What is Biological Aging?
What is aging? We used to think of our chronological age as the number of times the Earth circled the sun, but today we may think about the accumulation of cell and tissue damage (biological age). It’s an exciting time in aging science as we rapidly find how and why we age, as well as promising anti-aging therapies. We are beginning to notice that biological aging is a key to understanding the aging process and may lead to significant aging-related discoveries.
- Chromosome Instability. Researchers believe that DNA damage causes chromosomal instability, compromising the quality of the cells’ molecular machinery (proteins) that the DNA codes for. The accumulation of DNA mutations, or “mutational load,” adds significantly to chromosomal instability. The notion is that random, harmful DNA mutations accumulate over time, resulting in “mutational load.” However, DNA mutations seem to correspond with aging in tissues like skeletal muscle.
- Telomerase Shortening. Chromosome termination length is another hot issue in aging research. Telomeres are chromosomal ends that appear to disintegrate with age. The enzymes that help them mend (telomerase) can’t keep up with their fraying and deterioration as they age. So researchers looked at chromosomal end health to quantify biological age, but how telomere length impacts aging is yet unknown.
- Senescent Cells. When cells become senescent, that means they’ve reached an age-related, non-proliferating state. Researchers are still striving to understand senescence. Interestingly, telomere shortening appears to be associated with senescence. Overall, measuring senescent cell growth and burden may help measure biological aging. That this approach of measuring biological aging may soon enter clinical research and medical practice is encouraging. Yang et al. report in March 2021 that increasing intracellular NAD+ levels with its precusor delays aging.
- Mitochondrial Health. The mitochondria, the cell’s powerhouse, may also be used to monitor biological aging. Mitochondria are found in every cell in the body. Microsomes lose their capacity to create energy as we age, causing weariness and metabolic problems. Precursors of NAD+ such as nicotinamide mononucleotide (NMN) have been shown to improve mitochondrial activity.
- Vascular Health. Vascular health can act as a biological signal (biomarker) that predicts mortality.
These biomarkers of blood vessel health include blood pressure, altered blood flow, stiffness, plaque, and calcium buildup (calcification). Other aging markers of blood vessels include DNA mutations, interleukin (inflammatory) markers, and protein-based markers of blood vessel failure. We may be able to avoid age-related disorders and maximize solid health-related decisions in the future by looking at these blood vessel indicators in younger adults.
- Epigenetics. Epigenetics is a very wide term that refers to any alterations to the genome that are functionally significant but do not affect the nucleotide sequence. They are tiny chemical changes to DNA and histone that affect their activity and make them recognizable by other protein factors. DNA methylation, histone methylation, and histone acetylation are the most well-known epigenetic markers. Throughout life, all cells and tissues undergo a range of epigenetic changes. Unlike DNA mutations, epigenetic changes are reversible, allowing for the development of innovative anti-aging therapies. Replenishing NAD+ through NAD+ precursors may help increase Sirtuins activity and rejuvenate the epigenome.
- Altered Intercellular Communication. Humans are multicellular (an organism that consists of more than one cell). Endocrine, neuroendocrine, and neurological signals are all received, analyzed, and sent by our cells. Basic cellular property that aids in tissue homeostasis and many other physiological functions. Intercellular communication, like many other important functions, ages. Neurohormonal signaling is one of them that means neuroendocrine cells produce and release neurohormones into the circulation. Thus, neurohormones regulate neuronal metabolism. Aging disrupts adrenaline, insulin-IGF1, and renin-angiotensin signaling which degrade NAD+ and thus, NAD+ levels are reduced. Kang et al. studied the effects of the precursor of NAD+ on inflammation and oxidative stress in macrophages in April 2021. They discovered that the inflammatory gene expression in macrophages as well as the buildup of cellular reactive oxidative species are reduced.
Measuring biological age can help us predict age-related diseases as well as study how people age and what factors contribute to it. New molecules like NMN and other popular NAD+ precursors can help us slow down the aging process and maintain our health.