Rejuvenating senescent cells

IMAGE CREDIT: Dr Eva Latorre, Harries Lab, Univ of Exeter

Senisca

The image above is a 48 hour timelapse of rejuvenating senescent primary human dermal fibroblast cells.

A major cause of age-related diseases and the aesthetic signs of ageing is the accumulation of senescent cells in aged tissues and organs; removal of such cells has been shown to be capable of bringing about ‘rejuvenation’ of function in people and animals. Scientists at Senisca have discovered a new and druggable means to reverse senescence through modulation of RNA splicing.

Levels of splicing factors change during ageing, compromising our ability to carry out this ‘fine tuning’ of gene expression. This is a fundamental reason why cells become senescent. Compromised molecular resilience is a major cause of the ill health and frailty that accompanies ageing.

Senisca has demonstrated that restoration of splicing factor levels to those seen in younger cells is able to effectively turn back the ageing clock in old cells, bringing about reversal of senescence.

LEARN MORE: Senisca





Judith Campisi

Judith Campisi PhD

Judith Campisi received a PhD in biochemistry from the State University of New York at Stony Brook and completed her postdoctoral training in cell cycle regulation at the Dana-Farber Cancer Institute and Harvard Medical School. As an assistant and associate professor at the Boston University Medical School, she studied the role of cellular senescence in suppressing cancer and soon became convinced that senescent cells also contributed to aging. She joined the Lawrence Berkeley National Laboratory as a senior scientist in 1991.

In 2002, she started a second laboratory at the Buck Institute for Research on Aging. At both institutions, Dr Campisi established a broad program to understand the relationship between aging and age-related disease, with an emphasis on the interface between cancer and aging.

Dr Campisi has received numerous awards for her research, including two MERIT awards from the National Institute on Aging and awards from the AlliedSignal Corporation, Gerontological Society of America, and American Federation for Aging Research. She is a recipient of the Longevity prize from the IPSEN Foundation, the Bennett Cohen award from the University of Michigan, and the Schober award from Halle University, and she is the first recipient of the international Olav Thon Foundation prize in Natural Sciences and Medicine.

Dr Campisi currently serves on advisory committees for the Alliance for Aging Research, Progeria Research Foundation, and NIA’s Intervention Testing Program.



SENS

Strategies for Engineered Negligible Senescence (SENS) is the term coined by British biogerontologist Aubrey de Grey for the diverse range of regenerative medical therapies, either planned or currently in development, for the periodical repair of all age-related damage to human tissue with the ultimate purpose of maintaining a state of negligible senescence in the patient, thereby postponing age-associated disease for as long as the therapies are reapplied.

The term “negligible senescence” was first used in the early 1990s by professor Caleb Finch to describe organisms such as lobsters and hydras, which do not show symptoms of aging. The term “engineered negligible senescence” first appeared in print in de Grey’s 1999 book The Mitochondrial Free Radical Theory of Aging. De Grey called SENS a “goal-directed rather than curiosity-driven” approach to the science of aging, and “an effort to expand regenerative medicine into the territory of aging”.

Framework

The arrows with flat heads are notations meaning “inhibits,” used in the literature of gene expression and gene regulation.

The arrows with flat heads are a notation meaning "inhibits," used in the literature of gene expression and gene regulation.

The ultimate objective of SENS is the eventual elimination of age-related diseases and infirmity by repeatedly reducing the state of senescence in the organism. The SENS project consists in implementing a series of periodic medical interventions designed to repair, prevent or render irrelevant all the types of molecular and cellular damage that cause age-related pathology and degeneration, in order to avoid debilitation and death from age-related causes.

MORE: Wikipedia