Lifeboat Foundation

Naked mole rats are rodents that are about the size of a mouse with a key difference, aside from having no fur — they’re extremely long-lived — reaching ages of around 40 years old. For comparison, lab mice live an average of about three and a half years. To explain their extensive lifespans, researchers have sought to pinpoint how naked mole rats evade the onset of age-related diseases like cancer. In doing so, they’ve identified a form of gelatinous substance called hyaluronan, which has anti-inflammatory and anticancer properties. Now, the question of whether the benefits of the naked mole rat’s abundant levels of this form of hyaluronan — called high molecular mass hyaluronic acid (HMM-HA) — can be exported to other species has recently drawn attention.

Published in Nature, Gorbunova and colleagues from the University of Rochester show that genetically modifying mice to harbor an enzyme that produces HMM-HA extends their lifespan. The researchers go on to show that increasing HMM-HA reduces the prevalence of cancer. Additionally, the nmrHAS2 gene improves the healthspan of mice by countering physiological dysfunction, as measured with a frailty score. These findings provide the first evidence that genes from long-lived species can be exported to other species, perhaps conferring benefits to humans one day.

In this article, the fourth installment of our five-part series on different pathways of aging, we look at the rejuvenation of cells, tissues, and stem cells, a topic that has been gaining increasing popularity thanks to remarkable advancements in the field of epigenetic reprogramming. Recent research suggests that despite the accumulation of molecular damage over time, cells and tissues can indeed undergo rejuvenation. We’ll be exploring key subjects such as Epigenetic reprogramming, PGC1a and GSK3β, Telomerase (TERT), as well as Apoptosis and senescence. Join us on this enlightening journey as we uncover the groundbreaking discoveries that are shaping the future of aging research.

The idea for reprogramming was simple yet beautiful. Children are born young, even though their parents are old, because they have undergone a process of cellular reprogramming that leads to rejuvenation.

Welcome to another exciting episode of our podcast series, where we dive deep into the world of science and innovation! In today’s episode, we have the privilege of interviewing Prof. Michael Levin, a renowned researcher in the fields of bioelectricity, regenerative biology, and biophysics.

Prof. Levin is the director of the Allen Discovery Center at Tufts University and has been making groundbreaking discoveries that are revolutionizing the field of regenerative medicine. His research focuses on understanding the electrical communication within and between cells, and how this communication can be harnessed for tissue repair and regeneration.

Continue reading “-Electricity of Life💡: Wonders of Bioelectricity and Regenerative Biology Prof Michael Levin” »

AI systems are increasingly being employed to accurately estimate and modify the ages of individuals using image analysis. Building models that are robust to aging variations requires a lot of data and high-quality longitudinal datasets, which are datasets containing images of a large number of individuals collected over several years.

Numerous AI models have been designed to perform such tasks; however, many encounter challenges when effectively manipulating the age attribute while preserving the individual’s facial identity. These systems face the typical challenge of assembling a large set of training data consisting of images that show individual people over many years.

The researchers at NYU Tandon School of Engineering have developed a new artificial intelligence technique to change a person’s apparent age in images while ensuring the preservation of the individual’s unique biometric identity.

That’s why we were struck to see a team of scientists that includes researchers from the name-brand Harvard Medical School and Massachusetts Institute of Technology sounding off about what they say are promising new leads, published this month in the journal Aging.

“We identify six chemical cocktails, which, in less than a week and without compromising cellular identity, restore a youthful genome-wide transcript profile and reverse transcriptomic age,” reads the paper. “Thus, rejuvenation by age reversal can be achieved, not only by genetic, but also chemical means.”

Sounds big, right? The researchers claim they pinpointed six treatments that can reverse aging in cells and turn them into a more “youthful state,” according to a press release from Aging’s publisher, without causing dangerous unregulated cell growth.

Dr. Mark Hyman recommended Costco items including nuts, canned seafood, and fermented goods.

A short report on our satellite meeting at the Longevity Summit 2023.

How does the research conducted by Lige Leng at the Institute of Neuroscience of Xiamen University in China (I link it to you here)? It all starts with the study of the “inflamed brain”: many diseases of old age are associated with low-level chronic inflammation in the brain, organs, joints and circulatory system. A phenomenon sometimes called “inflammaging”.

You know it: over time all of our body’s repair systems deteriorate, our DNA and proteins accumulate damage, metabolism stumbles and cells stop doing their job. That’s life, beauty.

We’re all on our way to the exit, but research on worms, flies, mice and monkeys show that going at this speed isn’t inevitable. Diet and lifestyle changes (and, perhaps, upcoming anti-aging drugs) can curb decay and give us many more years of life, especially healthy life.

Continue reading “Discovered an aging ‘brake pedal’?” »

Several factors contribute to the development of inflamm-aging, including genetic susceptibility, visceral obesity, microbiota and gut permeability, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by mitochondrial dysfunction, immune cells dysregulation, and chronic infection (Ferrucci & Fabbri, 2018). The immune system becomes gradually dysregulated during aging, leading to elevated blood levels of pro-inflammatory mediators, such as TNFα, IL6, and C-reactive protein (Harris et al., 1999 ; Mooradian et al., 1991). Energy homeostasis also becomes dysregulated with aging, which results in the redistribution of subcutaneous fat to visceral regions and contributes to inflammation (Bouchard et al., 1993 ; Chumlea et al., 1989 ; Curtis et al., 2005). Metabolism-induced inflammation, also known as metaflammation, shares similarities with inflamm-aging, including the elevation of certain circulating pro-inflammatory cytokines (Prattichizzo et al., 2018). Therefore, the molecules that play a key role in the regulation of metabolic homeostasis potentially mediate the development of chronic inflammation during aging.

Forkhead box O1 (FOXO1) transcription factor has been indicated to be involved in the regulation of nutrient metabolism and energy homeostasis (Cheng et al., 2009 ; InSug et al., 2015 ; Matsumoto et al., 2007 ; Yang et al., 2019 ; Zhang et al., 2012). Deletion of hepatic Foxo1 improves glucose homeostasis in insulin resistant mice (Dong et al., 2008). FOXO1 inhibition by AS1842856 attenuates hepatic steatosis in diet-induced obesity mice (Ding et al., 2020). In mature macrophages, FOXO1 promotes inflammation through the activation of TLR4-and STAT6-mediated signaling pathways (Fan et al., 2010 ; Lee et al., 2022). In invertebrates, DAF-16, the Foxo homolog gene, mediates the effect of insulin/IGF signaling on lifespan (Ogg et al., 1997). Overexpression of FOXO in Drosophila and C.elegans increases their lifespan (Giannakou et al., 2004 ; Henderson & Johnson, 2001). However, studies in mammalians show that FOXO1 does not have a significant correlation with longevity (Chiba et al., 2009 ; Kleindorp et al., 2011). Considering the role of FOXO1 in regulating glucose metabolism and inflammation, we hypothesize that FOXO1 plays an important role in the regulation of aging-induced inflammation and dysregulation of glucose homeostasis.

Liver is an important metabolic organ that plays a key role in maintaining whole-body nutrient homeostasis by regulating energy metabolism, clearing xenobiotic and endobiotic, and synthesizing necessary molecules (Rui, 2014). As a result, aging-induced changes in liver contribute to systemic susceptibility to aging-related diseases. Different types of liver cells, including hepatocytes, endothelial cells, hepatic stellate cells (HSC), and macrophages, are all affected by the aging process (Hunt et al., 2019). However, most studies on liver aging focused on whole-liver tissue, which is mainly composed of parenchymal cells, hepatocytes. Thus, the effects of aging on liver nonparenchymal cells (NPCs) are less understood. In this study, we used bulk RNA-Seq and single-cell RNA (scRNA)-Seq technologies to analyze aging-induced changes, and the role of FOXO1 in aging-related processes in both whole-liver and individual liver cells, particularly liver macrophages. We found that insulin resistance, liver fat accumulation, liver inflammation, and systemic inflammation were significantly aggravated in old mice. Additionally, aging significantly increased pro-inflammatory response in Kupffer cells (KCs) and induced a functional quiescence in monocyte-derived macrophages (MDMs). FOXO1 activity was significantly enhanced in the livers of old mice and FOXO1 inhibition improved insulin resistance, hepatic steatosis, and inflammation in old mice. Furthermore, we found that FOXO1 inhibition attenuated aging-induced pro-inflammation in KCs and had a limited effect on aging-induced functional quiescence in MDMs. Taken together, this study indicates that FOXO1 plays an important role in the liver aging processes and suggests that FOXO1 is a potential therapeutic target for the treatment of aging-induced chronic diseases.