Lifeboat Foundation

With billions of dollars flooding into longevity, what role will epigenetic clocks play in measuring and intervening in aging?

When Horvath first described epigenetic clocks, scientists began to speculate that altering them could reverse aging. After all, if certain patterns of DNA methylation at certain sites in cells in certain tissues of your body are hallmarks of aging, could shifting them somehow reverse aging?

Looking at DNA in a tissue sample is now all you need to accurately work out the age of almost any mammal, and this reveals something fundamental about ageing.

The biotech platform that is leveraging one of the cornerstones of evolution – mitochondria.

Mitochondria play a crucial role in the aging process, activating factors and metabolic pathways involved in longevity. Their dysfunction impacts on both lifespan and healthspan, and whilst they have been identified as disease targets for some time, mitochondria have proven difficult to treat.

Continue reading “Unlocking the power of cell-derived medicines with Dr Alex Schueller, Cellvie’s CEO” »

With the aid of physics and a minuscule magnet, researchers have discovered a new structure of telomeric DNA. Telomeres are sometimes seen as the key to living longer. They protect genes from damage but get a bit shorter each time a cell divides. If they become too short, the cell dies. The new discovery will help us understand aging and disease.

Physics is not the first scientific discipline that springs to mind at the mention of DNA. But John van Noort from the Leiden Institute of Physics (LION) is one of the scientists who found the new DNA structure. A biophysicist, he uses methods from physics for biological experiments. This also caught the attention of biologists from Nanyan Technological University in Singapore. They asked him to help study the DNA structure of telomeres. They have published the results in Nature.

Biotech start-up Pretzel Therapeutics launched Monday with $72.5 million in Series A financing to develop novel, mitochondria-based therapies for rare genetic disorders and diseases of aging.

Pretzel plans to target mitochondrial diseases, a highly heterogenous group of conditions caused by DNA mutations in the mitochondria or the nucleus. These disorders are very rare, afflicting around one in 5,000 people.

Pretzel CEO Jay Parrish told BioSpace the funding “should enable us to get close to the clinic if not into the clinic with one or more programs.”

Hugo Cox.

At the end of a winding dirt track off Bear Creek Road, a few miles from Los Gatos in California’s Santa Cruz mountains is the home of Aubrey de Grey, the 53-year-old English research scientist from whom the claim originates. It looks exactly like the place you would expect a mad professor to live.

Summary: Determining the structure of vitronectin, a protein implicated in age-related macular degeneration and some neurodegenerative disorders, and using pressure to alter the protein shape may help in the development of new treatments for AMD.

Source: Sanford Burnham Prebys.

Research led by Sanford Burnham Prebys professor Francesca Marassi, Ph.D., is helping to reveal the molecular secrets of macular degeneration, which causes almost 90% of all age-related vision loss.

Japan is investing a lot into Longevity Research in hopes of keeping us young forever. And recently, they managed to bring about a new kind of vaccine which…

Senescent macrophages are in fact also found to express senescence-related markers p16(Ink4a) and β-galactosidase (β-gal), and promote inflammation in diseased tissues [25, 26]. Our previous work has indicated increased cellular senescence in dystrophic muscles of mdx/utr(−/−) mice [3], however, whether or not macrophages in particular develop cellular senescence and promote senescence associated phenotypes was still unknown. To this end, here we further examined mdx/utr(−/−) mice and solved these puzzles.

Immune cells in the skeletal muscle are activated during muscle injury and promote the process of muscle regeneration by coordinating with muscle stem cells. However, studies with severely diseased muscles further demonstrate that immune cells can become dominantly activated and is inductive of increased fatty infiltration and fibrosis formation, while at the same time potently repress the proliferation and function of muscle stem cells [27]. Our current results in severely dystrophic muscle reveal a similar situation of interaction between macrophages and MPCs, showing that the function of MPCs is repressed by the senescent macrophages. As senescent cells accumulate in the aged or diseased tissues, it can exert profound effects on the growth and function of normal cells by releasing SASPs [9, 10].