How does aging skin contain clues about aging brains?
Aging runs parallel to accumulation of stress. Aging is defined as a time sequential deterioration of living things that is prompted by increased susceptibility to disease and adverse events, leading to loss of viability and physiologic functions. In simpler terms, aging is characterized by the individual’s inability to respond in a useful way to stress.
Both skin cells and brain cells develop from the same kind of embryonic tissue (ectoderm). A brain biopsy to detect brain tissue aging is impractical but a skin biopsy is readily attainable and can provide an experimental model for aging research on the brain. The skin and brain age in similar ways. Influences include inherited genes, diet, environmental factors, sleep, exercise, and hormones. As we age, skin becomes dry and thin due to hormone decline.
How does the brain-skin interaction change as time goes on? What brain-skin magic can be done to help decrease the assault on both the brain and the skin?
As noted in an article by Chen and Lyga, “Skin is the primary sensing organ for external stressors, including heat, cold, pain, and mechanical tension. Three classes of receptors (thermoreceptors for heat and cold, nociceptor for pain and mechanoreceptors for mechanical changes) are responsible for transmitting the outside signals to the spinal cord, and then to the brain. The cutaneous sensory fibers also convey changes in temperature, pH, and inflammatory mediators to the central nervous system (CNS). The nerve terminals are often associated with receptors indicating close interaction. The brain responds to these signals, which in turn influence the stress responses in the skin.”
Perhaps the most vital component a person has for surviving the often harsh conditions and avoiding the friability of aging is their body’s immune system. Aside from simply thinking of being necessary to clear antigens from the body, the immune system is equally important in keeping the body’s own physiology in check by monitoring for reactions that may go awry and unchecked, leading to malignancies, or helping the body rebuild and reshape itself in the face of any stress (2). Decreased ability to cope with stressors would support the notion that aging, which by definition eventually brings about the onset of becoming “elderly,” and is marked by an increase in disease states and inability to withstand stresses that would be expected to be handled by the immune system, is itself a disease state (3). That lack of strength in the face of physiologic adversity implies that this disease state is brought about by an ever-decreasing efficiency of the human immune system and a decrease in the robust interaction between the brain and the skin.
In their conclusion, Chen and Lyga write, “In recent years, emerging research has demonstrated that skin is not only a target of psychological stress signaling modulation, it also actively participates in the stress response by a local HPA axis, peripheral nerve endings, and local skin cells including keratinocytes, mast cells, and immune cells. There are also feedback mechanisms and crosstalk between the brain and the skin, and pro-inflammatory cytokines and neurogenic inflammatory pathways play huge roles in mediating such responses.” The authors focus on major pathways and effector cells and how they negatively affect skin functions and diseases and how chronic stress can have a detrimental effect on skin aging.
We live in a time with a “silver tsunami” of aging; an unprecedented number of older population due to increased life expectancy and survival. Investigating the concept of how and when we age, immunity, and dermatological manifestations in our elderly is a complex and challenging task.
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