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
Contact: Megan Fellman