Lifeboat Foundation

Our bone marrow—the fatty, jelly-like substance inside our bones—is an unseen powerhouse quietly producing 500 billion new blood cells every day. That process is driven by hematopoietic stem cells that generate all of the various types of blood cells in our bodies and regenerating themselves to keep the entire assembly line of blood production operating smoothly.

As with any complex system, hematopoietic stem cells lose functionality as they age—and, in the process, contribute to the risk of serious diseases, including blood cancers. We know that the risk of developing aging-associated diseases is different among different individuals. Surprisingly, however, little is known about whether hematopoietic stem cells age differently between individuals.

“If you take a room full of 50-year-olds, some will be completely gray-haired, others will be salt-and-pepper, and a few will not have any gray hairs at all,” said Jennifer Trowbridge, Dattels Family Endowed Chair and professor at the Jackson Laboratory. “Logically, you’d expect to see the same kind of variation in the function of hematopoietic stem cells—but until now, nobody has studied that directly.”

Researchers from the University of Queensland have found that high-intensity interval training significantly enhances brain function in older adults, with cognitive improvements lasting up to five years. This study, led by Emeritus Professor Perry Bartlett and Dr. Daniel Blackmore, confirms that such exercise can not only improve but sustain cognition in aging populations, potentially reducing the risks and costs associated with dementia.

Researchers from the University of Queensland have conducted a longitudinal study demonstrating that high-intensity interval exercise can enhance brain function in older adults for up to five years. Led by Emeritus Professor Perry Bartlett and Dr. Daniel Blackmore of UQ’s Queensland Brain Institute, the study involved participants engaging in physical exercise and undergoing brain scans.

Continue reading “New Study Reveals Exercise Brain Boost Can Last for Years” »

New findings from the University Hospital Bonn (UKB), in collaboration with the University of Bonn, have revealed that specific early alterations in patients with age-related macular degeneration (AMD) can result in noticeable local vision loss. This breakthrough could enhance the treatment and monitoring of this eye condition in elderly patients, which typically progresses to central blindness, and facilitate the testing of new treatments.

AMD mainly affects elderly people. If left untreated, the disease leads to a progressive loss of central vision, which significantly impairs everyday activities such as reading or driving. Researchers around the world are intensively searching for ways to improve the early detection and treatment of this disease before major losses occur.

A research team from the UKB Eye Clinic, in cooperation with the University of Bonn and in close collaboration with basic and clinical scientists, has specifically examined patients with early forms of AMD. The researchers focused on the so-called iRORA lesions, which are very early anatomical signs of retinal damage.

Yes, we wish it were quicker too.

In this short video Dr. David Sinclair discusses the progress made with the new glaucoma treatment and upcoming human trials. Also, the timeline for potential availability of the treatment and reverse aging molecules which his company Metrobiotech is working on.

Continue reading “NEW Glaucoma Treatment & REVERSE Aging Molecules Jul 2024 Update | Dr David Sinclair” »

By analyzing co-evolution of mitochondrial and nuclear genomes across insect species, the authors uncover the evolutionary covariation of a group of non-mitochondrially targeted nuclear genes with mitochondrial genes, including the uncharacterized gene CG11837, which regulates insect lifespan.

University of Queensland researchers have unlocked crucial molecular secrets of ageing in cells, potentially paving the way to improve quality of life as people age.

The study decoded the process by which genes regulate how people mature as they grow and age, and was led by Dr Christian Nefzger from UQ’s Institute for Molecular Bioscience with key contributions from Dr Ralph Patrick and Dr Marina Naval-Sanchez.

Dr Nefzger said that until now the process of how genes change activity from birth to adulthood and into old age was largely unknown.

Helping to defend those tissues are innate lymphoid cells, or ILCs, which when faced with a threat, stimulate proteins called cytokines that further activate the immune system and control the intestinal microbiome.

These cells naturally diminish with aging or can be depleted by certain medical conditions.

ILCs are made inside bone marrow and circulate in the blood. But how are they activated to mobilize and travel to their target sites to replenish the depleted pool of tissue ILCs?

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Increased frailty, higher incidence of diseases, and death. As the population grows older, there is a need to reveal mechanisms associated with aging that could spearhead treatments to postpone the onset of age-associated decline, extend both healthspan and lifespan. One possibility is targeting the sirtuin SIRT1, the founding member of the sirtuin family, a highly conserved family of histone deacetylases that have been linked to metabolism, stress response, protein synthesis, genomic instability, neurodegeneration, DNA damage repair, and inflammation. Importantly, sirtuins have also been implicated to promote health and lifespan extension, while their dysregulation has been linked to cancer, neurological processes, and heart disorders. SIRT1 is one of seven members of sirtuin family; each requiring nicotinamide adenine dinucleotide (NAD⁺) as co-substrate for their catalytic activity. Overexpression of yeast, worm, fly, and mice SIRT1 homologs extend lifespan in each animal, respectively. Moreover, lifespan extension due to calorie restriction are associated with increased sirtuin activity. These findings led to the search for a calorie restriction mimetic, which revealed the compound resveratrol; (3, 5, 4′-trihydroxy-trans-stilbene) belonging to the stilbenoids group of polyphenols. Following this finding, resveratrol and other sirtuin-activating compounds have been extensively studied for their ability to affect health and lifespan in a variety of species, including humans via clinical studies.

Aging is associated with a progressive metabolic, physiological decline and can be genetically and environmentally modified (Helfand and Rogina, 2000). The search for the molecular basis of aging led to the identification of several pathways associated with longevity including insulin/IGF-1, target of rapamycin (TOR) and the Sirtuins (Kenyon, 2010; Chen et al., 2022). The sirtuins are a family of nicotinamide adenine dinucleotide (NAD⁺)-dependent histone deacetylases (Haigis and Sinclair, 2010; Hall et al., 2013; Bonkowski and Sinclair, 2016; Dai et al., 2018; Singh et al., 2018). Sirtuins are also categorized as deacetylases because they catalyze the post-translational modification of signaling molecules including decrotonylation, ADP-ribosylation, diacylation, desuccinylation, demalonylation, depropynylation, delipoamidation, and deglutarylation, and other long-chain fatty acid deacylations (Feldman, Baeza, and Denu, 2013; Choudhary et al., 2014; Fiorentino et al., 2022).

In mammals, there are seven members (SIRT1-SIRT7) including SIRT1, SIRT6 and SIRT7, which are localized to the nucleus, and SIRT3, SIRT4, and SIRT5 localized to the mitochondria, SIRT2 localized to the cytosol, and SIRT1 also localized to cytosol in some cell types (Bonkowski and Sinclair, 2016). As histone deacetylases, sirtuins function by removing acetyl groups from the target proteins resulting in either inhibition or activation. SIRT1, SIRT6 and SIRT7 have many functions including: regulators of transcription, control of cellular metabolism, DNA repair, cell survival, tissue regeneration, inflammation, circadian rhythms and neuronal signaling (Haigis and Sinclair, 2010). SIRT3-5 are important for switching to mitochondrial oxidative metabolism during CR and modulate stress tolerance (Verdin et al., 2010).