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.
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.
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