Danica Chen

Danica Chen

Title
Associate Professor
Department
Dept of Nutritional Sciences & Toxicology
Phone
(510) 642-0603
Research Expertise and Interest
aging, stem cell, metabolism, diseases of aging
Research Description

One of the most fundamental questions in biology is how we age. The past decades have witnessed a significant revision of a traditional view that aging is simply a random and passive process that is solely driven by entropy. In fact, the aging process is regulated genetically and lifespan can be extended by single gene mutations. The Chen Lab research aims to understand molecular and cellular mechanisms that regulate the aging process and explore therapeutic targets to slow aging and even reverse aging-associated degeneration. The most intriguing aspect of pharmaceutical intervention that targets the aging pathways is that, instead of targeting a specific disease, it has the potential of ameliorating a wide array of seemingly unrelated diseases associated with aging, such as cancer, tissue degeneration, metabolic syndrome, and immune dysfunction.

In the News

February 6, 2020

Molecular ‘switch’ reverses chronic inflammation and aging

Chronic inflammation, which results when old age, stress or environmental toxins keep the body’s immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.

In the News

February 6, 2020

Molecular ‘switch’ reverses chronic inflammation and aging

Chronic inflammation, which results when old age, stress or environmental toxins keep the body’s immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.

Featured in the Media

Please note: The views and opinions expressed in these articles are those of the authors and do not necessarily reflect the official policy or positions of UC Berkeley.
February 7, 2020
Michael Irving
Inflammation is an important function of our immune systems, but sometimes it gets stuck in overdrive, causing chronic pain and diseases such as multiple sclerosis, cancer, diabetes, Alzheimer's, and Parkinson's. Now, a team of Berkeley researchers has found a way of switching off a group of proteins that form the key culprit -- NLRP3 inflammasome -- in mice, and their results suggest that the "switch" could be used not only to turn off the reaction, but potentially reverse associated conditions and diseases and maybe even aging itself. "My lab is very interested in understanding the reversibility of aging," says associate nutritional sciences and toxicology professor Danica Chen, the study's senior author. "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." For more on this, see our press release at Berkeley News.
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