Sydney Brenner was one of the first to view James Watson and Francis Crick’s double helix model of DNA in April 1953. The 26-year-old biologist from South Africa was then a graduate student at the University of Oxford, UK. So enthralled was he by the insights from the structure that he determined on the spot to devote his life to understanding genes.

Iconoclastic and provocative, he became one of the leading biologists of the twentieth century. Brenner shared in the 2002 Nobel Prize in Physiology or Medicine for deciphering the genetics of programmed cell death and animal development, including how the nervous system forms. He was at the forefront of the 1975 Asilomar meeting to discuss the appropriate use of emerging abilities to alter DNA, was a key proponent of the Human Genome Project, and much more. He died on 5 April.

Brenner was born in 1927 in Germiston, South Africa to poor immigrant parents. Bored by school, he preferred to read books borrowed (sometimes permanently) from the public library, or to dabble with a self-assembled chemistry set. His extraordinary intellect — he was reading newspapers by the age of four — did not go unnoticed. His teachers secured an award from the town council to send him to medical school.

Brenner entered the University of the Witwatersrand in Johannesburg at the age of 15 (alongside Aaron Klug, another science-giant-in-training). Here, certain faculty members, notably the anatomist Raymond Dart, and fellow research-oriented medical students enriched his interest in science. On finishing his six-year course, his youth legally precluded him from practising medicine, so he devoted two years to learning cell biology at the bench. His passion for research was such that he rarely set foot on the wards — and he initially failed his final examination in internal medicine.


Sydney Brenner (right) with John Sulston, who both shared the Nobel Prize in Physiology or Medicine with Robert Horvitz in 2002.Credit: Steve Russell/Toronto Star/Getty

In 1952 Brenner won a scholarship to the Department of Physical Chemistry at Oxford. His adviser, Cyril Hinshelwood, wanted to pursue the idea that the environment altered observable characteristics of bacteria. Brenner tried to convince him of the role of genetic mutation. Two years later, with doctorate in hand, Brenner spent the summer of 1954 in the United States visiting labs, including Cold Spring Harbor in New York state. Here he caught up with Watson and Crick again.

Impressed, Crick recruited the young South African to the University of Cambridge, UK, in 1956. In the early 1960s, using just bacteria and bacteriophages, Crick and Brenner deciphered many of the essentials of gene function in a breathtaking series of studies.

Brenner had proved theoretically in the mid-1950s that the genetic code is ‘non-overlapping’ — each nucleotide is part of only one triplet (three nucleotides specify each amino acid in a protein) and successive ‘triplet codons’ are read in order. In 1961, Brenner and Crick confirmed this in the lab. The same year, Brenner, with François Jacob and Matthew Meselson, published their demonstration of the existence of messenger RNA. Over the next two years, often with Crick, Brenner showed how the synthesis of proteins encoded by DNA sequences is terminated.

This intellectual partnership dissolved when Brenner began to focus on whole organisms in the mid-1960s. He finally alighted on Caenorhabditis elegans. Studies of this tiny worm in Brenner’s arm of the legendary Laboratory of Molecular Biology (LMB) in Cambridge led to the Nobel for Brenner, Robert Horvitz and John Sulston.


Maxine Singer, Norton Zinder, Sydney Brenner and Paul Berg (left to right) at the 1975 meeting on recombinant DNA technology in Asilomar, California.Credit: NAS

And his contributions went well beyond the lab. In 1975, with Paul Berg and others, he organized a meeting at Asilomar, California, to draft a position paper on the United States’ use of recombinant DNA technology — introducing genes from one species into another, usually bacteria. Brenner was influential in persuading attendees to treat ethical and societal concerns seriously. He stressed the importance of thoughtful guidelines for deploying the technology to avoid overly restrictive regulation.

He served as director of the LMB for about a decade. Despite describing the experience as the biggest mistake in his life, he took the lab (with its stable of Nobel laureates and distinguished staff) to unprecedented prominence. In 1986, he moved to a new Medical Research Council (MRC) unit of molecular genetics at the city’s Addenbrooke’s Hospital, and began work in the emerging discipline of evolutionary genomics. Brenner also orchestrated Britain’s involvement in the Human Genome Project in the early 1990s.

From the late 1980s, Brenner steered the development of biomedical research in Singapore. Here he masterminded Biopolis, a spectacular conglomerate of chrome and glass buildings dedicated to biomedical research. He also helped to guide the Janelia Farm campus of the Howard Hughes Medical Institute in Ashburn, Virginia, and to restructure molecular biology in Japan.

Brenner dazzled, amused and sometimes offended audiences with his humour, irony and disdain of authority and dogma — prompting someone to describe him as “one of biology’s mischievous children; the witty trickster who delights in stirring things up.” His popular columns in Current Biology (titled ‘Loose Ends’ and, later, ‘False Starts’) in the mid-1990s led some seminar hosts to introduce him as Uncle Syd, a pen name he ultimately adopted.

Sydney was aware of the debt he owed to being in the right place at the right time. He attributed his successes to having to learn scientific independence in a remote part of the world, with few role models and even fewer mentors. He recounted the importance of arriving in Oxford with few scientific biases, and leaving with the conviction that seeing the double helix model one chilly April morning would be a defining moment in his life.

The Brenner laboratories (he often operated more than one) spawned a generation of outstanding protégés, including five Nobel laureates. Those who dedicated their careers to understanding the workings of C. elegans now number in the thousands. Science will be considerably poorer without Sydney. But his name will live forever in the annals of biology.

https://www.nature.com/articles/d41586-019-01192-9

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Remains from Callao Cave in the Philippines, including a foot bone, belong to a new hominin species, Homo luzonensis.Credit: Rob Rownd, UP-ASP Film Inst.

The human family tree has grown another branch, after researchers unearthed remains of a previously unknown hominin species from a cave in the Philippines. They have named the new species, which was probably small-bodied, Homo luzonensis.

The discovery, reported in Nature on 10 April1, is likely to reignite debates over when ancient human relatives first left Africa. And the age of the remains — possibly as young as 50,000 years old — suggests that several different human species once co-existed across southeast Asia.

The first traces of the new species turned up more than a decade ago, when researchers reported the discovery of a foot bone dating to at least 67,000 years old in Callao Cave on the island of Luzon, in the Philippines2. The researchers were unsure which species the bone was from, but they reported that it resembled that of a small Homo sapiens.

Further excavations of Callao Cave uncovered a thigh bone, seven teeth, two foot bones and two hand bones — with features unlike those of other human relatives, contends the team, co-led by Florent Détroit, a palaeoanthropologist at the National Museum of Natural History in Paris. The remains come from at least two adults and one child.

“Together, they create a strong argument that this is something new,” says Matthew Tocheri, a palaeoanthropologist at Lakehead University in Thunder Bay, Canada.

Hominin history
H. luzonensis is the second new human species to be identified in southeast Asia in recent years. In 2004, another group announced the discovery3 of Homo floresiensis — also known as the Hobbit — a species that would have stood just over a metre in height, on the Indonesian island of Flores.

But Détroit and his colleagues argue that the Callao Cave remains are distinct from those of H. floresiensis and other hominins — including a species called Homo erectus thought to have been the first human relative to leave Africa, some 2 million years ago.


Seven hominin teeth, including molars and premolars, were found in Callao Cave.Credit: Callao Cave Archaeology Project

The newly discovered molars are extremely small compared with those of other ancient human relatives. Elevated cusps on the molars, like those in H. sapiens, are not as pronounced as they were in earlier hominins. The shape of the internal molar enamel looks similar to that of both H. sapiens and H. erectus specimens found in Asia. The premolars discovered at Callao Cave are small but still in the range of those of H. sapiens and H. floresiensis. But the authors report that the overall size of the teeth, as well as the ratio between molar and premolar size, is distinct from those of other members of the genus Homo.

The shape of the H. luzonensis foot bones is also distinct. They most resemble those of Australopithecus — primitive hominins, including the famous fossil Lucy, thought not to have ever left Africa. Curves in the toe bones and a finger bone of H. luzonensis suggest that the species might have been adept at climbing trees.


Curves in the toe bones of H. luzonensis may have been adaptations for climbing.Credit: Callao Cave Archaeology Project

The researchers are cautious about estimating H. luzonensis’ height, because there are only a few remains to go on. But given its small teeth, and the foot bone reported in 2010, Détroit thinks that its body size was within the range of small H. sapiens, such as members of some Indigenous ethnic groups living on Luzon and elsewhere in the Philippines today, sometimes known collectively as the Philippine Negritos. Men from these groups living in Luzon have a recorded mean height of around 151 centimetres and the women about 142 centimetres.

The right fit
Researchers are split on how H. luzonensis fits into the human family tree. Détroit favours the view that the new species descends from a H. erectus group whose bodies gradually evolved into forms different from those of their ancestors.

“You get different evolutionary pathways on islands,” says palaeontologist Gerrit van den Bergh at the University of Wollongong in Australia. “We can imagine H. erectus arrives on islands like Luzon or Flores, and no longer needs to engage in endurance running but needs to adapt to spend the night in trees.”

But, given the species’ similarities to Australopithecus, Tocheri wonders whether the Callao Cave dwellers descended from a line that migrated out of Africa before H. erectus.

Genetic material from the remains could help scientists to identify the species’ relationship to other hominins, but efforts to extract DNA from H. luzonensis have failed so far. However, the bones and teeth were dated to at least 50,000 years old. This suggests that the species might have been roaming southeast Asia at the same time as H. sapiens, H. floresiensis and a mysterious group known as the Denisovans, whose DNA has been found in contemporary humans in southeast Asia.

“Island southeast Asia appears to be full of palaeontological surprises that complicate simple scenarios of human evolution,” says William Jungers, a palaeoanthropologist at Stony Brook University in New York.

https://www.nature.com/articles/d41586-019-01152-3?utm_source=Nature+Briefing&utm_campaign=669ddc32b9-briefing-dy-20190411&utm_medium=email&utm_term=0_c9dfd39373-669ddc32b9-44039353

by Antonio Regalado

Human intelligence is one of evolution’s most consequential inventions. It is the result of a sprint that started millions of years ago, leading to ever bigger brains and new abilities. Eventually, humans stood upright, took up the plow, and created civilization, while our primate cousins stayed in the trees.

Now scientists in southern China report that they’ve tried to narrow the evolutionary gap, creating several transgenic macaque monkeys with extra copies of a human gene suspected of playing a role in shaping human intelligence.

“This was the first attempt to understand the evolution of human cognition using a transgenic monkey model,” says Bing Su, the geneticist at the Kunming Institute of Zoology who led the effort.

According to their findings, the modified monkeys did better on a memory test involving colors and block pictures, and their brains also took longer to develop—as those of human children do. There wasn’t a difference in brain size.

The experiments, described on March 27 in a Beijing journal, National Science Review, and first reported by Chinese media, remain far from pinpointing the secrets of the human mind or leading to an uprising of brainy primates.

Instead, several Western scientists, including one who collaborated on the effort, called the experiments reckless and said they questioned the ethics of genetically modifying primates, an area where China has seized a technological edge.

“The use of transgenic monkeys to study human genes linked to brain evolution is a very risky road to take,” says James Sikela, a geneticist who carries out comparative studies among primates at the University of Colorado. He is concerned that the experiment shows disregard for the animals and will soon lead to more extreme modifications. “It is a classic slippery slope issue and one that we can expect to recur as this type of research is pursued,” he says.

Research using primates is increasingly difficult in Europe and the US, but China has rushed to apply the latest high-tech DNA tools to the animals. The country was first to create monkeys altered with the gene-editing tool CRISPR, and this January a Chinese institute announced it had produced a half-dozen clones of a monkey with a severe mental disturbance.

“It is troubling that the field is steamrolling along in this manner,” says Sikela.

Evolution story

Su, a researcher at the Kunming Institute of Zoology, specializes in searching for signs of “Darwinian selection”—that is, genes that have been spreading because they’re successful. His quest has spanned such topics as Himalayan yaks’ adaptation to high altitude and the evolution of human skin color in response to cold winters.

The biggest riddle of all, though, is intelligence. What we know is that our humanlike ancestors’ brains rapidly grew in size and power. To find the genes that caused the change, scientists have sought out differences between humans and chimpanzees, whose genes are about 98% similar to ours. The objective, says, Sikela, was to locate “the jewels of our genome”—that is, the DNA that makes us uniquely human.

For instance, one popular candidate gene called FOXP2—the “language gene” in press reports—became famous for its potential link to human speech. (A British family whose members inherited an abnormal version had trouble speaking.) Scientists from Tokyo to Berlin were soon mutating the gene in mice and listening with ultrasonic microphones to see if their squeaks changed.

Su was fascinated by a different gene, MCPH1, or microcephalin. Not only did the gene’s sequence differ between humans and apes, but babies with damage to microcephalin are born with tiny heads, providing a link to brain size. With his students, Su once used calipers and head spanners to the measure the heads of 867 Chinese men and women to see if the results could be explained by differences in the gene.

By 2010, though, Su saw a chance to carry out a potentially more definitive experiment—adding the human microcephalin gene to a monkey. China by then had begun pairing its sizeable breeding facilities for monkeys (the country exports more than 30,000 a year) with the newest genetic tools, an effort that has turned it into a mecca for foreign scientists who need monkeys to experiment on.

To create the animals, Su and collaborators at the Yunnan Key Laboratory of Primate Biomedical Research exposed monkey embryos to a virus carrying the human version of microcephalin. They generated 11 monkeys, five of which survived to take part in a battery of brain measurements. Those monkeys each have between two and nine copies of the human gene in their bodies.

Su’s monkeys raise some unusual questions about animal rights. In 2010, Sikela and three colleagues wrote a paper called “The ethics of using transgenic non-human primates to study what makes us human,” in which they concluded that human brain genes should never be added to apes, such as chimpanzees, because they are too similar to us. “You just go to the Planet of the Apes immediately in the popular imagination,” says Jacqueline Glover, a University of Colorado bioethicist who was one of the authors. “To humanize them is to cause harm. Where would they live and what would they do? Do not create a being that can’t have a meaningful life in any context.”

In an e-mail, Su says he agrees that apes are so close to humans that their brains shouldn’t be changed. But monkeys and humans last shared an ancestor 25 million years ago. To Su, that alleviates the ethical concerns. “Although their genome is close to ours, there are also tens of millions of differences,” he says. He doesn’t think the monkeys will become anything more than monkeys. “Impossible by introducing only a few human genes,” he says.

Smart monkey?

Judging by their experiments, the Chinese team did expect that their transgenic monkeys could end up with increased intelligence and brain size. That is why they put the creatures inside MRI machines to measure their white matter and gave them computerized memory tests. According to their report, the transgenic monkeys didn’t have larger brains, but they did better on a short-term memory quiz, a finding the team considers remarkable.

Several scientists think the Chinese experiment didn’t yield much new information. One of them is Martin Styner, a University of North Carolina computer scientist and specialist in MRI who is listed among the coauthors of the Chinese report. Styner says his role was limited to training Chinese students to extract brain volume data from MRI images, and that he considered removing his name from the paper, which he says was not able to find a publisher in the West.

“There are a bunch of aspects of this study that you could not do in the US,” says Styner. “It raised issues about the type of research and whether the animals were properly cared for.”

After what he’s seen, Styner says he’s not looking forward to more evolution research on transgenic monkeys. “I don’t think that is a good direction,” he says. “Now we have created this animal which is different than it is supposed to be. When we do experiments, we have to have a good understanding of what we are trying to learn, to help society, and that is not the case here.” One issue is that genetically modified monkeys are expensive to create and care for. With just five modified monkeys, it’s hard to reach firm conclusions about whether they really differ from normal monkeys in terms of brain size or memory skills. “They are trying to understand brain development. And I don’t think they are getting there,” says Styner.

In an e-mail, Su agreed that the small number of animals was a limitation. He says he has a solution, though. He is making more of the monkeys and is also testing new brain evolution genes. One that he has his eye on is SRGAP2C, a DNA variant that arose about two million years ago, just when Australopithecus was ceding the African savannah to early humans. That gene has been dubbed the “humanity switch” and the “missing genetic link” for its likely role in the emergence of human intelligence.

Su says he’s been adding it to monkeys, but that it’s too soon to say what the results are.

https://www.technologyreview.com/s/613277/chinese-scientists-have-put-human-brain-genes-in-monkeysand-yes-they-may-be-smarter/

by MIKE MCRAE

Transforming the microbial environment in the guts of children diagnosed with autism could significantly ease the severity of their condition’s signature traits, according to newly published research.

A study on the effects of a form of faecal transplant therapy in children on the autism spectrum found participants not only experienced fewer gut problems, but continued to show ongoing improvements in autism symptoms two years after the procedure.

Arizona State University researchers had already discovered a dose of healthy gut microflora caused characteristics associated with autism spectrum disorder (ASD) to ease or vanish for at least a couple of months after treatment ended.

But to be taken seriously as a potential therapy, there needed to be long term improvements. So a return to the original group of volunteers for another check-up was in order.

It turned out those new microbes were settling in nicely.

“In our original paper in 2017, we reported an increase in gut diversity together with beneficial bacteria after microbiota transfer therapy (MTT), and after two years, we observed diversity was even higher and the presence of beneficial microbes remained,” says biotechnologist Dae-Wook Kang.

The gut might seem like an odd place to start in developing therapies that assist individuals with a neurological condition such as autism.

But in addition to its defining characteristics of impaired social and communication skills, sensory challenges, and reduced core strength and motor control, for up to half of those with ASD the condition can come with a bunch of gut problems.

“Many kids with autism have gastrointestinal problems, and some studies, including ours, have found that those children also have worse autism-related symptoms,” says environmental engineer Rosa Krajmalnik-Brown.

Previous studies have repeatedly pointed to the potential benefits of swapping out a ‘bad’ microbial communities for a better one, either through using probiotics or courses of antibiotics.

Most showed promising short-term effects, suggesting there was more to be explored when it comes to gut-based therapies.

“In many cases, when you are able to treat those gastrointestinal problems, their behaviour improves,” says Krajmalnik-Brown.

In an attempt to elicit a more long-term result, the researchers pulled out the big guns. Forget dropping in a few microbial tourists or killing off a handful of trouble-makers – they went for a whole mass migration.

Using a customised process of gut microflora transplantation called microbiota transfer therapy, the researchers gave 18 kids aged between 7 and 16 a belly full of new microorganisms.

All of the volunteers had both an autism diagnosis and moderate to severe gastrointestinal problems. This group was compared with 20 equivalent control subjects who had neither gut problems nor an ASD diagnosis.

Both were treated for 10 weeks and then had follow-up test sessions for a further 8 weeks.

Admittedly, the experiment wasn’t blinded, so we do need to be cautious in how we read into the results. Placebo effects can’t be ruled out in cases like this.

But saying they were ‘promising’ isn’t too strong a claim to make. The children not only experienced an 80 percent reduction in gastrointestinal symptoms, they showed significant improvements when tested with common ASD diagnostic tools.

Two years later, those same tests indicate the conditions have only improved.

“The team’s new publication reports that the study demonstrated that two years after treatment stopped the participants still had an average of a 58 percent reduction in GI symptoms compared to baseline,” says Krajmalnik-Brown.

“In addition, the parents of most participants reported a slow but steady improvement in core ASD symptoms.”

An external evaluation using a standard ASD diagnostic tool concluded 83 percent of the initial test group could be considered as severe on the autistic spectrum. Two years later, this dropped to just 17 percent.

Amazingly, 44 percent no longer made the cut-off for being on the mild end of the spectrum at all.

Overall, the evaluator determined the severity of ASD traits was reduced by 47 percent compared with their baseline.

For a therapy that has barely any side-effects, and such remarkable improvements in challenges many with ASD struggle with, it’s surely a treatment that will continue to attract attention for further research.

Faecal transplants might sound a little gross, but you might as well get used to them. We’re bound to be seeing them used for a variety of things in the future, from treating superbugs to winning sports.

Now that we’re learning our neurological health is intimately connected with our digestive system, transplanting microbial communities from a healthy gut is seen as the next big thing in treating brain disorders.

This isn’t to say microflora cause autism. It’s a complex condition that has its roots in a diverse range of genes and environmental influences that nudge the brain’s development early in life.

But if we can swap out even a few of those influences, we just might be able to make life a little easier for those who need it.

This research was published in Scientific Reports.

https://www.sciencealert.com/autism-severity-cut-in-half-in-kids-who-underwent-radical-faecal-transplant-therapy

Summary: Newly identified ‘extinction neurons’ in the hippocampus suppress fearful memories when activated, and allow the memories to return when deactivated. The findings may provide new treatment avenues for PTSD, phobias, and anxiety.

Neuroscientists at The University of Texas at Austin have discovered a group of cells in the brain that are responsible when a frightening memory re-emerges unexpectedly, like Michael Myers in every “Halloween” movie. The finding could lead to new recommendations about when and how often certain therapies are deployed for the treatment of anxiety, phobias and post-traumatic stress disorder (PTSD).

In the new paper, out today in the journal Nature Neuroscience, researchers describe identifying “extinction neurons,” which suppress fearful memories when they are activated or allow fearful memories to return when they are not.

Since the time of Pavlov and his dogs, scientists have known that memories we thought we had put behind us can pop up at inconvenient times, triggering what is known as spontaneous recovery, a form of relapse. What they didn’t know was why it happened.

“There is frequently a relapse of the original fear, but we knew very little about the mechanisms,” said Michael Drew, associate professor of neuroscience and the senior author of the study. “These kinds of studies can help us understand the potential cause of disorders, like anxiety and PTSD, and they can also help us understand potential treatments.”

One of the surprises to Drew and his team was finding that brain cells that suppress fear memories hid in the hippocampus. Traditionally, scientists associate fear with another part of the brain, the amygdala. The hippocampus, responsible for many aspects of memory and spatial navigation, seems to play an important role in contextualizing fear, for example, by tying fearful memories to the place where they happened.

The discovery may help explain why one of the leading ways to treat fear-based disorders, exposure therapy, sometimes stops working. Exposure therapy promotes the formation of new memories of safety that can override an original fear memory. For example, if someone becomes afraid of spiders after being bitten by one, he might undertake exposure therapy by letting a harmless spider crawl on him. The safe memories are called “extinction memories.”

“Extinction does not erase the original fear memory but instead creates a new memory that inhibits or competes with the original fear,” Drew said. “Our paper demonstrates that the hippocampus generates memory traces of both fear and extinction, and competition between these hippocampal traces determines whether fear is expressed or suppressed.”

Given this, recommended practices around the frequency and timing of exposure therapy may need revisiting, and new pathways for drug development may be explored.

In experiments, Drew and his team placed mice in a distinctive box and induced fear with a harmless shock. After that, when one of the mice was in the box, it would display fear behavior until, with repeated exposure to the box without a shock, the extinction memories formed, and the mouse was not afraid.

Scientists were able to artificially activate the fear and suppress the extinction trace memories by using a tool called optogenetics to turn the extinction neurons on and off again.

“Artificially suppressing these so-called extinction neurons causes fear to relapse, whereas stimulating them prevents fear relapse,” Drew said. “These experiments reveal potential avenues for suppressing maladaptive fear and preventing relapse.”

The studies were led by graduate student Anthony Lacagnina of The University of Texas at Austin, with contributions from Emma Brockway, Chelsea Crovetti, Francis Shue, Meredith McCarty and Kevin Sattler of The University of Texas; and Sean Lim, Sofia Leal Santos and Christine Denny of Columbia University.

https://neurosciencenews.com/ptsd-hippocampus-fear-10966/

Beauty might only be skin deep, but for those wondering how to keep that skin young, scientists may have found an answer in the form of a protein that encourages cell competition.

The prosaically named COL17A1 might not sound like a fountain of youth, but the new study suggests it does the heavy lifting when it comes to keeping skin intact and unimpaired.

The protein works by encouraging cell competition, a key process to maintain tissue fitness. That effectively “drives out” weaker cells while encouraging replication of stronger ones.

“Damaged or stressed stem cells can be selectively eliminated by intact stem cells every day in our skin,” said Emi Nishimura, a professor at the Tokyo Medical and Dental University’s Stem Cell Biology department, who led the research.

But ageing results in a depletion of COL17A1, as do familiar enemies of youthful skin, like UV radiation and other stress factors.

And when that happens, weaker cells replicate, leaving the skin thinner, more prone to damage and slower to heal.

The research published Thursday in the journal Nature is based on investigations using mice tails, which share many of the same characteristics as human skin.

After confirming the importance of COL17A1, the team decided to investigate whether they could stimulate the protein once it was depleted—effectively looking for compounds that could kickstart the anti-ageing process in skin.

They isolated two chemical compounds—Y27632 and apocynin—and tested both on skin cells, with positive results.

“Application of these drugs to full-thickness skin wounds significantly promoted wound repair,” the study said.

The two compounds point to ways of “facilitating skin regeneration and reducing skin ageing,” the study added.

In a review of the study commissioned by Nature, two professors from the University of Colorado said cell competition had previously only been studied extensively in fruit flies.

The research “provides evidence that healthy cells in mammals can also efficiently repopulate adult tissues, replacing unfit or damaged cells,” wrote professors Ganna Bilousova and James DeGregori.

And they said the research offered “proof-of-principle” that the two chemical compounds could combat ageing.

“Future studies are needed to determine the mechanisms of cell competition in other tissues, and to identify compounds capable of reversing ageing in other organs,” they said.

Nishimura told AFP that the work could eventually lead to products like creams or tablets that could stop skin deterioration and promote repair.

“We are going to collaborate with pharmaceutical or cosmetic companies for the clinical use of the chemicals,” she said.

She said additional research would investigate whether the same process might also be at work in other parts of the body that have so-called epithelial cells like skin does.

“We are working on other epithelial organs as well to find out (whether) similar competition may underlie long-term tissue maintenance as well as organ ageing,” she said.

https://medicalxpress.com/news/2019-04-young-uncovers-protein-skin-youthful.html

by Carly Cassella

Over a dozen dolphins, stranded on the beaches of Florida and Massachusetts, have been found with brains full of amyloid plaques, a hallmark of Alzheimer’s disease. The scientists who made the discovery think it may be a warning to us all: alongside the Alzheimer’s-like plaques, the team also found the environmental toxin BMAA.

Produced by blue-green algae blooms, this neurotoxin is easily caught up in the ocean food web, and chronic dietary exposure has long been suspected to be a cause of neurological disease, including Alzheimers, Parkinson’s and Amyotrophic Lateral Sclerosis (ALS).

The presence of both BMAA and amyloid plaques in 13 stranded dolphins now adds even more weight to this hypothesis.

“Dolphins are an excellent sentinel species for toxic exposures in the marine environment,” says neurologist Deborah Mash from the University of Miami.

“With increasing frequency and duration of cyanobacterial blooms in coastal waters, dolphins might provide early warning of toxic exposures that could impact human health.”

They might also be a good animal model for how BMAA could trigger Alzheimer’s disease. In 2017, it was discovered that dolphins are the only known wild animal to show signs of this common human disease.

Meanwhile, dolphins that inhabit Florida coastal waters are also commonly exposed to recurring harmful algae blooms (HABs). This might just be a coincidence, but experiments have shown that chronic BMAA dietary exposure can trigger neurodegenerative changes in both humans and non-human primates.

“Acute and chronic exposures to such toxins can be harmful to both humans and animals resulting in respiratory illnesses, severe dermatitis, mucosal damage, cancer, organ failure and death,” the authors write.

As the world warms at a rapid rate, these HABs are only becoming more frequent, and the authors worry that dolphins will accumulate even more BMAA as a result, “both by exposure to HABs and by the ingestion of prey previously exposed to the cyanotoxin”.

As such, these creatures may very well be our first indication of poor environmental conditions, and while it’s still not clear if these blooms directly lead to Alzheimer’s in dolphins or in humans, the researchers say it’s a risk we shouldn’t be willing to take.

“The $64,000 question is whether these marine mammals experienced cognitive deficits and disorientation that led to their beaching,” says co-author Paul Alan Cox, an ethnobotanist at the Brain Chemistry Labs in Jackson Hole.

“Until further research clarifies this question, people should take simple steps to avoid cyanobacterial exposure.”

This study has been published in PLOS ONE.

https://www.sciencealert.com/beached-dolphins-had-alzheimer-s-like-plaques-and-it-s-a-warning-to-us-all