Lifeboat Foundation

The world’s largest genetic study of hypertension finds that the number of genetic loci involved is three times larger than previously thought.

This study investigated the portrayal of “personalized” and “precision” medicine (PM) in North American news over the past decade. Content analysis of print and online news was conducted to determine how PM has been defined and to identify the frames used to discuss PM, including associated topics, benefits, and concerns.

A data set was built using the FACTIVA database, searching for popular North American publications with the terms “personalized (personalised) medicine” and/or “precision medicine” from 1 January 2005 to 15 March 2016. The final set of publications totaled 774.

PM is almost exclusively defined as related to genetics and is often part of a story related to cancer. The PM story is overwhelmingly one of highlighting (potential) benefits and optimism, especially in shorter publications, and ones where PM is not the main focus. This promotional PM discourse has remained fairly consistent over the past decade.

A well-known biohacker wants to help you channel your inner geneticist.

A famed biohackers is selling a kit that allows anyone to genetically engineer mutant frogs that are more massive than their natural counterparts.

Research has shed new light on genetic processes that may one day lead to the development of therapies that can slow, or even reverse, how our cells age.

A study led by the University of Exeter Medical School has found that certain genes and pathways that regulate splicing factors – a group of proteins in our body that tell our genes how to behave—play a key role in the ageing process. Significantly, the team found that disrupting these genetic processes could reverse signs of ageing in cells.

The study, published in the FASEB Journal, was conducted in human cells in laboratories. Aged, or senescent, cells are thought to represent a driver of the ageing process and other groups have shown that if such cells are removed in animal models, many features of ageing can be corrected. This new work from the Exeter team found that stopping the activity of the pathways ERK and AKT, which communicate signals from outside the cell to the genes, reduced the number of senescent cells in in cultures grown in the laboratory. Furthermore, they found the same effects from knocking out the activity of just two genes controlled by these pathways—FOX01 and ETV6.

Continue reading “Disrupting genetic processes reverses ageing in human cells” »

A wonderfully written, very friendly essay on the discoveries, carrier and life of Prof Dr David Sinclair and of course on sirtuins, the epigenetic theory of aging, resveratrol, nicotinamide dinucleotide NAD+ and healthy aging.

Since my recent visit to the Harvard Medical School laboratory run by Australian geneticist David Sinclair, I’ve been struggling with a shamefully greedy impulse. How can I get my hands on the wonder molecules that Sinclair is trialling to amazing effect in mice, not only slowing down their ageing but reversing it? My fear of missing out has flared up since I learnt from Sinclair that he estimates at least a third of his scientific colleagues are taking some version of these “anti-ageing” molecules, just as he does, in the belief it will increase their health spans by as much as 10 years. This means not just having a chance at living an extra decade, but living it in good health, avoiding the age-related diseases and general frailty that can make those years harrowing.

It becomes difficult to remain impartial when a respected scientist tells you he will soon turn 50, does not have a single grey hair and, according to regular blood and genetic tests, has the biological age of 31.4, even though he’s a workaholic and doesn’t exercise much. Or that he likes to think his mother prolonged her life – post lung cancer, with only one lung – for 20 years by taking the molecules he gave her, and that his 79-year-old father, who has taken several different kinds of them for years, currently lists whitewater rafting and mountaineering among his hobbies. Sinclair’s wife, Sandra Luikenhuis, even gives these molecules to the family dogs. (Luikenhuis, who has a PhD in genetics from Massachusetts Institute of Technology, only began taking the molecules herself after she noticed the irrefutably positive effect they’d had on their pets.)

Continue reading “Can David Sinclair cure old age?” »

An international consortium involving over 50 institutions has announced an ambitious project to assemble high-quality genome sequences of all 66,000 vertebrate species on Earth, including all mammals, birds, reptiles, amphibians, and fish. With an estimated total cost of $600 million dollars, it’s a project of biblical proportions.

It’s called the Vertebrate Genomes Project (VGP), and it’s being organized by a consortium called Genome 10K, or G10K. As its name implies, this group had initially planned to sequence the genomes of at least 10,000 vertebrate species, but now, owing to tremendous advances and cost reductions in gene sequencing technologies, G10K has decided to up the ante, aiming to sequence both a male and female individual from each of the approximately 66,000 vertebrate species on Earth.

A new study on adult neurogenesis and Alzheimer’s disease.

According to a study led by scientists at Massachusetts General Hospital, exercise-induced neurogenesis improves cognition in a mouse model of Alzheimer’s disease, yielding more benefits than drug-induced adult neurogenesis. The scientists were able to figure out the difference between the two types of induced neurogenesis and pharmacologically reproduce the same benefits provided by exercise [1].

Study abstract

Continue reading “Exercise Induces Adult Neurogenesis and Ameliorates Alzheimer’s Disease in Mice” »

Today, we are going to take a look at the topic of NAD+, its precursor, nicotinamide mononucleotide, and the debate surrounding the ability of these molecules to pass through the cell membrane.

NAD+ is critical for cellular function

Nicotinamide adenine dinucleotide (NAD+) is a redox cofactor, but it is also a critical signaling molecule that regulates cell function and survival in response to environmental changes such as nutrient intake and cellular damage. Age-related changes to the level of NAD+ in the cell impacts mitochondrial function, nutrient sensing and metabolism, redox reactions, circadian rhythm, immune and inflammatory responses, DNA repair, cell division, protein-to-protein signaling, chromatin, and epigenetics.

The Alzheimer’s Hypothesis

Introduction

Continue reading “The Alzheimer's Hypothesis” »