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The risk of morbidity and mortality increases exponentially with age. Chronic inflammation, accumulation of DNA damage, dysfunctional mitochondria, and increased senescent cell load are factors contributing to this. Mechanistic investigations have revealed specific pathways and processes which, proposedly, cause age-related phenotypes such as frailty, reduced physical resilience, and multi-morbidity. Among promising treatments alleviating the consequences of aging are caloric restriction and pharmacologically targeting longevity pathways such as the mechanistic target of rapamycin (mTOR), sirtuins, and anti-apoptotic pathways in senescent cells. Regulation of these pathways and processes has revealed significant health-and lifespan extending results in animal models. Nevertheless, it remains unclear if similar results translate to humans. A requirement of translation are the development of age-and morbidity associated biomarkers as longitudinal trials are difficult and not feasible, practical, nor ethical when human life span is the endpoint. Current biomarkers and the results of anti-aging intervention studies in humans will be covered within this paper. The future of clinical trials targeting aging may be phase 2 and 3 studies with larger populations if safety and tolerability of investigated medication continues not to be a hurdle for further investigations.

As age increases, so does the susceptibility to a series of chronic diseases which ultimately result in fatal endings. This is such a basic part of life that we rarely consider if there is anything we can do to postpone it. So far, the principal of “one-disease-one-treatment” has brought medical sciences far but this line of thought may soon be outdated when it comes to aging related conditions. It is like fighting a many-headed monster: If one condition is treated successfully, another emerges shortly after. This point is illustrated as eradicating the two leading causes of death (cancer and cardiovascular disease) extends mean life span by 3.3 and 4 years, respectively (Arias et al., 2013). Interestingly, the gain of treating multiple diseases combined exceeds the sum of these numbers.

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Levine’s Biological age calculator is embedded as an Excel file in this link from my website:
https://michaellustgarten.com/2019/09/09/quantifying-biological-age/

NOTE FROM TED: Research around aging discussed in this talk remains an ongoing field of study. Please do not look to this talk for health advice. TEDx events are independently organized by volunteers. The guidelines we give TEDx organizers are described in more detail here: http://storage.ted.com/tedx/manuals/tedx_content_guidelines.pdf.

Have you ever wondered how long you will live? And if so, how could you change that number to live drastically longer? The science might be in your favor: follow David Sinclair, Australian biologist and professor of genetics at Harvard University, as he shares his research on slowing and reversing the process of aging in mice, and how the same technology may someday be transferable to humans. David Sinclair, Australian biologist and professor of genetics at Harvard Universityhis insightful research into the science of age reversal and anti-aging medicine.

Continue reading “Is Aging Reversible? A Scientific Look with David Sinclair | David Sinclair | TEDxBoston” »

Scientists have managed to safely reverse the signs of aging in mice by genetically reprogramming some of their cells.

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Scientists said this full picture of the genome will give humanity a greater understanding of our evolution and biology while also opening the door to medical discoveries in areas like aging, neurodegenerative conditions, cancer and heart disease.

“We’re just broadening our opportunities to understand human disease,” said Karen Miga, an author of one of the six studies published Thursday.

The research caps off decades of work. The first draft of the human genome was announced in a White House ceremony in 2000 by leaders of two competing entities: an international publicly funded project led by an agency of the U.S. National Institutes of Health and a private company, Maryland-based Celera Genomics.

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Identifying dual-purpose therapeutic targets implicated in aging and disease will extend healthspan and delay age-related health issues.

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A substantial percentage of the human clinical trials, including those evaluating investigational anti-aging drugs, fail in Phase II, a phase where the efficacy of the drug is tested. This poor success is in part due to inadequate target choice and the inability to identify a group of patients who will most likely respond to specific agents. This challenge is further complicated by the differences in the biological age of the patients, as the importance of therapeutic targets varies between the age groups. Unfortunately, most targets are discovered without considering patients’ age and being tested in a relatively younger population (average age in phase I is 24). Hence, identifying potential targets that are implicated in multiple age-associated diseases, and also play a role in the basic biology of aging, may have substantial benefits.

Identifying dual-purpose targets that are implicated in aging and disease at the same time will extend healthspan and delay age-related health issues – even if the target is not the most important in a specific patient, the drug would still benefit that patient.

Continue reading “Insilico identifies therapeutic targets implicated in aging using AI and hallmarks of aging framework” »