News

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."

The research by neuroscientists at the URMC was presented at the annual meeting of the Society for Neuroscience in San Diego Nov. 3-7. The work was highlighted as part of a press conference on potential environmental influences on Alzheimer's disease.

The team found that copper damages a molecule known as LRP (low-density lipoprotein receptor-related protein), a molecule that acts like an escort service in the brain, shuttling amyloid-beta out of the brain and into the body. The molecule's role in Alzheimer's was revealed more than a decade ago by another author of the work, Berislav Zlokovic, M.D., Ph.D., professor of Neurosurgery and Neurology and director of the Frank P. Smith Laboratory for Neuroscience and Neurosurgery Research. Zlokovic is widely recognized for demonstrating that blood vessels, blood flow, and the blood-brain barrier are central to the development of Alzheimer's disease.

In the experiment at the University of Rochester Medical Center, worms that are hermaphrodites (with characteristics of both females and males) went for the buttery smell, while the males - the other of the two sexes in these worms - opted for the scent of fresh vegetables. But when researchers tricked a few nerve cells in hermaphrodites into sensing that they were in a male worm, suddenly they too preferred the smell of fresh vegetables.

Geneticist Douglas Portman, Ph.D., and graduate student KyungHwa Lee ultimately hope to understand gender differences in diseases like autism, depression, and attention-deficit disorder. Many more boys than girls are diagnosed with ADD and autism, and many more girls than boys are diagnosed with depression. While proposed explanations abound, few scientists debate the notion that the brains of the sexes are in some ways fundamentally different.

Scientists at the University of Rochester Medical Center have received $1.37 million to continue their work looking at some of the earliest events that occur at the start of Alzheimer's disease - a condition that now generally goes undetected until the death of key brain cells has been underway for decades.

The team led by William Bowers, Ph.D., associate professor of Neurology and a scientist in the Center for Neural Development and Disease, is focusing on the role of inflammation in the evolution of the disease. Just as rheumatoid arthritis can ravage the body's joints because of the inflammation it causes, scientists are realizing that the same thing happens to the brain in patients with Alzheimer's disease. The brain can be under assault for decades as the body attempts to fend off some perceived threat.

Scientists are trying a plumber's approach to rid the brain of the amyloid buildup that plagues Alzheimer’s patients: Simply drain the toxic protein away.

That’s the method outlined in a paper published online August 12^th by Nature Medicine. A team of scientists from the University of Rochester Medical Center, led by neuroscientist Berislav Zlokovic, M.D., Ph.D., show how the body's natural way of ridding the body of the substance is flawed in people with the disease. Then the team demonstrated an experimental method in mice to fix the process, dramatically reducing the levels of the toxic protein in the brain and halting symptoms. The team is now working on developing a version of the protein that could be tested in people with the disease.

This summer the University of Rochester Medical Center boasts winners of two of the most prestigious awards available to young scientists - and the winners are from the same family.

Edward Brown, Ph.D., has been named a Pew Scholar in the Biomedical Sciences, and his spouse Ania Majewska, Ph.D., has received an award from the Alfred P. Sloan Foundation. Brown, one of just 20 scientists in the nation to be recognized by the Pew Charitable Trusts this year, will receive $240,000 toward his research, while Majewska will receive $45,000 to continue her work.

In the June 1^st issue of the Journal of Clinical Investigation, a team of scientists from the University of Rochester Medical Center shows that a key inflammatory regulator, a known villain when it comes to parsing out damage after a stroke and other brain injuries, seems to do the opposite in Alzheimer’s disease, protecting the brain and helping get rid of clumps of material known as plaques that are a hallmark of the disease.

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.