Press Releases & Research Commentary
July 28, 2009
A compound strikingly similar to the common food additive that gives M&Ms and Gatorade their blue tint may offer promise for preventing the additional – and serious – secondary damage that immediately follows a traumatic injury to the spinal cord. In an article published online today in the Proceedings of the National Academy of Sciences, researchers report that the compound Brilliant Blue G (BBG) stops the cascade of molecular events that cause secondary damage to the spinal cord in the hours following a spinal cord injury, an injury known to expand the injured area in the spinal cord and permanently worsen the paralysis for patients.
This research builds on landmark laboratory findings first reported five years ago by researchers at the University of Rochester Medical Center. In the August 2004 cover story of Nature Medicine, scientists detailed how ATP, the vital energy source that keeps our body's cells alive, quickly pours into the area surrounding a spinal cord injury shortly after it occurs, and paradoxically kills off what are otherwise healthy and uninjured cells.
This surprising discovery marked a milestone in establishing how secondary injury occurs in spinal cord patients. It also laid out a potential way to stop secondary spinal injury, by using oxidized ATP, a compound known to block ATP's effects. Rats with damaged spinal cords who received an injection of oxidized ATP were shown to recover much of their limb function, to the point of being able to walk again, ambulating effectively if not gracefully.
July 27, 2009
The same blue food dye that gives your Gatorade its turquoise tint and turns your tongue a peculiar shade of purple might also protect your nerves in the case of spinal cord injury.
By lucky accident, researchers discovered that the commonly used food additive FD&C blue dye No. 1 is remarkably similar to a lab compound that blocks a key step in nerve inflammation. When rats with spinal cord injury were given an infusion of blue dye, they recovered much faster than rats that didn't get the treatment. And researchers reported only one adverse effect: The rats turned blue.
"One of the reasons no one had done this before is that food science is very separate from neuroscience," said neuroscientist Maiken Nedergaard of the University of Rochester Medical Center, who co-authored the study published Monday in the Proceedings of the National Academy of Science. "Those two fields don't interact at all."
March 23, 2009
A type of brain cell that was long overlooked by researchers embodies one of very few ways in which the human brain differs fundamentally from that of a mouse or rat, according to researchers who published their findings as the cover story in the March 11 issue of the Journal of Neuroscience.
Scientists at the University of Rochester Medical Center found that human astrocytes, cells that were long thought simply to support flashier brain cells known as neurons that send electrical signals, are bigger, faster, and much more complex than those in mice and rats.
"There aren't many differences known between the rodent brain and the human brain, but we are finding striking differences in the astrocytes. Our astrocytes signal faster, and they're bigger and more complex. This has big implications for how our brains process information," said first author Nancy Ann Oberheim, Ph.D., a medical student who recently completed her doctoral thesis on astrocytes.
September 23, 2008
Maiken Nedergaard, M.D., D.M.Sc., has been elected a member of the Royal Danish Academy of Sciences, the premier scientific society in Denmark. The society elects only six new members worldwide every other year.
Nedergaard has been a pioneer in brain research, demonstrating that brain cells known as astrocytes play a role in a host of human diseases. For decades, much of the attention of neuroscientists had been focused on brain cells known as neurons, which send electrical signals. Astrocytes were long considered cells whose primary function was to support the neurons.
Nedergaard has turned that notion on its head, showing that astrocytes themselves play an important role in epilepsy, spinal cord disease, migraine headaches, stroke, and Alzheimer's disease.
December 24, 2007
A brain chemical that makes us sleepy also appears to play a central role in the success of deep brain stimulation to ease symptoms in patients with Parkinson's disease and other brain disorders. The surprising finding is outlined in a paper published online Dec. 23 in Nature Medicine.
The work shows that adenosine, a brain chemical most widely known as the cause of drowsiness, is central to the effect of deep brain stimulation, or DBS. The technique is used to treat people affected by Parkinson's disease and who have severe tremor, and it's also being tested in people who have severe depression or obsessive-compulsive disorder.
Patients typically are equipped with a
brain pacemaker,a small implanted device that delivers carefully choreographed electrical signals to a very precise point in the patient's brain. The procedure disrupts abnormal nerve signals and alleviates symptoms, but doctors have long debated exactly how the procedure works.
Certainly the electrical effect of the stimulation on neurons is central to the effect of deep brain stimulation,said Maiken Nedergaard, M.D., Ph.D., the neuroscientist and professor in the Department of Neurosurgery who led the research team.
But we also found a very important role for adenosine, which is surprising.
May 17, 2007
Scientists have found evidence that the cox-2 inhibitor celecoxib, a common pain reliever used to treat arthritis, may offer a new way to reduce the risk of the most common cause of brain damage in babies born prematurely.
The work involves shoring up blood vessels in a part of the brain that in premature infants is extremely fragile and vulnerable to dangerous bleeding, which affects an estimated 12,000 children a year, leaving many permanently affected by cerebral palsy, mental retardation, and seizures.
The laboratory research was done primarily in a laboratory at New York Medical College led by neonatologist Praveen Ballabh, M.D. Ballabh's team worked with Rochester neuroscientists including Maiken Nedergaard, M.D., D.M.Sc., Steven Goldman, M.D., Ph.D., and Nanhong Lou, B.M.
August 25, 2006
More than a dozen Rochester scientists seeking ways to reverse or lessen the effects of paralysis and other effects of spinal cord injury will begin new projects and continue promising research, thanks to motorists in New York State who push the gas medal a little too far.
Three research projects at the University of Rochester Medical Center are among the programs funded this year through the Spinal Cord Injury Research Program run by the New York State Department of Health. The program, created in 1998, uses fines paid by speeding motorists to fund research into spinal cord injury, whose number-one cause nationwide is motor vehicle accidents. In Rochester this year the grants are going to Roman Giger, Ph.D.; Maiken Nedergaard, M.D., Ph.D.; and Mark Noble, Ph.D.
May 15, 2006
By blowing gentle puffs of air onto a mouse's whiskers and watching how its brain reacts, scientists are discovering that a long-overlooked signaling system in the brain is crucial to our everyday activity.
The work is the latest in a growing body of evidence that star-shaped brain cells known as astrocytes aren't simply support cells but are stars of the brain in their own right, say researchers at the University of Rochester Medical Center who did the study. The work will be reported in a paper in the June issue of Nature Neuroscience and is now available online.
Now people have to take astrocytes seriously,said Maiken Nedergaard, M.D., Ph.D., professor in the Department of Neurosurgery and a member of the Center for Aging and Developmental Biology, whose team did the research. In the past few years she has found that the cells, long thought to simply nourish other cells and clean up their wastes, are central to diseases like epilepsy, spinal cord injury, and maybe even Alzheimer's disease.
January 6, 2006
New findings that long-overlooked brain cells play an important role in regulating blood flow in the brain call into question one of the basic assumptions underlying today's most sophisticated brain imaging techniques and could open a new frontier when it comes to understanding Alzheimer's disease.
In a paper to appear in the February issue of Nature Neuroscience and now available on-line, scientists at the University of Rochester Medical Center demonstrate that star-shaped brain cells known as astrocytes play a direct role in controlling blood flow in the brain, a crucial process that allows parts of the brain to burst into activity when needed. The finding is intriguing for a disease like Alzheimer's, which has long been considered a disease of brain cells known as neurons, and certainly not astrocytes.
For many years, astrocytes have been considered mainly as housekeeping cells that help nourish and maintain a healthy environment for neurons. But it's turning out that astrocytes may play a central role in many human diseases,said neuroscientist Maiken Nedergaard, M.D., Ph.D., who has produced a string of publications fingering astrocytes in diseases like epilepsy and spinal cord injury.
August 15, 2005
Star-shaped brain cells that are often overlooked by doctors and scientists as mere support cells appear to play a key role in the development of epilepsy, researchers say in a study published on-line August 14 in Nature Medicine. It's one of the first times scientists have produced firm evidence implicating the cells, known as astrocytes, in a common human disease.
Scientists found that astrocytes can serve as ground zero in the brain, setting off a harmful cascade of electrical activity in the brain by sending out a brain chemical that triggers other brain cells to fire out of control.
While it's impossible to tell at this early stage what effect the finding will have on treatment, the investigators at the University of Rochester Medical Center are hopeful the results will give doctors and pharmaceutical firms a new target in efforts to treat and prevent the disease.
This opens up a new vista in efforts to treat epilepsy. It might be possible to treat epilepsy not by depressing or slowing brain function, as many of the current medications do, but by targeting brain cells that have been completely overlooked,says Maiken Nedergaard, M.D., Ph.D., professor in the Department of Neurosurgery and a researcher in the Center for Aging and Developmental Biology, who led the research.
We are hopeful that someday, this will be very beneficial to patients.
July 28, 2004
ATP, the vital energy source that keeps our body's cells alive, runs amok at the site of a spinal cord injury, pouring into the area around the wound and killing the cells that normally allow us to move, scientists report in the cover story of the August issue of Nature Medicine.
The finding that ATP is a culprit in causing the devastating damage of spinal cord injury is unexpected. Doctors have known that initial trauma to the spinal cord is exacerbated by a cascade of molecular events over the first few hours that permanently worsen the paralysis for patients. But the finding that high levels of ATP kill healthy cells in nearby regions of the spinal cord that were otherwise uninjured is surprising and marks one of the first times that high levels of ATP have been identified as a cause of injury in the body.
While the work opens up a promising new avenue of study, the work is years away from possible application in patients, cautions Maiken Nedergaard, M.D., Ph.D., the researcher who led the study. In addition, the research offers promise mainly to people who have just suffered a spinal cord injury, not for patients whose injury is more than a day old. Just as clot-busting agents can help patients who have had a stroke or heart attack who get to an emergency room within a few hours, so a compound that could stem the damage from ATP might help patients who have had a spinal cord injury and are treated immediately.
- Contributions of the Na(+) /K(+) -ATPase, NKCC1, and Kir4.1 to hippocampal K(+) clearance and volume responses. Glia. 62, 608-22. (2014 Apr 01).
- Assessment of NgR1 Function In Vivo After Spinal Cord Injury. Neurosurgery. In press. (2014 Mar 03).
- Rapid manifestation of reactive astrogliosis in acute hippocampal brain slices. Glia. 62, 78-95. (2014 Jan 01).