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SENS has kindly commented about MMTP and the impact our research should have on aging. We launch a fundraiser in April to test senolytics (ApoptoSENS) with a planned follow up to combine this with stem cell therapy (RepleniSENS). It is time to put the engineering approach to aging to the test!


Some drugs tested have been found to increase mouse lifespan such as Metformin and Rapamycin for example and are considered for human testing. Many more substances have never been tested and we do not know if they might extend healthy lifespan.

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CRISPR may have burst on the scene as a revolutionary gene editing tool, but it’s proving to be so much more. Tagging the targeting system with a gene silencing component could revolutionise stem cell work and enable a new level of genetic control we’ve never seen before.

A wonder tool

Efficient and accurate, CRISPR may be in the throes of a patent battle but it’s undoubtedly going down in history as a landmark in biological science. There may be other similar systems out there, but CRISPR makes things quick and comparatively cheap — which tends to revolutionise any industry.

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Innovative new project the MMTP aims to fast forward translation from lab to clinic with rapid, parallel mice testing. We caught up with Steve Hill and Elena Milova from the MMTP team to discuss the program and why being pro-actively involved with longevity advocacy is so important.

What’s the gap in the market you’re aiming to fill and the major motivation behind the MMTP?

Steve – The bridge between basic research and taking it to clinical trials. People like The SENS Foundation are spinning a lot of plates doing the high risk, nitty gritty research that isn’t profitable, but crowdfunding can get that done. We want to create a solid gold standard testing platform without the restrictions of government, where any team can come to us for parallel testing and halve development time. The problem with animal testing is there’s this disconnect; it’s not sexy science basically. A common response is let me know when it’s available in humans, but it’s not going to be! No animal data means no human testing, organizations like the FDA, NHS and EMA all insist on a battery of animal testing before human trials. Period. It’s not sexy, it’s not available in humans next week, but if MMTP or other projects don’t get things done on mice for example, it’s never going to get done. It doesn’t matter if one theory turns out to be wrong, let’s get stuck in and find out!

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CRISPR may be revolutionary; however, it’s not nearly as easy as it’s made out to be. But thanks to this company, individuals can alter the source code of life without ever needing to enter a lab.

A new genome editing technique is allowing us to alter DNA—the source code of life—with unprecedented precision. It is known as CRISPR, and with it, we can target and change a gene from any cell of any species without interfering with any other genes. If that’s not enough, we are able to edit these genes at just a fraction of the cost of previous methods.

So not only is this technique remarkably precise, it’s also remarkably cheap.

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It won’t be long now before cancer is nothing but a terrible, terrible memory.

Never soon enough, though.


Recent advances in an immune-cell cancer treatment called immunotherapy* (using engineered antibodies that can target specific molecules on cancer cells) are producing dramatic results for people with cancer, according to Stanley Riddell, MD, an immunotherapy researcher and oncologist at Seattle’s Fred Hutchinson Cancer Research Center.**

Riddell and his colleagues have refined new methods of engineering a patient’s own immune cells to better target and kill cancer cells while decreasing side effects. In laboratory and clinical trials, the researchers are seeing “dramatic responses” in patients with tumors that are resistant to conventional high-dose chemotherapy, “providing new hope for patients with many different kinds of malignancies,” Riddell said.

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The MDI Biological Laboratory has announced new discoveries about the mechanisms underlying the regeneration of heart tissue by Assistant Professor Voot P. Yin, Ph.D., which raise hope that drugs can be identified to help the body grow muscle cells and remove scar tissue, important steps in the regeneration of heart tissue.

Heart disease is a leading cause of death in the western world. Yin is using zebrafish to study the regeneration of tissue because of the amazing capacity of these common aquarium fish to regenerate the form and function of almost any body part, including heart, bone, skin and blood vessels, regardless of their age. In contrast, the adult mammalian cardiovascular system has limited regenerative capacity.

“Although zebrafish look quite different from humans, they share an astonishing 70 percent of their genetic material with humans, including genes important for the formation of new heart muscle,” Yin said. “These genes are conserved in humans and other mammals, but their activity is regulated differently after an injury like a .”

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Allen Institute working with Baylor on reconstructing neuronal connections.


The Intelligence Advanced Research Projects Activity (IARPA) has awarded an $18.7 million contract to the Allen Institute for Brain Science, as part of a larger project with Baylor College of Medicine and Princeton University, to create the largest ever roadmap to understand how the function of networks in the brain’s cortex relates to the underlying connections of its individual neurons.

The project is part of the Machine Intelligence from Cortical Networks (MICrONS) program, which seeks to revolutionize machine learning by reverse-engineering the algorithms of the brain.

“This effort will be the first time that we can physically look at more than a thousand connections between neurons in a single cortical network and understand how those connections might allow the network to perform functions, like process visual information or store memories,” says R. Clay Reid, Ph.D., Senior Investigator at the Allen Institute for Brain Science, Principal Investigator on the project.

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