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A carboxyfullerene SOD mimetic improves cognition and extends the lifespan of mice
Kevin L Quick1, Sameh S Ali, Robert Arch
1Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States.
Abstract:
In lower organisms, such as Caenorhabditis elegans and Drosophila, many genes identified as key regulators of aging are involved in either detoxification of reactive oxygen species or the cellular response to oxidatively-damaged macromolecules. Transgenic mice have been generated to study these genes in mammalian aging, but have not in general exhibited the expected lifespan extension or beneficial behavioral effects, possibly reflecting compensatory changes during development. We administered a small-molecule synthetic enzyme superoxide dismutase (SOD) mimetic to wild-type (i.e. non-transgenic, non-senescence accelerated) mice starting at middle age. Chronic treatment not only reduced age-associated oxidative stress and mitochondrial radical production, but significantly extended lifespan. Treated mice also exhibited improved performance on the Morris water maze learning and memory task. This is to our knowledge the first demonstration that an administered antioxidant with mitochondrial activity and nervous system penetration not only increases lifespan, but rescues age-related cognitive impairment in mammals. SOD mimetics with such characteristics may provide unique complements to genetic strategies to study the contribution of oxidative processes to nervous system aging.
Insights
Administering a synthetic superoxide dismutase (SOD) mimetic to middle-aged mice extended lifespan and improved cognitive function. This antioxidant treatment reduced oxidative stress, offering a potential therapeutic strategy for aging mammals.
Area of Science:
- Biogerontology
- Neuroscience
- Oxidative Stress Research
Background:
- Aging research in lower organisms identifies genes in reactive oxygen species detoxification and oxidative damage response.
- Transgenic mouse models often fail to show expected lifespan extension or behavioral benefits, possibly due to developmental compensation.
Purpose of the Study:
- To investigate the effects of a small-molecule synthetic superoxide dismutase (SOD) mimetic on aging in wild-type mice.
- To determine if SOD mimetic administration can mitigate age-associated oxidative stress and cognitive decline.
Main Methods:
- Wild-type mice were treated with a synthetic SOD mimetic starting at middle age.
- Evaluated effects on oxidative stress markers, mitochondrial radical production, lifespan, and performance on the Morris water maze.
Main Results:
- Chronic SOD mimetic treatment reduced age-associated oxidative stress and mitochondrial radical production.
- Significant lifespan extension was observed in treated mice.
- Treated mice showed improved learning and memory performance in the Morris water maze.
Conclusions:
- Administered antioxidants with mitochondrial activity and nervous system penetration can extend lifespan and rescue age-related cognitive impairment in mammals.
- SOD mimetics represent a promising therapeutic approach to complement genetic strategies for studying aging and oxidative stress in the nervous system.
