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Other than speeding up bone healing, slowing Alzheimer’s in mice, ultrasound has been found to help with speedy wound healing. Ultrasound application can help diabetic patients, who suffer from helping defects, up to 30% to decrease the healing time of wounds.

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These type of sound waves, trigger a protein pathway essential for fibroblast cells to work. Fibroblast cells help in blood clotting. The number and speed of blood clotting cells are increased in the area of the wound, and the healing process begins. This technique could lower the instances of amputation in case of chronic healing defects in diabetic patients.

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The SENS Research Foundation has finally published this anticipated and important paper on mitochondrial gene transfer which has ramifications for mitochondrial diseases and more importantly one of the processes of aging. It is great to see that finally after a decade of criticism Aubrey de Grey has proven his approach is viable.


We explore the possibility of re-engineering mitochondrial genes and expressing them from the nucleus as an approach to rescue defects arising from mitochondrial DNA mutations. We have used a patient cybrid cell line with a single point mutation in the overlap region of the ATP8 and ATP6 genes of the human mitochondrial genome. These cells are null for the ATP8 protein, have significantly lowered ATP6 protein levels and no Complex V function. Nuclear expression of only the ATP8 gene with the ATP5G1 mitochondrial targeting sequence appended restored viability on Krebs cycle substrates and ATP synthesis capabilities but, failed to restore ATP hydrolysis and was insensitive to various inhibitors of oxidative phosphorylation. Co-expressing both ATP8 and ATP6 genes under similar conditions resulted in stable protein expression leading to successful integration into Complex V of the oxidative phosphorylation machinery. Tests for ATP hydrolysis / synthesis, oxygen consumption, glycolytic metabolism and viability all indicate a significant functional rescue of the mutant phenotype (including re-assembly of Complex V) following stable co-expression of ATP8 and ATP6. Thus, we report the stable allotopic expression, import and function of two mitochondria encoded genes, ATP8 and ATP6, resulting in simultaneous rescue of the loss of both mitochondrial proteins.

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For cancer research, meanwhile, the situation is more akin to an economic revolution, or disruptive advance in technology. Because all cancers must lengthen their telomeres, and because telomere lengthening is governed by a small number of processes, there is the opportunity to change the focus of cancer research from an endless procession of expensive new therapies, each targeting a tiny number of the hundreds of subtypes of cancer, to one single therapy that can effectively suppress all cancers.


The last few days have arrived for this year’s SENS Research Foundation crowdfunding campaign, focused on important groundwork to establish a universal therapy for all types of cancer. There are still a few thousand dollars left in the matching fund, so donations are still being matched. Cancer is just as much a part of aging that must be ended, brought completely under control, as all of the other line items in the SENS rejuvenation research portfolio, and this year is the first time that the SENS Research Foundation has run a fundraiser for this program.

Hopefully there is no need to remind the audience here that the SENS Research Foundation, and important ally the Methuselah Foundation, have in recent years achieved great progress in the field of rejuvenation research on the basis of our donations and our support. Some of the high points you’ll find mentioned here and there at Fight Aging!: support and ongoing expansion of the mitochondrial repair technologies now under development at Gensight; seed funding Oisin Biotechnologies for senescent cell clearance; unblocking efforts to clear glucosepane cross-links that stiffen tissues; running the lauded Rejuvenation Biotechnology conferences; and many more. If only all charities produced as great an impact with as few resources — and if only we were further along in the bootstrapping of an industry focused on the development of rejuvenation therapies.

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The year was 2012, and IBM’s AI software Watson was in the midst of its heyday.

Watson beat two of Jeopardy’s all-time champions a year earlier in 2011, and the world was stunned. It was the first widespread and successful demonstration of a natural language processing computer of its class. Combined with the popularity of Jeopardy, Watson became an immediate mainstream icon.

Later in 2012, IBM announced one of the first major practical partnerships for Watson—a Cleveland Clinic collaboration to bring the system into medical training.

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Professor YongKeun Park of the Physics Department at the Korea Advanced Institute of Science and Technology and his research team have developed a powerful method for 3D imaging of live cells without staining.

The new microscopic tool is called the holotomography (HT)-1. It was announced to the global marketplace through a Korean start-up that Professor Park co-founded called TomoCube.

From the measurement of multiple 2D holograms of a cell, coupled with various angles of laser illuminations, the 3D refractive index (RI) distribution of the cell can be reconstructed. This 3D map provides structural and chemical information, such as dry mass and protein concentration.

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Brain is the most complex biological computing system and performs almost every activity with jet speed and precision. Despite the numerous advancements in the interaction of technology and science, there is no machine that functions as swift as a brain. Nevertheless, the recent experiment by the researchers of Okinawa Institute of Science and Technology Graduate University in Japan and Forschungszentrum Jülich in Germany is a milestone in the history of producing human brain simulations by a computer.

The team of researchers from Japan and Germany have managed to produce the most accurate simulation of a human brain in Japan’s computer. The single second worth of activity in the human brain from just one percent of the complex organ was able to be produced in 40 minutes by the world’s fourth largest computer.

The computer used is the K computer in Japan to simulate human brain activity. The computer has 705,024 processor cores and 1.4 million GB of RAM, but still took 40 minutes to crunch the data for just one second of brain activity. The open-source Neural Simulation Technology (NEST) tool is used to replicate a network consisting of 1.73 billion nerve cells connected by 10.4 trillion synapses.

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Traditional cancer research is well funded but ALT cancers are not. SENS Research is aiming to raise funds to address this vital gap in our scientific knowledge. Most scary thing of all is that some regular cancers that abuse telomerase can switch to this ALT method to keep growing when telomerase blocking therapies are used.


The paper I’ll point out today is a timely one, given that the SENS Research Foundation’s fundraiser for early stage work on a therapy for alternative lengthening of telomeres (ALT) cancers is nearing its close. There are still thousands of dollars left in the matching fund, so give it some thought if you haven’t yet donated. The search for ways to safely sabotage ALT is a useful, important line of research because blocking telomere lengthening is a path to a universal cancer therapy, those research groups presently working on it are all looking to achieve this goal by interfering in the activities of telomerase, cancers can switch from using telomerase to using ALT, and next to no-one is working on ways to suppress ALT mechanisms. It seems fairly clear based on the evidence to date that the universal cancer therapy that lies ahead, built by inhibiting telomere lengthening, must involve a blockade of both telomerase and ALT. The open access paper below reinforces this point, the authors investigating how exactly cancers switch from telomerase to ALT to maintain their dangerous growth.

Cancer research today has a grand strategy problem. There is only so much funding and only so many researchers, but hundreds of subtypes of cancer. Therapies tend to be highly specific to the peculiarities of one type of cancer or a small class of cancers, meaning that great expense and time leads to a treatment that is only applicable for a fraction of cancer patients, all too often a tiny fraction. Further, since tumors evolve at great speed, any one individual patient’s cancer may find its way out from under the hammer by changing its signature and mode of operation. All is not doom and gloom, however. Consider that the research community could build a therapy applicable to all cancers with little to no modification, where the cost of development would be no greater than any one of the highly specific therapies presently in use and under development. That therapy would be, of course, based on the blockade of telomere lengthening.

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Calico, a company focused on aging research and therapeutics, today announced that Daphne Koller, Ph.D., is joining the company as Chief Computing Officer. In this newly created position, Dr. Koller will lead the company’s computational biology efforts. She will build a team focused on developing powerful computational and machine learning tools for analyzing biological and medical data sets. She and her team will work closely with the biological scientists at Calico to design experiments and construct data sets that could provide a deeper understanding into the science of longevity and support the development of new interventions to extend healthy lifespan.

Calico will try to use machine learning to understand the complex biological processes involved in aging.

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