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“We were able to show that there is only a single type of microglia in the brain that exist in multiple flavours,” says project head Prof. Dr. Marco Prinz, medical director of the Institute of Neuropathology at the Medical Center — University of Freiburg. “These immune cells are very versatile all-rounders, not specialists, as has been the textbook opinion up to now,” sums up Prof. Prinz.


A team of researchers under the direction of the Medical Center — University of Freiburg has created an entirely new map of the brain’s own immune system in humans and mice. The scientists succeeded in demonstrating for the first time ever that the phagocytes in the brain, the so-called microglia, all have the same core signature but adopt in different ways depending on their function. It was previously assumed that these are different types of microglia. The discovery, made by means of a new, high-resolution method for analyzing single cells, is important for the understanding of brain diseases. Furthermore, the researchers from Freiburg, Göttingen, Berlin, Bochum, Essen, and Ghent (Belgium) demonstrated in detail how the human immune system in the brain changes in the course of multiple sclerosis (MS), which is significant for future therapeutic approaches. The study was published on 14. February 2019 in the journal Nature.

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Not all damaged cells die. Some stick around as senescent cells, unable to divide but still able to produce chemical signals — and they could play a major role in the battle against aging.

“It is thought that these cells and the substances they produce are involved in the process of aging,” longevity researcher Nicolas Musi from the University of Texas at Austin told MIT Technology Review.

“The idea is that removing these cells may be beneficial to promote healthy aging and also to prevent diseases of aging.”

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Circa 2011


Bill Andrews’s feet are so large, he tells me, that back when he was 20 he was able to break the Southern California barefoot-waterskiing distance record the first time he put skin to water. Then he got ambitious and went for the world speed record. When the towrope broke at 80 mph, he says, “they pulled me out of the water on a stretcher.”

The soles of the size-15 New Balances that today shelter those impressive feet strike a steady clap-clap on the macadam as Andrews and I lope down a path along the Truckee River that takes us away from the clutter of cut-rate casino hotels, strip malls and highway exit ramps that is downtown Reno, Nevada. Andrews, 59, is a lean 6-foot-3 and wears a close-cropped salt-and-pepper Vandyke and, for today’s outing, a silver running jacket, nicely completing a package that suggests a Right Stuff–era astronaut. He is in fact one of the better ultramarathoners in America. I am an out-of-shape former occasional runner, so it gives me pause to listen as Andrews describes his racing exploits. “I can run 100 miles, finish, turn around, and meet friends of mine on the course who are still coming in,” he says. “I’ve been in many races where I’m stepping over bodies of people who have collapsed, and I’m feeling great.”

“I want to cure my aging, my friends’ and family’s aging, my investors’ aging, and I want to make a ton of money,” Andrews says. His return to running after a middle-aged break was, he says, inspired by a revelation he had at a time when he and a small team of scientists at his biotech start-up, Sierra Sciences, had been working 14 to 18 hours a day in the lab for five years, rather obsessively pursuing a particular breakthrough. Finally, his doctor told him he was headed for an early grave. “I thought, god, I don’t want to cure aging and then drop dead,” Andrews says.

Researchers from Texas A&M University, led by Dr. Akhilesh K. Gaharwar, have developed a new way to deliver treatment for cartilage regeneration.

Gaharwar, assistant professor in the Department of Biomedical Engineering at Texas A&M, said the nanoclay-based platform for sustained and prolonged delivery of protein therapeutics has the potential to impact treating osteoarthritis, a degenerative disease that affects nearly 27 million Americans and is caused by breakdown of cartilage that can lead to damage of the underlying bone.

As America’s population ages, the number of osteoarthritis incidences is likely to increase. One of the greatest challenges with treating osteoarthritis and subsequent joint damage is repairing the damaged tissue, especially as cartilage tissue is difficult to regenerate.

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  • Spherical nucleic acids are a class of personalized medicines for treating cancer and other diseases
  • SNAs are challenging to optimize because their structures can vary in many ways
  • Northwestern University team developed a library approach and machine learning to rapidly synthesize, analyze and select for potent SNA medicines

EVANSTON, Ill.— With their ability to treat a wide a variety of diseases, (SNAs) are poised to revolutionize medicine. But before these digitally designed nanostructures can reach their full potential, researchers need to optimize their various components.

A Northwestern University team led by nanotechnology pioneer Chad A. Mirkin has developed a direct route to optimize these challenging particles, bringing them one step closer to becoming a viable treatment option for many forms of cancer, , neurological disorders and more.

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Neural stimulation is a developing technology that has beneficial therapeutic effects in neurological disorders, such as Parkinson’s disease. While many advancements have been made, the implanted devices deteriorate over time and cause scarring in neural tissue. In a recently published paper, the University of Pittsburgh’s Takashi D. Y. Kozai detailed a less invasive method of stimulation that would use an untethered ultrasmall electrode activated by light, a technique that may mitigate damage done by current methods.

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There are many instances in medicine when it would be helpful to stop, or greatly slow down, time. Doing so could spare a limb from amputation, prevent paralysis after a stroke or save your life following a heart attack.

Across the tree of life, there are many organisms that can essentially cheat time by decelerating their biology. Chief among them is the tardigrade, a creature no bigger than a speck of sand that can survive severe temperatures and pressures, outer space and all sorts of apocalyptic scenarios by entering a dormant state called anhydrobiosis.

A team at Harvard Medical School is studying tardigrades in hopes of finding medical treatments that halt tissue damage. In particular, the scientists are drawing inspiration from special proteins suspected to help tardigrades achieve suspended animation. They aim to synthesize a version of these proteins that can enter human cells and pause processes leading to cell death.

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Tuberculosis (TB) is one of the top 10 causes of death worldwide. In 2017, 10 million people around the world fell ill with TB and 1.3 million died. The genome of the bacterium that causes TB holds a special toxin-antitoxin system with a surprising function: Once the toxin is activated, all bacterial cells die, stopping the disease. An international research team co-led by the Wilmanns group at EMBL in Hamburg investigated this promising feature for therapeutic targets. They now share the first high-resolution details of the system in Molecular Cell.

Mycobacterium tuberculosis is the bacterium that causes TB in humans. Its genome holds 80 so-called toxin-antitoxin (TA) systems, sets of closely linked genes that encode both a toxic protein and an antitoxin—a toxin-neutralising antidote.

When the bacteria are growing normally, toxin activity is blocked by the antitoxin’s presence. But under stress conditions such as lack of nutrients, dedicated enzymes rapidly degrade the antitoxin molecules. This activates the toxin proteins in the cell and slows down the growth of the bacteria, allowing them to survive the stressful environment.

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