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Category: biotech/medical – Page 1,816

Psilocybin startup Compass Pathways goes public at more than $1B. Here’s why Wall Street is starting to see the value in psychedelics.

For several years, investors and psychonauts have predicted that psychedelic medicine would become the next billion-dollar industry, with some value estimates as high as $100 billion. They said substances like MDMA or psilocybin mushrooms would follow a similar regulatory path that cannabis took to the mainstream, going from a Schedule 1 narcotic to a legal, regulated, and highly lucrative medicine.

At least some of these predictions have rung true. On September 18th, Compass Pathways Plc., a London-based company developing psilocybin into a prescription drug in assisted psychotherapy, went public, listing on Nasdaq. The company’s stock jumped 71 percent on its first day of trading and is now estimated to be worth $1.3 billion. Compass Pathways declined to comment for this article. Numinus Wellness Inc and Champignon Brands Inc are two other psychedelic companies that have gone public this year.

This month, another psychedelic research company, Mind Medicine Inc. (“Mindmed”), announced their intent to appear on Nasdaq, as well, and some analysts predict it will soon be the next billion-dollar psychedelic company. Havn Life Sciences, which has earned permission from the Canadian government to work with psilocybin, also squeezed onto the Canadian Stock Exchange in September.

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Stem cells are a promising experimental treatment for a variety of diseases. Now researchers at the University of Wisconsin-Madison have found that transplanting neurons grown from stem cells into the brains of mice with Parkinson’s disease repaired the damaged brain circuits, improving the animals’ motor skills.

In people afflicted with Parkinson’s, neurons that produce dopamine begin to break down and die. The disease gradually presents as tremors, involuntary movements, and trouble with walking, speaking and other actions. While it currently can’t be cured, studies are suggesting new ways to slow progression and reduce severity of symptoms through new drugs or repurposed old ones, deep brain stimulation or probiotic treatments.

But an emerging and potentially ground-breaking treatment involves stem cells. In several studies, researchers have used stem cells to grow new dopamine-producing neurons, and then transplant them into animals. And now the UW-Madison team’s work has shown that doing so can help restore brain circuits damaged by Parkinson’s.

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In a study of gorilla skeletons collected in the wild, Johns Hopkins Medicine researchers and their international collaborators report that aging female gorillas do not experience the accelerated bone loss associated with the bone-weakening condition called osteoporosis, as their human counterparts often do. The findings, they say, could offer clues as to how humans evolved with age-related diseases.

The study was published on Sept. 21, 2020, in Philosophical Translations of the Royal Society B.

“Osteoporosis in humans is a really interesting mechanical problem,” says Christopher Ruff, Ph.D., professor at the Center for Functional Anatomy and Evolution at the Johns Hopkins University School of Medicine. “In terms of natural selection, there is no evolutionary advantage in developing with aging to the point of a potential fracture. By looking at close relatives of humans on the evolutionary tree, we can infer more about the origins of this condition.”

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Some people are at higher risk of developing obesity because they possess genetic variants that affect how the brain processes sensory information and regulates feeding and behavior. The findings from scientists at the University of Copenhagen support a growing body of evidence that obesity is a disease whose roots are in the brain.

Over the past decade, scientists have identified hundreds of different genetic variants that increase a person’s risk of developing obesity. But a lot of work remains to understand how these variants translate into obesity. Now scientists at the University of Copenhagen have identified populations of cells in the that play a role in the development of the disease—and they are all in the brain.

“Our results provide evidence that outside the traditional organs investigated in obesity research, such as , play a key role in human obesity,” says Associate Professor Tune H Pers from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR), at the University of Copenhagen, who published his team’s findings in the internationally-recognized journal eLife.

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Two active genetics strategies help address concerns about gene-drive releases into the wild.

In the past decade, researchers have engineered an array of new tools that control the balance of genetic inheritance. Based on CRISPR technology, such gene drives are poised to move from the laboratory into the wild where they are being engineered to suppress devastating diseases such as mosquito-borne malaria, dengue, Zika, chikungunya, yellow fever and West Nile. Gene drives carry the power to immunize mosquitoes against malarial parasites, or act as genetic insecticides that reduce mosquito populations.

Although the newest gene drives have been proven to spread efficiently as designed in laboratory settings, concerns have been raised regarding the safety of releasing such systems into wild populations. Questions have emerged about the predictability and controllability of gene drives and whether, once let loose, they can be recalled in the field if they spread beyond their intended application region.

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For the first time, Senckenberg scientist Mónica Solórzano-Kraemer, together with lead authors David Peris and Kathrin Janssen of the University of Bonn and additional colleagues from Spain and Norway, successfully extracted genetic material from insects that were embedded in six- and two-year-old resin samples. DNA—in particular, DNA from extinct animals—is an important tool in the identification of species. In the future, the researchers plan to use their new methods on older resin inclusions, as well. The study was published today in the scientific journal PLOS ONE.

The idea of extracting DNA from resin-embedded organisms inevitably invokes memories of the blockbuster “Jurassic Park.”

“However, we have no intention of raising dinosaurs,” says Dr. Mónica Solórzano-Kraemer of the Senckenberg Research Institute and Natural History Museum. “Rather, our current study is a structured attempt to determine how long the DNA of insects enclosed in resinous materials can be preserved.”

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Quantum computers, which harness the strange probabilities of quantum mechanics, may prove revolutionary. They have the potential to achieve an exponential speedup over their classical counterparts, at least when it comes to solving some problems. But for now, these computers are still in their infancy, useful for only a few applications, just as the first digital computers were in the 1940s. So isn’t a book about the communications network that will link quantum computers — the quantum internet — more than a little ahead of itself?

Surprisingly, no. As theoretical physicist Jonathan Dowling makes clear in Schrödinger’s Web, early versions of the quantum internet are here already — for example, quantum communication has been taking place between Beijing and Shanghai via fiber-optic cables since 2016 — and more are coming fast. So now is the perfect time to read up.

Dowling, who helped found the U.S. government’s quantum computing program in the 1990s, is the perfect guide. Armed with a seemingly endless supply of outrageous anecdotes, memorable analogies, puns and quips, he makes the thorny theoretical details of the quantum internet both entertaining and accessible.

Readers wanting to dive right in to details of the quantum internet will have to be patient. “Photons are the particles that will power the quantum internet, so we had better be sure we know what the heck they are,” Dowling writes. Accordingly, the first third of the book is a historical overview of light, from Newton’s 17th century idea of light as “corpuscles” to experiments probing the quantum reality of photons, or particles of light, in the late 20th century. There are some small historical inaccuracies — the section on the Danish physicist Hans Christian Ørsted repeats an apocryphal tale about his “serendipitous” discovery of the link between electricity and magnetism — and the footnotes rely too much on Wikipedia. But Dowling accomplishes what he sets out to do: Help readers develop an understanding of the quantum nature of light.

For an entertaining overview of the physics and technological advances paving the way for the quantum internet, read ‘Schrödinger’s Web.’

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Not too much here, but longevity research fans might like.

Time may be our worst enemy, and aging its most powerful weapon. Our hair turns gray, our strength wanes, and a slew of age-related diseases represent what is happening at the cellular and molecular levels. Aging affects all the cells in our body’s different tissues, and understanding its impact would be of great value in fighting this eternal enemy of all ephemeral life forms.

The key is to first observe and measure. In a paper published in Cell Reports, scientists led by Johan Auwerx at EPFL started by asking a simple question: how do the tissues of aging mice differ from those of mice that are mere adults?

To answer the question, the researchers used the multiple techniques to measure the expression of everyone one of the thousands of mouse’s genes, and to identify any underlying epigenetic differences. The researchers not only measured different layers of information, but they did it across three different tissues: liver, heart, and muscle.

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Stopping the cannibalistic behavior of a well-studied enzyme could be the key to new drugs to fight age-related diseases, according to a new study published online in Nature Cell Biology. For the first time, researchers in the Perelman School of Medicine at the University of Pennsylvania show how the self-eating cellular process known as autophagy is causing the SIRT1 enzyme, long known to play a role in longevity, to degrade over time in cells and tissue in mice. Identifying an enzymatic target is an important step that may lead to new or modified existing therapeutics.

“Blocking this pathway could be another potential approach to restore the level of SIRT1 in patients to help treat or prevent age-related organ and immune system decline,” said first author Lu Wang, Ph.D., a postdoctoral researcher in the lab of Shelly Berger, Ph.D., a professor of Cell and Developmental Biology in the Perelman School of Medicine and a professor of Biology in the School of Arts and Sciences at Penn. Berger also serves as senior author on the paper.

“The findings may be of most interest to the immune aging field, as autophagy’s role in SIRT1 in immune is a concept that hasn’t been shown before,” Wang added. “Exploiting this mechanism presents us with a new possibility of restoring immune function.”

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