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Monash researchers have unlocked a key process in all human cells that contributes to diseases like cancer and neurodegenerative diseases as well as ageing. The discovery reveals how cells efficiently get rid of cellular junk, which when it accumulates, can trigger death and the health problems associated with getting older.

Autophagy is the ‘clean-up crew’ of the cell—used by cells to break-down debris like broken proteins, bits of cell , viruses or bacteria. To capture this trash, cells use specialised membranes to trap the cargo for recycling into new parts and energy. Without efficient autophagy cells become choked by their own damaged components, which can contribute to the development of a range of diseases, including diabetes, muscular dystrophy, Parkinson’s and Alzheimer’s disease.

Dr. Michael Lazarou’s laboratory from the Monash Biomedicine Discovery Institute have today published data in Nature Communications that debunks previously held beliefs about how cells target their trash. Cells target different types of cargo by using ‘autophagy receptors’, which can bind the cargo as well as the ensnaring membranes. Until recently these autophagy receptors were thought to recruit the membranes to the cargo, but research led by Dr. Benjamin Padman from the Lazarou lab now shows that this is not the case.

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Three men with severe spinal cord injuries have walked for the first time in years after receiving targeted electrical stimulation of the spinal cord.

Breakthrough: Spinal cord injuries can severely reduce a person’s range of motion or lead to complete leg paralysis. In two new papers published in Nature and Nature Neuroscience, researchers describe implanting electrical stimulators into the damaged spinal cords of three men who all had partial or complete lower-leg paralysis. The stimulators then delivered targeted electric pulses in time with the patients’ walking gait.

The patients wore a series of sensors on their legs and feet that wirelessly communicated to the stimulators as they began to walk. Within a week, the men were able to leave the treadmill and walk on the ground with continued electrical stimulation. After a few months, they regained the ability to walk without any electrical stimulation at all.

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GDF11 is an endogenous (meaning it’s natural, and you have it in you) signaling molecule whose primary mechanism of action is stem cell DNA repair. Most of the aging is likely caused by the atrophy of your stem cell populations due to declining GDF11 levels, and many believe this is natural selection’s way of programming lifespan. Fortunately, adding exogenous GDF11 can generally repair enough of senescent stem cells to reverse your age 5 to 10 years.

Steve will take some time providing information on the topic and answering questions.

“I’ve always been interested in stopping the aging process, and as a lifelong software guy, coupled with plenty of evidence from parabiosis experiments, I believe lifespan is programmed by natural selection, specifically group selection.

The primary mechanism for determining lifespan is a naturally occurring, blood born peptide called GDF11. Interestingly enough, the molecular structure of GDF11 is maintained across all vertebrate species. You have GDF in you right now, but unless you are 18, you don’t have enough of it.

“Human players must explicitly manage an ‘economy of attention’ to decide where to focus the camera,” said the DeepMind team. “However, analysis of AlphaStar’s games suggests that it manages an implicit focus of attention. On average, agents ‘switched context’ about 30 times per minute,” the team wrote, which was similar to Komincz’s and Wünsch’s behaviors.

Ultimately, the DeepMind team concluded that AlphaStar won against both pros because of “superior macro and micro-strategic decision-making, rather than superior click-rate, faster reaction times, or the raw interface.”

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In the new paper, Jason Snyder, Ph.D., a University of British Columbia behavioral neuroscientist, argues that if you take a close look at all the studies on animals from mice to humans, the facts are quite clear: Animals probably don’t develop significant amounts of new brain cells as we enter adulthood. There’s still hope for some neurogenesis, but not a huge amount.

“In some respects, it’s just one of the things that humanity has always hoped for — staying young,” he tells Inverse. “So I think it’s been disconcerting that there might not be as many of these young cells that are malleable, that are adaptive, that are capable of learning earlier in life. Of course we want those things to be there, but I think that introduces some bias.”

To be clear, Snyder doesn’t argue that the field is biased. Instead, his argument is based on the analysis of past studies that have looked into this topic in humans, primates, and mice. There he admits that there’s been some confusion — some studies seem to show that the brain can continue to develop new cells later in life, while others show that it can’t. Specifically, he says that it’s been hard to let go of the idea of neurogenesis because of the results of animal studies (many on mice) “demonstrating persistent neurogenesis throughout life.”

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  • In an age where innovative technologies like gene and cell therapy are transforming how we think about medical treatments, some CEOs are wondering what’s being left on the table.
  • Business Insider spoke to three companies developing new uses for old drugs, and they told us now might be a good time to rethink what we consider innovation.
  • Simply changing how drugs are dosed or delivered could open up the doors to more uses for existing medications in tough-to-treat conditions like female sexual arousal dysfunction or antibiotic-resistant infections.

The key to tackling hard-to-treat diseases could have less to do with flashy new technologies than with finding new uses for old drugs.

A range of smaller drugmakers are exploring the back catalogs of big pharma companies to discover old drugs that could be used in new ways, they told Business Insider. They’re seeking treatments for conditions including a rare lung disease, antibiotic-resistant infections, and female sexual arousal disorder. Along the way, they’re seeking to redefine what we think of as medical innovation.

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NK-cell function appears to be impaired during spaceflights over long durations according to a new study published this week. This means that immune systems could be broken down somewhat during the long trips NASA hopes to take with astronauts in the distant future. The research here was done by a team of researchers at the University of Arizona, the University of Houston, Louisiana State University, and NASA-Johnson Space Center.

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