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In general, biological aging clocks and biomarkers of aging are expected to find many uses in biological research since age is a fundamental characteristic of most organisms. Accurate measures of biological age (biological aging clocks) could be useful for testing the validity of various theories of biological aging,
Genetic theories of aging propose that aging is programmed within each individual's genes. According to this theory, genes dictate cellular longevity. Programmed cell death, or apoptosis, is determined by a "biological clock" via genetic information in the nucleus of the cell. Genes responsible for apoptosis provide an explanation for cell ...
Steve Horvath is a German–American aging researcher, geneticist, and biostatistician.He is a professor at the University of California, Los Angeles known for developing the Horvath aging clock, which is a highly accurate molecular biomarker of aging, and for developing weighted correlation network analysis.
Circadian clock, a molecular mechanism that results in a circadian rhythm in a living organism; Circadian rhythm, biological process that displays an oscillation about 24 hours, such as the human sleep-wake cycle (the "body clock") Epigenetic clock, a set of DNA sites whose methylation levels can be used to measure aging throughout the body
Overview, including some physiological parameters, of the human circadian rhythm ("biological clock"). Chronobiology is a field of biology that examines timing processes, including periodic (cyclic) phenomena in living organisms, such as their adaptation to solar- and lunar-related rhythms. [1] These cycles are known as biological rhythms.
Until recently, epigenetic clocks have primarily been used in the lab, but a few are now available to consumers. Some have price tags upwards of $500. ... Understanding biological aging can be ...
The somatic mutation theory of ageing states that accumulation of mutations in somatic cells is the primary cause of aging. A comparison of somatic mutation rate across several mammal species found that the total number of accumulated mutations at the end of lifespan was roughly equal across a broad range of lifespans. [ 16 ]
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