Lifeboat Foundation

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In this episode, Peter and Elon hop on X Spaces to discuss Data-driven optimism, solving grand challenges, uplifting humanity, Digital Super Intelligence, Longevity, Education, and Abundance in 2024.

Elon Musk is a businessman, founder, investor, and CEO. He co-founded PayPal, Neuralink and OpenAI; founded SpaceX, and is the CEO of Tesla and the Chairman of X.

Continue reading “Elon Musk Discusses Abundance, AGI, and Media in 2024 with Peter Diamandis” »

During our lives, normal exposures cause DNA damage to build up. Eventually, this causes cancer and age-related diseases. Studying DNA-repairing animals could help treat these issues.

Several techniques currently are used to determine the pace of aging in animals and, to a lesser degree, in humans. However, the techniques used in humans lack accuracy, don’t assess aging in specific organs, are not widely available, and are expensive.

A multi-institutional research team measured the levels of nearly 5,000 human proteins in 5,676 people of all ages who were followed for as long as 15 years in five prospective longitudinal cohorts. Each measured protein was associated with specific organs, based on previous studies: adipose tissue, artery, brain, heart, immune tissue, intestine, kidney, liver, lung, muscle, or pancreas. Combinations of proteins indicated the pace of aging in each organ. Accelerated aging of one organ was found in nearly 20% of people, and accelerated aging of multiple organs was noted in ≈2%. Accelerated aging in a specific organ correlated with risk for developing disease in that organ. For example, people with accelerated heart aging (vs. those without it) had 250% higher risk for developing heart failure, and people with accelerated brain and vascular aging had nearly 60% higher risk for developing Alzheimer disease.

Various tools — from sequencing a person’s genome to measuring gene expression (e.g., the “methylome”) — are becoming available to predict a person’s risk for developing particular diseases. Will these predictions lead to interventions that lower risk? The jury is still out on that question.

😀 They say we could even regenerate human limbs this way aswell as repair human blood vessels.

Cell tubes, made entirely from a patient’s own cells, are just as elastic as blood vessels but much stronger. Skin cells cultured into lumps are skewered on needles on a base, similar to a Kenzan, a tool used in Japanese flower arrangements, and formed into a tube. The technique, called the Kenzan Method, was made possible by a 3D bioprinter. A clinical trial is underway in Japan to transplant these tubes into humans in place of blood vessels. Studies are being done to apply them to nerves and organs.

Taking out the trash: Autophagy genes help extrude protein aggregates from neurons in the nematode C elegans.

In a recent study published in Molecular Psychiatry, researchers explored the effects of a small humanin-like peptide 2 (SHLP2) variant on mitochondrial function.

Mitochondria are implicated in Parkinson’s disease (PD) pathogenesis. Mitochondrial-derived peptides (MDPs) are microproteins encoded from small open reading frames (sORFs) in the mitochondrial DNA (mtDNA). SHLP2 is an MDP with an essential role in multiple cellular processes, and it improves mitochondrial metabolism by increasing biogenesis and respiration and reducing oxidation.

Recent studies link mitochondrial single nucleotide polymorphisms (mtSNPs) within coding regions of MDPs to age-related deficits. For instance, m.2706 A G, an mtSNP in humanin, predicts reduced circulating levels of humanin and worse cognitive decline. Moreover, another mtSNP, m.2158 T C, is associated with reduced PD risk, albeit the underlying mechanisms are unknown.

Despite the excitement, caution remains paramount.

Just as healthy organs are vital to our well-being, healthy organelles are vital to the proper functioning of the cell. These subcellular structures carry out specific jobs within the cell; for example, mitochondria power the cell, and lysosomes keep the cell tidy.

Although damage to these two organelles has been linked to aging, cellular senescence, and many diseases, the regulation and maintenance of these organelles have remained poorly understood. Now, researchers at Osaka University have identified a protein, HKDC1, that plays a key role in maintaining these two organelles, thereby acting to prevent cellular aging.

There was evidence that a protein called TFEB is involved in maintaining the function of both organelles, but no targets of this protein were known. By comparing all the genes of the cell that are active under particular conditions and by using a method called chromatin immunoprecipitation, which can identify the DNA targets of proteins, the team was the first to show that the gene encoding HKDC1 is a direct target of TFEB, and that HKDC1 becomes upregulated under conditions of mitochondrial or lysosomal stress.