MIT professor Dina Katabi is building a gadget that can sit in one spot and track everything from breathing to walking, no wearables required.
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Category: biotech/medical – Page 2,479
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.
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While blood stem cells from bone marrow have long been a cornerstone of treating blood cancers like leukemia and lymphoma, Mackenzie’s trial extracting the cells from a pregnant woman to treat a developing fetus in utero is just one of several innovative uses of stem cells to treat a growing list of diseases with cells instead of drugs. And promising studies are inching more of these stem-cell-based treatments closer to finally being tested in people.
With stem cells like those found in bone marrow, scientists are taking advantage of what the body does naturally: generate itself anew. Many of the adult body’s organs and tissues, including fat cells and blood, are equipped with their own stash of stem cells whose sole job is to regenerate cells and tissues when older ones are damaged or die off and which can be harvested for research and growth outside the body.
Some organs are not endowed with these large stem-cell reservoirs, however, most notably the brain and heart muscle. So more than two decades ago, scientists found another source of these flexible cells–in embryos that were donated for research from in vitro fertilization clinics. They learned how to grow these cells in the lab into any cells in the body. That opened the possibility that conditions like heart disease, diabetes or even psychiatric disorders might eventually be treated by replacing damaged tissues or organs with healthy ones, which could provide cures and treatments that didn’t require drugs or surgery.
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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.)
If all goes well, and these anti-ageing molecules live up to their promise, Sinclair and his family will be proof it’s still possible to be going strong on the other side of the private apocalypse each of us has to face, what Philip Roth famously called the “massacre” of ageing. Imagine if you could still be standing tall after the dust clears, not one of the walking wounded, not just surviving, but thriving.
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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.
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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
Adult hippocampal neurogenesis (AHN) is impaired before the onset of Alzheimer’s disease (AD) pathology. We found that exercise provided cognitive benefit to 5×FAD mice, a mouse model of AD, by inducing AHN and elevating levels of brain-derived neurotrophic factor (BDNF). Neither stimulation of AHN alone, nor exercise, in the absence of increased AHN, ameliorated cognition. We successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels. Suppressing AHN later led to worsened cognitive performance and loss of preexisting dentate neurons. Thus, pharmacological mimetics of exercise, enhancing AHN and elevating BDNF levels, may improve cognition in AD. Furthermore, applied at early stages of AD, these mimetics may protect against subsequent neuronal cell death.
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The Next-Generation Nonsurgical Neurotechnology (N3) program will fund research on tech that can transmit high-fidelity signals between the brain and some external machine without requiring that the user be cut open for rewiring or implantation. It hasn’t escaped DARPA’s attention that no-surgery-required brain gear that gives people superpowers may find applications beyond the military. The proof-of-concept tech that comes out of the N3 program may lead to consumer products, says Justin Sanchez, director of DARPA’s Biological Technologies Office. “This will spawn new industries,” he says…
The N3 program will create no-surgery-required neurotech that the general public may also find useful.
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Researchers have discovered a way to kill #cancer cells and stop #glioblastoma formation by blocking casein kinase 1 gene.
Scientists with the Virginia Tech Carilion Research Institute say a gene involved in the body’s circadian rhythms is a potential target for therapies to help patients with a deadly form of brain cancer known as glioblastoma.
This discovery, to be published in the journal Scientific Reports on Tuesday, Sept. 11, points to a subtype of a particular gene that apparently is enabling the survival of cancer cells, although it is more commonly associated with circadian rhythms — the body’s 24-hour biological clock.
“The world is desperately seeking new treatments for glioblastoma and no one has ever before pointed to this gene as a target upon which to base therapies,” said Zhi Sheng, an assistant professor at the Virginia Tech Carilion Research Institute, whose team pinpointed the gene from 20 suspects it had previously identified.
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An incurable affliction that gradually destroys a person’s ability to walk, speak, and eventually breathe can also deteriorate the mind, new research suggests. People with amyotrophic lateral sclerosis (ALS) are more likely to have other mental and behavioral health problems than people without the condition, the study found.
ALS, also called Lou Gehrig’s disease, is a progressive neurologic condition that affects some 20,000 Americans at any one time. In ALS, a person’s motor neurons throughout their body and brain steadily die off. These neurons are responsible for helping us carry out voluntary movement.
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