Press Releases & Research Commentary

Chances are if you're a senior managing your health, you've already had a conversation with your doctor about stroke risk. While many patients know the warning signs of stroke -- slurred speech, weakness on one side of the body, coordination problems, double vision, and headaches -- health care providers often fail to educate patients about their risk for silent or mini-strokes, which can cause progressive, permanent damage and lead to dementia.

A new study published in the Journal of Neuroscience, examined the effects of these so-called mini-strokes. They frequently are not diagnosed or detected by a doctor because a patient does not immediately present with stroke signs. Mini-strokes may lead to permanent neurological damage and increase risk for full blown stroke.

Maiken Nedergaard, MD, lead author of the study and professor of neurosurgery at the University of Rochester Medical Center, says at least half of individuals over the age of 60 will experience one mini-stroke in their lifetime. She calls the prevalence of mini-strokes "an epidemic."

The University of Rochester Medical Center has opened the doors on a new facility that will enable researchers to create, study, and ultimately use stem cells and their offspring in early-phase experimental human therapies. The Upstate Stem Cell cGMP Facility – which will be used by academic and private-sector scientists from across the state – was created with $3.5 million in support from the Empire State Stem Cell Board.

“One of the critical barriers to moving cell-based therapies into clinical trials is the requirement that these cells be manufactured in a facility that meets strict federal requirements,” said Steve Dewhurst, Ph.D., chair of the URMC Department of Microbiology and Immunology and principal investigator for the state grant. “Without this resource, much of this science remains stuck in the lab.”

A new study appearing today in the Journal of Neuroscience details for the first time how "mini-strokes" cause prolonged periods of brain damage and result in cognitive impairment. These strokes, which are often imperceptible, are common in older adults and are believed to contribute to dementia.

"Our research indicates that neurons are being lost as a result of delayed processes following a mini-strokes that may differ fundamentally from those of acute ischemic events," said Maiken Nedergaard, M.D., D.M.Sc., the lead author of the study and professor of Neurosurgery at the University of Rochester Medical Center. "This observation suggests that the therapeutic window to protect cells after these tiny strokes may extend to days and weeks after the initial injury."

When the era of regenerative medicine dawned more than three decades ago, the potential to replenish populations of cells destroyed by disease was seen by many as the next medical revolution. However, what followed turned out not to be a sprint to the clinic, but rather a long tedious slog carried out in labs across the globe required to master the complexity of stem cells and then pair their capabilities and attributes with specific diseases.

In a review article appearing today in the journal Science, University of Rochester Medical Center scientists Steve Goldman, M.D., Ph.D., Maiken Nedergaard, Ph.D., and Martha Windrem, Ph.D., contend that researchers are now on the threshold of human application of stem cell therapies for a class of neurological diseases known as myelin disorders -- a long list of diseases that include conditions such as multiple sclerosis, white matter stroke, cerebral palsy, certain dementias, and rare but fatal childhood disorders called pediatric leukodystrophies.

Stem cell biology has progressed in many ways over the last decade, and many potential opportunities for clinical translation have arisen, said Goldman. In particular, for diseases of the central nervous system, which have proven difficult to treat because of the brain's great cellular complexity, we postulated that the simplest cell types might provide us the best opportunities for cell therapy.

A previously unrecognized system that drains waste from the brain at a rapid clip has been discovered by neuroscientists at the University of Rochester Medical Center. The findings were published online August 15 in Science Translational Medicine.

The highly organized system acts like a series of pipes that piggyback on the brain's blood vessels, sort of a shadow plumbing system that seems to serve much the same function in the brain as the lymph system does in the rest of the body -- to drain away waste products.

"Waste clearance is of central importance to every organ, and there have been long-standing questions about how the brain gets rid of its waste," said Maiken Nedergaard, M.D., D.M.Sc., senior author of the paper and co-director of the University's Center for Translational Neuromedicine. "This work shows that the brain is cleansing itself in a more organized way and on a much larger scale than has been realized previously.

"We're hopeful that these findings have implications for many conditions that involve the brain, such as traumatic brain injury, Alzheimer's disease, stroke, and Parkinson's disease," she added.

A type of cell plentiful in the brain, long considered mainly the stuff that holds the brain together and oft-overlooked by scientists more interested in flashier cells known as neurons, wields more power in the brain than has been realized, according to new research published today in Science Signaling.

Neuroscientists at the University of Rochester Medical Center report that astrocytes are crucial for creating the proper environment for our brains to work. The team found that the cells play a key role in reducing or stopping the electrical signals that are considered brain activity, playing an active role in determining when cells called neurons fire and when they don't.

That is a big step forward from what scientists have long considered the role of astrocytes -- to nurture neurons and keep them healthy.

"Astrocytes have long been called housekeeping cells -- tending to neurons, nurturing them, and cleaning up after them," said Maiken Nedergaard, M.D., D.M.Sc., professor of Neurosurgery and leader of the study. "It turns out that they can influence the actions of neurons in ways that have not been realized."

Acupuncture has been used for more than 2,000 years in traditional Chinese medicine to treat pain and other ailments. This technique was traditionally thought to work by channeling energy or Qi (pronounced chee) through body 'meridians' with acupuncture needles. In reality, meridians are not associated with any discrete anatomical structures. However, virtually all acupuncture points are located in deep tissues that are rich in sensory innervation, suggesting an intimate association between acupuncture points and peripheral somatosensory afferents. Although opioid peptides, the body's natural painkillers, contribute centrally to the pain-relieving effects of acupuncture, it is currently unclear what peripheral mechanisms are engaged by this ancient remedy.

Scientists have taken another important step toward understanding just how sticking needles into the body can ease pain.

In a paper published online May 30 in Nature Neuroscience, a team at the University of Rochester Medical Center identifies the molecule adenosine as a central player in parlaying some of the effects of acupuncture in the body. Building on that knowledge, scientists were able to triple the beneficial effects of acupuncture in mice by adding a medication approved to treat leukemia in people.

The new findings add to the scientific heft underlying acupuncture, said neuroscientist Maiken Nedergaard, M.D., D.M.Sc., who led the research. Her team is presenting the work this week at a scientific meeting, Purines 2010, in Barcelona, Spain.

Millions of people worldwide use acupuncture to ease a variety of painful conditions, but it’s still not clear how the ancient treatment works. Now a new study of mice shows that insertion of an acupuncture needle activates nearby pain-suppressing receptors. What’s more, a compound that boosts the response of those receptors increases pain relief—a finding that could one day lead to drugs that enhance the effectiveness of acupuncture in people.

Researchers have developed two hypotheses for how acupuncture relieves pain. One holds that the needle stimulates pain-sensing nerves, which trigger the brain to release opiumlike compounds called endorphins that circulate in the body. The other holds that acupuncture works through a placebo effect, in which the patient's thinking releases endorphins. Neuroscientist Maiken Nedergaard of the University of Rochester Medical Center in New York state was skeptical about both hypotheses because acupuncture doesn’t hurt and often works only when needles are inserted near the sore site. Nedergaard instead suspected that when acupuncturists insert and rotate needles, they cause minor damage to the tissue, which releases a compound called adenosine that acts as a local pain reliever.

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.

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."

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.

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.

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."

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.

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.

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.

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.

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."

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.