Age-related cognitive decline: a transposon storm?
April 15, 2013
With the growing elderly population in the United States and around the world, questions about age-related cognitive decline are on everyone’s mind. Despite massive research into possible causes for age-related decline, numerous mysteries remain. A recent article in Nature Neuroscience, led by researcher Josh Dubnau at Cold Spring Harbor, suggests a new mechanism that may drive cognitive decline.
Josh’s lab uses Drosophila melanogaster (above) as a model system because of the feasibility of genetic manipulation in that species. The focus of their current paper is transposable elements: DNA sequences that can change where they are in the genome, potentially creating mutations or changing the size of the genome altogether. Readers who are not genetic experts might still remember Barbara McClintock’s famous corn that exposed the existence of transposable elements.
This new study identified transposable elements in drosophila that were active during normal aging. That might have been just a coincidence, except they found that a mutant with extra transposon expression had even more age-dependent cognitive decline. It was as if the mutants lost their cognitive sharpness more quickly than their wild type siblings. The mechanism by which this abnormal transposon activation affects cognition remains a mystery and the lab has yet to show that the abnormal transposons cause the cognitive decline. Nevertheless, this research suggests a new avenue through which we might understand, and ultimately prevent, the cognitive decline that so often accompanies aging. Perhaps the work might also provide insight into the variability in this process: might adults who suffer more rapid cognitive decline have more abnormal transposon activity? If so, what might be the cause of this? Answering such questions could cause a dramatic improvement in the lives of a large population.