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Cellular cues identified for stroke recovery
December 26, 2006New insight into how the brain regenerates after stroke
When a stroke strikes, the supply of blood to the part of the brain affected is interrupted, starving it of oxygen. Brain cells can be seriously damaged or die, impairing local brain function.
But the brain is a battler. Within weeks of a stroke, new blood vessels begin to form, and, like marching ants, newly born neurons migrate long distances to the damaged area to aid the regeneration process. What's not known is what the right cellular environment is, and what the cellular cues are for this process of regeneration and migration to take place.
Now, in the Journal of Neuroscience, currently online, S. Thomas Carmichael, M.D., Ph.D., an assistant professor in the Department of Neurology at the UCLA Geffen School of Medicine, and colleagues report that in the mouse model, this neuron march is the direct result of signaling from the newly blooming blood vessels, thus casually linking angiogenesis the development of new blood vessels and neurogenesis, the birth of new neurons. Further, they have identified what these molecular signals are. The results hold promise for eventual clinical applications that may spur brain repair after stroke.
Stroke is the leading cause of adult disability, said Carmichael. And while much is known about the mechanisms of cell death in stroke, little is known about the mechanisms of neurological recovery after a stroke. His lab studies the mechanisms of brain repair and the recovery of function after a stroke.
Recent research has revealed that in the adult brain, new neurons form in a region of the forebrain known as the subventricular zone (SVZ). In mice, after a stroke was initiated in a part of the brain located far from the SVZ, the researchers, using a combination of mitotic, genetic, and viral labeling, tracked newly formed neuroblasts (immature brain cells from which mature adult neurons form) as they traveled through healthy brain tissue to the stroke area. Once there, these immature neurons wrapped themselves around the immature vascular cells that were in the process of forming new blood vessels in the damaged area. The neurons were found to arrive at the site within the first two to four weeks after the stroke.
Further, the researchers found that two proteins, stromal-derived factor 1 (SDF1) and angiopoietin 1 (Ang1), that are given off by these newly-forming blood vessels, are what trigger the thousands of immature neurons to the site of damage.
"The SDF1 and Ang1 proteins are what link the two processes of neurogenesis and angiogenesis together by promoting post-stroke neuroblast migration," said Carmichael. They also appear to effect behavioral recovery as well, he noted. The researchers produced the stroke in an area of the brain that controls the mouse's facial whiskers. When the mouse was infused by the researchers with Ang1 and SDF1, improvement in the function of the whisker's was seen to the same levels as the control (non-stroke) mice.
If harnessed properly, said Carmichael, the molecular mechanisms for neuronal regeneration hold the promise of regenerating and reconnecting brain cells near the area where stroke occurs. While the process may vary between mice and humans, he said, it's known that neurogenesis occurs in humans. "We're hopeful that we can take advantage of the brain's plasticity," said Carmichael. "This work could lead to the development of new therapies that will promote brain repair after stroke."
University of California - Los Angeles
Now, in the Journal of Neuroscience, currently online, S. Thomas Carmichael, M.D., Ph.D., an assistant professor in the Department of Neurology at the UCLA Geffen School of Medicine, and colleagues report that in the mouse model, this neuron march is the direct result of signaling from the newly blooming blood vessels, thus casually linking angiogenesis the development of new blood vessels and neurogenesis, the birth of new neurons. Further, they have identified what these molecular signals are. The results hold promise for eventual clinical applications that may spur brain repair after stroke.
Stroke is the leading cause of adult disability, said Carmichael. And while much is known about the mechanisms of cell death in stroke, little is known about the mechanisms of neurological recovery after a stroke. His lab studies the mechanisms of brain repair and the recovery of function after a stroke.
Recent research has revealed that in the adult brain, new neurons form in a region of the forebrain known as the subventricular zone (SVZ). In mice, after a stroke was initiated in a part of the brain located far from the SVZ, the researchers, using a combination of mitotic, genetic, and viral labeling, tracked newly formed neuroblasts (immature brain cells from which mature adult neurons form) as they traveled through healthy brain tissue to the stroke area. Once there, these immature neurons wrapped themselves around the immature vascular cells that were in the process of forming new blood vessels in the damaged area. The neurons were found to arrive at the site within the first two to four weeks after the stroke.
Further, the researchers found that two proteins, stromal-derived factor 1 (SDF1) and angiopoietin 1 (Ang1), that are given off by these newly-forming blood vessels, are what trigger the thousands of immature neurons to the site of damage.
"The SDF1 and Ang1 proteins are what link the two processes of neurogenesis and angiogenesis together by promoting post-stroke neuroblast migration," said Carmichael. They also appear to effect behavioral recovery as well, he noted. The researchers produced the stroke in an area of the brain that controls the mouse's facial whiskers. When the mouse was infused by the researchers with Ang1 and SDF1, improvement in the function of the whisker's was seen to the same levels as the control (non-stroke) mice.
If harnessed properly, said Carmichael, the molecular mechanisms for neuronal regeneration hold the promise of regenerating and reconnecting brain cells near the area where stroke occurs. While the process may vary between mice and humans, he said, it's known that neurogenesis occurs in humans. "We're hopeful that we can take advantage of the brain's plasticity," said Carmichael. "This work could lead to the development of new therapies that will promote brain repair after stroke."
University of California - Los Angeles
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The benefits of exercise
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Heart and bone damage from low vitamin D tied to declines in sex hormones
Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone.
New study links vitamin D deficiency to cardiovascular disease and death
While mothers have known that feeding their kids milk builds strong bones, a new study by researchers at the Heart Institute at Intermountain Medical Center in Salt Lake City suggests that Vitamin D contributes to a strong and healthy heart as well - and that inadequate levels of the vitamin may significantly increase a person's risk of stroke, heart disease, and death, even among people who've never had heart disease.
Early end to key study on benefits of niacin, a B vitamin, in keeping arteries open was premature
Heart experts at Johns Hopkins are calling premature the early halt of a study by researchers at Walter Reed Army Medical Center and Washington Hospital Center on the benefits of combining extended-release niacin, a B vitamin, with cholesterol-lowering statin medications to prevent blood vessel narrowing.
Study finds many people with hemianopia have difficulty detecting pedestrians while driving, advocates for individual testing
Schepens Eye Research Institute scientists have found that--when tested in a driving simulator--patients with hemianopia (blindness in one half of the visual field in both eyes) have significantly more difficulty detecting pedestrians (on their blind side) than normally sighted people.
Texas Children's discharges first pediatric patient with implanted mechanical heart device
Texas Children's Hospital is the nation's first pediatric hospital to discharge a child while on an intracorporeal ventricular assist device (VAD), a feat previously accomplished only at adult institutions.
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