MIAMI BEACH --- Researchers from Northwestern University will present findings from their studies at the Society for Neuroscience's annual meeting to be held in Miami Beach, Fla., Oct. 23-28, 1999. The Northwestern presentations include studies of the genetic gears of the biological clock, gene therapy and its effect on Parkinson's disease and an understanding of memory and loss of memory. A summary of these three presentations follows:
Study points to genetic basis for aging of biological clock
Results from a recent study conducted at Northwestern University should help neuroscientists better understand the genes that drive human beings' biological clocks and how those genes might change as people age.
The findings, which will be presented by Northwestern graduate student Daniel Kolker, suggest that in old age the Clock gene, or one of the genes that its protein product interacts with, fails to function as well as it does in youth. This may help explain why the circadian rhythms of many species of animals, including humans, function differently or more irregularly in old age.
Kolker and colleagues studied two different groups of mice, one a normal group of animals and the other a group that had a mutation in the Clock gene, which gives those mice an abnormally functioning biological clock. The animals? circadian timing systems were monitored when they where young and later old, and all the mice exhibited a change in their daily rhythms (e.g., exercise and activity-rest cycle) when older. However, the mice with a mutated Clock gene showed a significantly greater disruption in their circadian rhythms than the normal mice. This would indicate that the Clock gene is important to the functioning of the biological clock.
Kolker, who works with circadian rhythm expert Fred Turek, Charles E. and Emma H. Morrison Professor of Biology at Northwestern, has repeated the study and is currently analyzing the data. Although no experiments have yet looked at the role that the Clock gene plays in the aging of human circadian systems, the biological clocks of all animals, including humans, share similar characteristics.
The research was funded by the National Institutes of Health.
Kolker can be reached during the Neuroscience Meeting at (305) 531-1331.
Gene therapy effective for Parkinson's disease
A new study from Northwestern University Medical School and the Children's Memorial Institute for Education and Research in Chicago provides strong support for the development of gene therapy approaches to treat Parkinson's disease.
Findings from the study, which will be presented by Martha C. Bohn and colleagues from Northwestern, indicated that glial cell line-derived factor (GDNF) gene therapy used in a laboratory model of Parkinson's disease rescued dying brain cells and decreased the movement problems associated with nerve cell death. GDNF is a growth-promoting factor for glia cells, which make dopamine and also are the cells that die in Parkinson's disease.
Bohn is a professor of pediatrics at Northwestern University Medical School and director of the neurobiology program at Children's Memorial Institute for Education and Research.
Results of several tests showed that animals that received the GDNF gene therapy maintained over 50 percent of the connections between the substantia nigra, the area of brain that degenerates in Parkinson's disease, and the striatum, which receives connections from the substantia nigra. The animals that did not receive the gene therapy maintained only 25 percent of the nerve connections.
In addition, the animals that received the GDNF gene therapy had less-severe Parkinson-like motor deficits. These results were observed only if the GDNF gene was injected into the substantia nigra, as opposed to when it was injected into the striatum, the area that receives connections.
To further determine if GDNF gene therapy is effective, it must be tested in larger animal models of Parkinson's disease. In addition, improved and safer methods of inserting genes into the brain must be developed. The Northwestern researchers are pursuing both avenues of research.
Bohn can be reached during the Neuroscience Meeting at m-bohn@nwu.edu or through her office in Chicago at (773) 868-8052.
Northwestern researchers measure memory -- and the loss of it
Neuroscientists at Northwestern University are a step closer to learning how memories are stored in the brain and how memory sometimes fails in both healthy people and those suffering from neurological disease or brain injury.
Ken A. Paller, assistant professor of psychology at the Weinberg College of Arts and Sciences, and co-researchers at Northwestern University will describe experiments that measured an individual's ability to recognize other persons.
Using a set of face photographs, each of which was associated with a unique name and a short, spoken vignette, they measured brain activity during person recognition with two methods that provided information about relevant neural events. The first method was based on electrical activity extracted from an electroencephalogram (EEG), and the other was based on a blood oxygenation measure derived from magnetic resonance imaging (MRI).
Together, these methods provided information about brain networks that are responsible for representing and retrieving the information constituting person identity.
Results of the Northwestern study suggest that person recognition depends on prefrontal brain regions that presumably exert a modulatory influence on processing in other brain regions. Person recognition also requires networks in the posterior part of the neocortex, including parietal and fusiform regions, that are necessary for the storage and retrieval of information associated with each face.
The researchers also showed that right prefrontal activity is associated with generic aspects of memory retrieval, whereas left prefrontal activity is more closely associated with successful recollection.
This study was supported by a grant from the National Institute of Neurological Diseases and Stroke.
Paller can be reached during the Neuroscience Society meeting at kap@nwu.edu or through his office at Northwestern at (847) 491-3370.