(NewsNation) — Researchers at the University of Rochester transferred a longevity gene from naked mole rats to mice, calling it a “groundbreaking endeavor.”

According to the University of Rochester, naked mole rats have long captured the attention of scientists for their lengthy lifespans and resistance to age-related diseases.

The Conboys’ statement on plasma dilution is important:

The pair are quick to add that this isn’t going to have a Benjamin Button effect, and the research “wasn’t geared to make old people young” – even if this idea is being bio-hacked around the world. “It was clear that there were improvements after a couple of procedures,” says Irina. “[But] it’s not really healthy or rejuvenating to drain somebody of 70% of their blood and replace it with something.” She warns people to wait until more research is done.

Still, they believe that in the next five years we will see huge advancements in prolonging life treatments – including taking a pill instead of getting blood, and a “fountain of middle age”. “People will be able to have this high quality, productive life where they are healthy for many more decades,”

A fascinating and often terrifying new podcast delves into the lengths ‘longevity superstars’ will go to make 90 the new 50, from swapping blood with the young to designing the first ‘post-humans’

Although the German scientist Hanns Kaiser published a number of articles in the 1970s relating inflammation to diseases in the elderly (Kaiser, 1971), the last 20 years have seen a burst in the study of the aging immune system, inflammation and the associated diseases. One of the most iconic studies in aging and immunity was the OCTO and NONA longitudinal study of healthy 80–90 year old people that took place in Jonkoping Sweden in the 1990s (Wikby AJ and Ferguson, 2003). These studies were unique for several reasons. First, they were longitudinal studies of elderly individuals. Second, the 80-and 90-year-olds were very healthy. As people age, they naturally acquire more disease and it becomes increasingly difficult to distinguish the effects of disease vs. aging on the immune parameters being measured. To overcome these confounders, the OCTO and NONA immune longitudinal study was a community population-based study that continually and carefully evaluated individual health parameters. Study participants had normal cognition, were not on drugs that would influence their immune responses, and were non-institutionalized (Wikby AJ and Ferguson, 2003). Several important findings resulted from these studies; 1) the establishment of an Immune Risk Profile (IRP) based on altered CD4/CD8 T cell ratios (decreasing CD4⁺ T cell numbers and often increasing CD8⁺ T cell numbers) (Wikby et al., 1998) and 2) germane to this review, the discovery of a link between elevated plasma IL-6 levels, mortality and IRP in the very old (Wikby et al., 2006).

An optimal immune response requires the appropriate interaction between the innate and the adaptive arms of the immune system as well as a proper balance of activation and regulation. After decades of life, the aging immune system is continuously exposed to immune stressors and inflammatory assaults that lead to immune senescence (Salama et al., 2014; Aiello et al., 2019; Di Micco et al., 2021). In this review, we will discuss inflammaging in the elderly, specifically concentrating on IL-6 and IL-1β in the context of T lymphocytes, and how inflammation is related to mortality and morbidities, specifically cardiovascular disease and cancer. Although a number of studies suggests that the anti-inflammatory cytokine TGF-β is elevated in the elderly, heightened inflammation persists. Thus, the regulation of the immune response and the ability to return the immune system to homeostasis is also important. Therefore, we will discuss cellular alterations in aging, concentrating on senescent T cells and CD4⁺ CD25 ⁺ FOXP3+ regulatory T cells (T_regs) in aging.

Inflammaging is a phenomenon of inflammatory pathogenesis characterized by chronic low-grade inflammation, and is a significant risk factor for morbidity and mortality in elderly people. Claudio Franceschi first coined the term “inflammaging” in the manuscript “Inflamm-aging.

Telomerase helps maintain telomere length in our cells, influences how our bodies age, and why we develop diseases like cancer. If cells had enough telomerase, telomeres might not shorten at all. But in most somatic cells, it’s present in very low amounts — only enough to slow the telomere shortening down.

This is part of a short series of videos where we explore telomeres, telomere length and telomerase, as well as the impacts they have on our health.

Chapters:
00:00 What is telomerase?
00:25 What happens when telomeres are too short?
00:38 How does telomerase work?
01:23 How does telomerase affect cancer risk and aging?

Watch the next video explaining Telomere Biology Disorders: https://youtu.be/sVTd0ZkTH3k.

Missed the previous video on the end replication problem, and how telomere shortening affects aging? https://youtu.be/pluI6SOd-_I

RepeatDx is a leading clinical laboratory for telomere length testing. You can find out more on our website: https://repeatdx.com/