Human senescent phenotypes

Published on June 30, 2016   51 min

Other Talks in the Series: Aging

Hello, my name is Robert Arking, I'm a professor of Biological Sciences at Wayne State University. I've long been interested in understanding the genetic aspects of the biology of longevity and aging. I've been asked to discuss with you today the topic of human senescent phenotypes, what are they, how do they begin, do they use the same or different mechanisms, can they be averted, and most interestingly, can they be reversed. Let us begin.
We experience our life as being a long and continuous sequence of events. Our conscious experience is not, however, a reliable guide, for the lifespan is actually composed of several different phases. Each distinguished by different patterns of gene expression, functional levels, and mortality rates. These phases are the developmental span, the health span, the transition phase, and then the senescent span. The developmental span begins at our conception, or for certain epigenetic based events, it might well begin when your mother was a fetus in your grandmother's womb. Much of this phase is concerned with proper physical and mental development and ends by about 20 years of age when we reach our maximum physical fitness. The minimum human age specific mortality rate has reached just prior to sexual maturation. Humans differ from most other mammals in the fact that we are sexually mature long before we are developmentally mature. The health span occurs roughly from ages 20 to 55 or 60 or so. Gene-dependent longevity assurance mechanisms are operative. There are high levels of repair and maintenance, high levels of homeostasis, and sufficient reserve capacity to deal with various stressors. If you are healthy, the age specific mortality rate usually increases at a very slow rate and is at a low level to begin with. The transition phase is when the age specific mortality begins to significantly increase, beginning at about 55 to 60 years. When the age related senescent human phenotypes begin to make themselves felt and experienced. The senescent phase extends form age 55 until the end of life. And many senescent phenotypes that steal away our functional ability are highly individualized. In all cases, what occurs is that the cells burden of damage increases and we undergo a loss of homeostasis. Eventually, a critical threshold is passed and cell function ceases. Note that aging can be reversed in certain highly controlled, entirely different situations in laboratory animals. Thus, the idea that aging is non-reversible is not strictly true. But there are for now no obvious ways of translating these exceptional reversals into a more ordinary event. Although the research is very encouraging, I must say. Perhaps, one of you might be involved in that work some day. Thus the senescent human phenotypes occur mostly during the last 20 years of the ordinary human life but as you will see, they mostly have their beginnings much earlier in the health span.