Even though medical care has advanced significantly in recent decades, and the average human lifespan enjoyed a steady rise for a very long time, it seems we are starting to reach the limits of human longevity; around one in 6,000 people lives for more than 100 years, but only around one in every 7 million people lives to be a supercentenarian–over 110 years old; and almost no one has lived for more than 120 years. But we might gain new insights into extending the health of older people by studying supercentenarians. Two new studies have revealed more about the genetics of long-lived people, and one could help individuals who suffer from a disorder that causes children to age rapidly.
One study that was published in Cell Reports Medicine analyzed health data, including the metabolomics, proteomics, and genomics of one supercentenarian: a woman named Maria Branyas, who lived for more than 117 years. The researchers determined that this individual had some of the unmistakable hallmarks of aging, such as short telomeres and increases in inflammation.
But she also carried features that indicated some aspects of her health were being protected; there were genetics signs of improved neurological and cardiological health, a microbiome that carried high levels of a beneficial microbe known as bifidobacteria, and epigenetic characteristics that would be seen in a person of much younger age.
She also maintained a strong social support network, a good diet, and healthy habits, the researchers noted, though there is not enough data to link specific behaviors to longevity.
In another study published in Signal Transduction and Targeted Therapy, scientists found a genetic variant in long-lived people that can lower the levels of damage or fibrosis in heart tissue, which could benefit people who have progeria. Progeria is a disease in which people age too quickly at a young age.
The variant was found in a gene called BPI fold containing family B, member 4 (BPIFB4). Previous work has indicated that this genetic variant can delay and even reverse aging in animal models of cardiovascular disease. Now, the researchers have shown that this variant can exert a protective effect, halting fibrosis and promoting cell survival in an animal model of progeria.
"This is the first study to indicate that a longevity-associated gene can counteract the cardiovascular damage caused by progeria. The results pave the way for new treatment strategies for this rare disease, which urgently requires innovative cardiovascular drugs capable of improving both long-term survival and patient quality of life. Looking ahead, the administration of the LAV-BPIFB4 gene through gene therapy could be replaced and/or complemented by new protein- or RNA-based delivery methods,” said co-corresponding study author Professor Annibale Puca, a Research Group Leader at IRCCS MultiMedica and Dean of the Faculty of Medicine at the University of Salerno.
"We are currently conducting numerous studies to investigate the potential of LAV-BPIFB4 in counteracting the deterioration of the cardiovascular and immune systems in various pathological conditions, with the goal of translating these experimental findings into a new biologic drug."
Sources: Cell Reports Medicine, Signal Transduction and Targeted Therapy