Many scientists work on mechanisms that determine lifespan in model organisms such as worms, flies and mice, but what will it take to develop strategies to increase human lifespan? In a Review “Puzzles, promises and a cure for aging” appearing in Nature this week, Jan Vijg and Judith Campisi discuss current knowledge and outline questions for future research.
The inevitability of aging and death and attempts to subvert mortality have fascinated humanity for more than 5,000 years. Today research involving yeast, flies, worms and mice encourages the notion that we may yet manipulate lifespan with drugs, genetic knowledge or nutritional fine-tuning. In the Review, Buck Institute faculty members Judith Campisi, PhD (who is also senior scientist at Lawrence Berkeley National Laboratory) and Jan Vijg PhD (now professor and chair of genetics at Albert Einstein College of Medicine of Yeshiva University) discuss current knowledge and argue that there is no question human lifespan will almost certainly increase modestly over the coming decades. However, they critically analyze whether current knowledge has reached the state where postponing human aging and natural death for many decades, possibly indefinitely, is feasible. They further posit that only a more complete understanding of basic aging mechanisms and their relationship with disease will allow us to develop integrated strategies to safely and effectively increase human health and lifespan.
“Current findings involving simple organisms leave no doubt that lifespan is plastic,” said Campisi, “But research needs to take into account the idiosyncrasies of model organisms, and the complexity of humans who do not live in laboratories.” In the review Campisi and Vijg say future research should focus on comparing the differences in aging between simple animals and humans. They also advocate a search for biomarkers that would better define and characterize the degenerative processes underlying mortality.
“There is much work that remains to be done to unravel the causes of aging,” said Vijg. “All interventions currently on the horizon will fail to increase longevity substantially if the ultimate cause(s) of aging does not lend itself to available treatments.” The authors contend that there is no known scientific reason why aging cannot be prevented, similar to the goal of preventing individual age-related diseases. But, they conclude, our understanding of basic aging processes is too shallow to know whether an indefinite postponement of aging is really possible. They call for studies that delve deeper into theories that assume aging is caused by random changes, as well as the lifelong accumulation of molecular and cellular damage. Campisi and Vijg also say future research should focus on the potential relationship between cancer, neurodegenerative and cardiovascular disorders with the basic molecular processes of aging.
Source: Buck institute for Age Research