Researchers are trying to figure out how to manipulate the aging process in hopes to delay age related disease such as Alzheimer’s, osteoporosis, heart disease, diabetes, and cancer. Potential treatments for aging could unlock cures to a variety of illnesses, even possibly in one fell swoop.
Aging is the underlying shared factor of many common causes of death, new insight into the aging process could act as a skeleton key of sorts providing sure for many of these conditions. Being immortal is not the goal says Felipe Sierra of the NIH, rather to improve the health of the elderly of which living healthier for longer is a fortunate side effect.
This is most welcome to those in the anti-aging industry as they have never really said that anti-aging has any scientific value, to some this is a game changer and this is the equivalent of admitting that anti-aging research is the ultimate road to success in age and related disease.
Aging research has gained momentum, of all the anti-aging drugs being investigated 2 potentials are most interesting to Sierra: 1) Rapamycin that blocks pathways within the body related to metabolism, immune function, and energy; and 2) Senolytics which can kill senescent cell types within the body that cause inflammation and damage.
Sierra explains by understanding aging manipulations can be made, wherein we don’t just delay one disease of aging rather we dealy them all, it’s a better solution; all roads lead to TOR. TOR is a popular pathway in regards to anti-aging as well as senolytics. Studies on humans and animals restricting caloric intake has been shown to help protect against cancer, CVD, diabetes, and potentially extend lifespans. Rapamycin may produce similar outcomes by targeting the TOR signalling pathway that is linked to cell growth and aging.
According to Manuel Serrano rapamycin mimics calorie restriction even when consuming the same amounts of food, the biochemical machinery of cells think there are no nutrients which is beneficial. Originally used as an immuno-suppressive drug for organ transplant patients, rapamycin was found to be able to block the TOR pathway.
Making reference to a Novartis study Sierra said a drug similar to rapamycin acting on TOR pathways in elderly patient’s immune response and risk for infection decreased rate of respiratory tract infections by more than 65% during peak winter cold and flu season; which is significant as it was done in humans and showed these approaches addressing aging are useful against disease of the elderly that are the paradigm they are working with.
The science in the anti-aging field has progressed enough to start translating into humans, increasing data suggests aging is not just due to random wear and tear but also biology related regulated by signalling pathways. Targeting fundamental pathways contributing to aging is a new way to treat aging and age related conditions, such as killing zombie senescent cells that lose many functions with age but don’t die as normal cells would and become damaging leading to inflammation, cancer, and nearby cells to enter the same state.
Dr. James Kirkland of the Mayo clinic explains the immune system eliminates some senescent cells, but with age the ability declines, these zombie cells accumulate in tissue as a result of aging, chronic disease, chemotherapy, and exposure to radiation. Such cells have been associated with osteoporosis and also frailty in the elderly.
Mayo Clinic researchers used computer analysis to identify pathways in the cells that protect against inflammatory toxic secretions. Dasatinib and the flavonoid Quercetin were used in experiments with attempts to eliminate senescent cells, this combination was found to help older mice to live 36% longer. Kirkland said elimination of the zombie cells alleviated radiation induced injury and frailty, and increased cardiac function and blood flow, while improving symptoms of diabetes and osteoporosis. All of which findings Sierra of the NIH said were amazing.
Senolytics are hoped to be brought into clinical trials for the elderly with serious pulmonary fibrosis or other age related dysfunctions to investigate whether they can improve lung and other physical functions, Kirkland adds, as the only side effect is that they may delay wound healing.
Another controversial contending anti-aging treatment would be a modern day version of parabiosis. Sierra says it may seem like is is science fiction but it is an important approach to research if only as proof of principle. Blood from young mice was shown to rejuvenate older mice brains, while blood from older mice inflamed younger mice brains in Wyss-Coray’s research. Other parabiosis research has shown ability to restore function in kidney, liver, heart, bone, skin, and muscles; as well as specific part of blood plasma treating AD which had positive early trials in 2017 which have moved onto phase II trials.
Sierra goes on to say that lifespans are being extended, but there is a rapid increase in the number of diseases and disabilities indicating that there hasn’t been a good job being done to extend healthspans to go along with living longer, making it more expensive to care for aging populations as 80% of older adults have at least 1 chronic disease and 77% have at least 2. According to the National Council on Aging 75% of the money spent in healthcare within the USA is on chronic diseases. The population is aging rapidly, in 2016 there were 49.2 million people aged 65+, by 2035 that number is projected to hit 78 million.
The oncoming silver tsunami will put additional strain on healthcare systems. Targeting aging will allow science to intervene earlier in chains of events leading to many chronic and age related disease such as diabetes, stroke, cancer, and heart disease that cause close to two thirds of all deaths each year.
Aging is now considered to be the biggest risk factor for most chronic diseases, it was not understood that it may be a modifiable risk factor in the past that could be targeted with a drug. If studies continue to be positive it could open a whole new area of medicine, according to Mannick.
