Lifeboat Foundation

The field of epigenetics sits precariously on the precipice of the classic nature versus nurture debate. Instead of a simple environment versus genetics dichotomy, epigenetic examines how specific genes are either switched on or off through external forces encountered in a person’s lifetime. Striking new research from scientists at the University of British Columbia and Harvard University is suggesting that adults who were victims of abuse as children may carry an imprint of that trauma in regions of their DNA.

Today, we would like to share with you a talk by Dr. Michael West from AgeX Therapeutics, a company developing therapies to combat age-related diseases by encouraging the body to regenerate cells and tissues.

On July 12th, we hosted our first conference, Ending Age-Related Diseases: Investment Prospects & Advances in Research, at the Frederick P. Rose Auditorium, which is part of the Cooper Union campus in New York City. The packed event saw a range of people from research, investment, and the wider community coming together for a day of science and biotech business presentations and panels.

Continue reading “The Reversibility of Human Aging” »

To rapidly detect the presence of E. coli in drinking water, Cornell University food scientists now can employ a bacteriophage — a genetically engineered virus — in a test used in hard-to-reach areas around the world.

Be gone flat earthism.

The nature-versus-nurture argument of intelligence just got a lot more complicated with the discovery that the environment can modify the expression of a key gene in the brain, affecting intelligence far more than we previously thought.

Such a finding may not come as a surprise if you remember that numerous genes influence our IQ and stressful experiences can lock and unlock genes in our brains. Yet having hard evidence of the link will no doubt stir debate on just what it means to be “smart”.

Continue reading “Your Environment Could Be Changing Your IQ on a Genetic Level, Study Finds” »

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The GTPases constitute a very large protein family, whose members are involved in the control of cell growth, transport of molecules, synthesis of other proteins, etc. Despite the many functions of the GTPases, they follow a common cyclic pattern (Figure 1). The activity of the GTPases is regulated by factors that control their ability to bind and hydrolyse guanosine triphosphate (GTP) to guanosine diphosphate (GDP). So far, it has been the general assumption that a GTPase is active or “on” when it is bound to GTP and inactive or “off” in complex with GDP. The GTPases are therefore sometimes referred to as molecular “switches.”

The bacterial translational elongation factor EF-Tu is a GTPase, which plays a crucial role during the synthesis of proteins in bacteria, as the factor transports the amino acids that build up a cell’s proteins to the cellular protein synthesis factory, the ribosome. Previous structural studies using X-ray crystallography have shown that EF-Tu occurs in two markedly different three-dimensional shapes depending on whether the factor is “on” (i.e. bound to GTP) or “off” (i.e. bound to GDP) (Figure 2). The binding of GTP/GDP have therefore always been thought to be decisive for the factor’s structural conformation.

Continue reading “Molecular switches are not just ‘on’ or ‘off’” »

With the introduction of more products aimed at gauging the effectiveness of mental health treatments, science is getting left behind, some experts say.

A recent open-access mouse study published by Xi’an Institute of Tissue Engineering and Regenerative Medicine scientists in the journal Bone Research describes how the ALPL gene affects bone aging and suggests that metformin might constitute a viable therapeutic option to prevent it [1].

Study abstract

Mutations in the liver/bone/kidney alkaline phosphatase (Alpl) gene cause hypophosphatasia (HPP) and early-onset bone dysplasia, suggesting that this gene is a key factor in human bone development. However, how and where Alpl acts in bone ageing is largely unknown. Here, we determined that ablation of Alpl induces prototypical premature bone ageing characteristics, including bone mass loss and marrow fat gain coupled with elevated expression of p16INK4A (p16) and p53 due to senescence and impaired differentiation in mesenchymal stem cells (MSCs). Mechanistically, Alpl deficiency in MSCs enhances ATP release and reduces ATP hydrolysis. Then, the excessive extracellular ATP is, in turn, internalized by MSCs and causes an elevation in the intracellular ATP level, which consequently inactivates the AMPKα pathway and contributes to the cell fate switch of MSCs.

Continue reading “Switching Off ALPL Gene Contributes to Bone Aging” »

That conclusion is based on a study that reviewed genetic testing results from 1.45 million individuals and found that nearly 25 percent of “variants of uncertain significance” were subsequently reclassified — sometimes as less likely to be associated with cancer, sometimes as more likely.

The study appears in the Journal of the American Medical Association (JAMA).

When variations from the norm are discovered in a gene, the variants are classified as “benign,” “likely benign,” “variant of uncertain significance,” “likely pathogenic,” or “pathogenic.”

Today, we have an interview with Dr. Michael Bonkowski, an expert on NAD+ biology and aging from the David Sinclair Lab, Harvard Medical School.

Michael Bonkowski aims to advance our understanding of the links between metabolism, aging, and age-associated diseases. He has published 35 peer-reviewed journal articles and has conducted multiple successful longevity studies. In Dr. David Sinclair’s lab, his research efforts are focused on the role of nutrient sensors’ regulation of endocrine signaling and aging in the mouse. He is also working on direct and indirect ways to drive the activity of these nutrient sensors by using dietary manipulations, small molecules, and chemical treatments.

Michael is trained as a pharmacologist, physiologist, and animal scientist. Some of his areas of expertise include animal physiology, genetics, glucose, and insulin homeostasis, metabolism, assay development, protein biochemistry, and transmission electron microscopy imaging.