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Berkeley scientists discover switch for aging

March 24, 2020

Scientists at the University of California, Berkeley, have discovered a “switch” that controls chronic inflammation in the human body
The group has identified a protein called NLRP3 that senses threats and launches an inflammatory response
The researchers believe that switching off this protein can potentially delay aging
The finding has given the scientific community a better understanding of the reversibility of age-associated chronic diseases

During times of stress or exposure to environmental toxins as well as in aging human bodies, the body’s immune system goes into overdrive, leading to chronic inflammation. Inflammation is a contributing factor in many debilitating age-associated diseases like Parkinson’s, Alzheimer’s, cancer, and diabetes. Now, a group of researchers at UC Berkeley have identified a molecular “switch” that controls the immune response in the body through chronic inflammation. The findings were published in the journal Cell Metabolism in February 2020. The group is optimistic that the discovery could lead to new ways of slowing or reversing many age-related diseases. “My lab is very interested in understanding the reversibility of aging,” says senior author Danica Chen, associate professor of metabolic biology, nutritional sciences and toxicology at UC Berkeley. “In the past, we showed that aged stem cells can be rejuvenated. Now, we are asking: to what extent can aging be reversed? And we are doing that by looking at physiological conditions, like inflammation and insulin resistance, that have been associated with aging-related degeneration and diseases.” Chen and her colleagues have demonstrated that a protein called NLRP3 inflammasome can be essentially “switched off” through a process called deacetylation in which a small part of the molecule is removed. NLRP3 senses threats in the body and launches an inflammatory reaction in response. Switching it off can prevent the inflammation from occurring. Overactivity of NLRP3 is linked to many chronic diseases such as diabetes, cancer, multiple sclerosis, and dementia. The new study shows that drugs that deacetylate NLRP3 may be able to prevent or reverse age-related degenerative conditions. “This acetylation can serve as a switch,” says Chen. “So, when it is acetylated, this inflammasome is on. When it is deacetylated, the inflammasome is off.” The group conducted their experiments in mice and found that a protein called SIRT2 can deacetylate NLRP3. Mice with a genetic mutation that prevented SIRT2 production had higher levels of NLRP3 and consequently more signs of chronic inflammation and higher insulin resistance in old age. Insulin resistance is associated with diabetes type 2 and metabolic syndrome. The researchers further went on to destroy the immune system of some mice with radiation and then reconstituted it with either acetylated or deacetylated versions of NLRP3 inflammasome. After six weeks, the scientists noted that the mice that got the switched off (deacetylated) version had better insulin resistance. “I think this finding has very important implications in treating major human chronic diseases,” Chen said. “It’s also a timely question to ask, because in the past year, many promising Alzheimer’s disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return. So, I think it’s more urgent than ever to understand the reversibility of aging-related conditions and use that knowledge to aid a drug development for aging-related diseases.” The study was co-authored by scientists at UC Berkeley, Harvard Medical School, and Fudan University.

References: https://news.berkeley.edu/2020/02/06/molecular-switch-reverses-chronic-inflammation-and-aging

Berkeley scientists discover switch for aging

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