Previous studies suggested that GDF10 is involved in the early stages of axial tagging, but its exact role in the process was unclear. The research team behind the new study took a close look at factor GDF10 to determine how it can contribute to axial outgrowth.
Examining animal models of strokes as well as human tissue autopsies, the research team found that GDF10 is triggered very early after the stroke. Then using rodent and human neurons in Petri dishes, the researchers tested the effect of GDF10 along axon axons, which carry messages between the brain cells. They discovered that GDF10 stimulates axonal growth while increasing their length.
“We found that GDF10 caused many different neurons in a dish to grow, including human neurons derived from stem cells,” the study said.
The researchers also found that GDF10 may be important for functional recovery after a stroke. The results of the study showed that the increase in GDF10 levels was associated with significantly faster recovery after the stroke. When the researchers blocked GDF10, the animals did not perform as well in kinetic work, indicating that the repair mechanisms were impaired, and that the natural levels of GDF10 in the brain are a means of recovery.
Researchers report in the study that more research is needed to determine whether GDF10 may be a possible cure for stroke recovery.

Discovery Could Lead to Better Recovery After Stroke

Well fuck, sound the alarm, a breakthrough. It will just take 100+ years to make it to clinical practice because there is no strategy or plan to followup research like this. Our fucking failures of stroke associations would rather put out press releases on F.A.S.T. or World Stroke Day. Neither of which does one fucking thing for survivors or future survivors.
http://www.biosciencetechnology.com/news/2015/10/discovery-could-lead-better-recovery-after-stroke?
UCLA researchers have identified a molecule that, after a stroke, signals brain tissue to form new connections to compensate for the damage and initiate repairs to the brain.
The finding could eventually lead to a new treatment to promote brain repair and functional recovery in people who have suffered a stroke, which is the leading cause of serious long-term disability in adults.
The five-year study, performed in an animal model, was the first to identify growth differentiation factor 10, or GDF10, a molecule that previously had no known role in the adult brain, said Dr. S. Thomas Carmichael, the study’s senior author and a professor and vice chair for research and programs in the UCLA department of neurology.
“The brain has a limited capacity for recovery after stroke,” Carmichael said. “Most stroke patients get better after their initial stroke, but few fully recover. If the signals that lead to this limited recovery after stroke can be identified and turned into a treatment, then it might be possible to enhance brain repair after stroke.”
The study, which appears Oct. 26 in the peer-reviewed journal Nature Neuroscience, also showed that GDF10 is released after a stroke in humans and in many different animals.
During a previous study, Carmichael and his team determined which molecules become more prevalent in the brain during the recovery period after a stroke, and listed all of the genes that are up- or down-regulated.
Heading into the new study, Carmichael said, researchers believed that one of the molecules on the list could be a signal telling the brain to repair itself after a stroke, and they screened for the molecules that saw the biggest increase in the brain after stroke. After finding that GDF10 was a possible signal for brain repair, the team analyzed the molecule in a petri dish.
The scientists found that GDF10 promotes brain cells’ ability to form new connections, and they identified the signaling systems that control the process.
“We found that GDF10 induces new connections to form in the brain after stroke, and that this mediates the recovery of the ability to control bodily movement,” Carmichael said.
Finally, the team identified all of the molecules that are turned on or off by GDF10 in brain cells after a stroke and compared the cells’ RNA to RNA in comparable cells during brain development and normal learning, and to RNA in the brain cells of people with other diseases.
They found that GDF10 regulates a unique collection of molecules that improves recovery after stroke. The discovery indicates that brain tissue regenerating after a stroke is a unique process rather than just a reactivation of the molecules that are active in brain development.
The team also administered GDF10 to the animals that had experienced strokes and then mapped the connections in the brain that are tied to body movement. They compared those to the connections in animals who had experienced a stroke but were not given GDF10, in animals with healthy brains and with animals that had experienced a stroke and had a reduced level of GDF10.
“The results indicated that GDF10 normally is responsible for the very limited process of the formation of new connections after stroke,” Carmichael said. “Delivering more GDF10 markedly enhances the formation of new connections and does so mostly in a specific brain circuit. The formation of connections in this circuit with GDF10 administration significantly enhanced recovery of limb control after stroke.”
Going forward, Carmichael and his team hope to identify a small molecule that activates the GDF10 signaling systems and that could eventually lead to the development of a drug to enhance recovery from strokes.
Stroke kills nearly 130,000 Americans each year — one of every 20 deaths in the U.S. — according to the Centers for Disease Control. Every year, more than 795,000 people in the U.S. have a stroke, about 610,000 of them for the first time. Stroke costs the U.S. an estimated $34 billion each year, including the cost of health care, medications and missed days of work.
The study was funded by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health, the American Heart Association, the Richard Merkin Foundation for Neural Regeneration at UCLA, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation and the Edwin W. and Catherine Davis Foundation.
Source: University of California Los Angeles