People are living longer lives than ever before because of public health policies and modern medicine. According to predictions, the population over the age of 65 will more than quadruple by 2050. Longer life implies that a growing portion of the population will face the tell-tale signs of aging, such as weakened muscles, deteriorating memory, and slowed metabolism.
A molecule called urolithin-A has piqued the curiosity of a lot of researchers as one of the various strategies to address individual aging. Scientists at the life science business Amazentis and the Swiss Federal Institute of Technology in Lausanne have been researching the molecule for more than a decade, and Amazentis currently manufactures a supplement containing it. Urolithin A is created spontaneously by gut microorganisms in certain people when they metabolize a precursor molecule present in pomegranates, berries, and walnuts, and has been linked to mitochondrial health.
In a 2016 study published in Nature Medicine, these researchers discovered that urolithin A greatly enhanced worm longevity while improving muscular strength and endurance in mice. They have spent the last five years researching the compound’s potential advantages for people, emphasizing mitochondrial and muscle health. They published phase I clinical trial data in Nature Metabolism in 2019 that urolithin A is safe for human intake. They recently conducted a study to investigate the relationship between mitochondrial health and muscular strength.
Biologists quickly discovered novel linkages between mitochondria and aging, connections that drew on mitochondria’s peculiar origins. Some 1.4 billion years ago, somewhere in Earth’s primeval waters, a eukaryotic cell absorbed an oxygen-respiring bacteria, which evolved into mitochondria over generations. Despite being completely integrated cellular organelles, mitochondria never lost their original genome, which is now known as mitochondrial DNA (mtDNA). Today, mtDNA generates 13 essential mitochondrial proteins.
As mitochondria age, their structure changes, and they become less active. They eventually fail and release mtDNA. Researchers believe that because mitochondria originated as a foreign entity, the released mtDNA causes an immunological response. Several studies show that this causes chronic inflammation in aging organisms, a condition known as ‘inflammaging,’ which can contribute to age-related disorders.
mtDNA changes with aging as well. The mitochondrial genome acquires mutations and deletions quicker than the genes in the cell’s nucleus as a person ages. These mutations have been associated with aging signs. For example, mice with a faulty DNA-replication enzyme called mtDNA polymerase have more mutations in their mitochondria DNA (mtDNA) than the ordinary mouse. They also have gray fur, osteoporosis, and die young.
However, such relationships may correlate with rather than cause aging, according to Toren Finkel, director of the Aging Institute at the University of Pittsburgh Medical Center. “Mitochondrial dysfunction is most likely caused by various abnormalities in the mitochondria, not necessarily by its DNA.”
