Developmental Biology - Theory of Aging Redrawn|
What Causes Organs to Deteriorate and Age?
Cell lifespan is extended by lower temperatures, but controlled by genes...
Why do we age? Despite more than a century of research and a vast industry of youth-promising products, cells in our organs continue to deteriorate with age in a process not completely understood.
We do know that cooler temperatures extend many animal species lives, over those animals living in warmer temperatures. As such, "there are people out there who believe, strongly, that if you take a cold shower every day it will extend your lifespan," says Kristin E. Gribble PhD, of the Marine Biological Laboratory (MBL). But a new study from the laboratories of Gribble and David Mark Welch PhD, MBL Director of Research, indicates it's not simply a matter of turning down the thermostat. Rather, the extent temperature affects lifespan depends on an individual's genes.
The MBL study published in Experimental Gerentology, was conducted in the rotifer, a tiny animal that Gribble, Mark Welch, and colleagues have been developing as a model system for aging research. They exposed 11 genetically distinct strains of Brachionus rotifers to low temperature, with the idea that if lifespan extension is purely the result of a thermodynamic response, all strains should have a similar lifespan increase.
"Generally, it was thought that if an organism is exposed to lower temperature, it passively lowers its metabolic rate and that slows the release of ROS, which slows down cellular damage, delaying aging and extending lifespan," explains Gribble. Reactive oxygen species (ROS) is formed as a natural by product of oxygen metabolism and is important to cell signaling and cell homeostasis.
However, the median lifespan increase across the eleven strains of rotifers varied from 6 percent to 100 percent.
The study clarifies the role of temperature in the free-radical theory of aging, which has dominated the field since the 1950s. That theory proposes animals age due to the accumulation of cell damage from reactive oxidative species (ROS), a form of oxygen generated by normal metabolic processes.
Research results, however, indicate that change in lifespan under low temperature is more likely controlled by specific genes.
"This means we really need to pay more attention to genetic variability in thinking about aging therapies. That is going to be really important when we try to move some of these therapies into humans."
Kristin E. Gribble PhD, Josephine Bay Paul Center for Comparative Molecular Biology and Evolution, Marine Biological Laboratory, Woods Hole, Massachusetts, USA.
• Congeneric [animals belonging to the same genus] strains displayed variable lifespan change in response to lower temperature.
• Low temperature reduced reproductive senescence suggesting healthspan extension.
• The cold-sensor TRPA1 does not mediate chemoreception in Brachionus rotifers.
• Results suggest that lifespan extension under low temperature is an active genetic process.
Lifespan extension under low temperature is well conserved across both endothermic and exothermic taxa, but the mechanism underlying this change in aging is poorly understood. Low temperature is thought to decrease metabolic rate, thus slowing the accumulation of cellular damage from reactive oxygen species, although recent evidence suggests involvement of specific cold-sensing biochemical pathways. We tested the effect of low temperature on aging in 11 strains of Brachionus rotifers, with the hypothesis that if the mechanism of lifespan extension is purely thermodynamic, all strains should have a similar increase in lifespan. We found differences in change in median lifespan ranging from a 6% decrease to a 100% increase, as well as differences in maximum and relative lifespan extension and in mortality rate. Low temperature delays reproductive senescence in most strains, suggesting an extension of healthspan, even in strains with little to no change in lifespan. The combination of low temperature and caloric restriction in one strain resulted in an additive lifespan increase, indicating these interventions may work via non- or partially-overlapping pathways. The known low temperature sensor TRPA1 is present in the rotifer genome, but chemical TRPA1 agonists did not affect lifespan, suggesting that this gene may be involved in low temperature sensation but not in chemoreception in rotifers. The congeneric [animals belonging to the same genus] variability in response to low temperature suggests that the mechanism of low temperature lifespan extension is an active genetic process rather than a passive thermodynamic one and is dependent upon genotype.
Kristin E. Gribble, Benjamin M. Moran, Shannon Jones, Emily L. Corey and David B. Mark Welch.
The Marine Biological Laboratory (MBL) is dedicated to scientific discovery - exploring fundamental biology, understanding marine biodiversity and the environment, and informing the human condition through research and education. Founded in Woods Hole, Massachusetts in 1888, the MBL is a private, nonprofit institution and an affiliate of the University of Chicago.
This work was financed by grants from the National Institute on Aging to DMW (R01 AG037960-01) and to KEG (K01 AG049049-01) and by funding from the Vetlesen Foundation to the Josephine Bay Paul Center for Comparative Molecular Biology and Evolution at the Marine Biological Laboratory.
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In 1702, Antonie van Leeuwenhoek was the first to publish observations of this species.
Not until 1838 were rotifers recognized as multicellular animals. Image: Wikipedia.