Tag: brain

Exploring Leonardo da Vinci’s knowledge of the brain

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Summary: A new study looks at Leonardo da Vinci’s contribution to neuroscience and the advancement of modern sciences.

Source: Profiles, Inc

May 2, 2019, marks the 500th anniversary of Leonardo da Vinci’s death. A cultural icon, artist, engineer and experimentalist of the Renaissance period, Leonardo continues to inspire people around the globe. Jonathan Pevsner, PhD, professor and research scientist at the Kennedy Krieger Institute, wrote an article featured in the April edition of The Lancet titled, “Leonardo da Vinci’s studies of the brain.” In the piece, Pevsner highlights the exquisite drawings and curiosity, dedication and scientific rigor that led Leonardo to make penetrating insights into how the brain functions.

Through his research, Pevsner shares that Leonardo was the first to identify the olfactory nerve as a cranial nerve. He details how Leonardo performed intricate studies on the peripheral nervous system, challenging the findings of earlier authorities and introducing methods centuries earlier than other anatomists and physiologists. Pevsner also delves into Leonardo’s pioneering experiment on the ventricles by replicating his technique of injecting wax to make a cast of the ventricles in the brain to determine their overall shape and size. This further demonstrates Leonardo’s original thinking and advanced intelligence.

“Leonardo’s work reflects the emergence of the modern scientific era and forms a key part of his integrative approach to art and science,” said Pevsner.

“He asked questions about how the brain works in health and in disease. He sought to understand changes in the brain that occur in epilepsy, or why the mental state of a pregnant mother can directly affect the physical well-being of her child. At the Kennedy Krieger Institute, many of us struggle to answer the same questions. While science and technology have advanced at a breathtaking pace, we still need Leonardo’s qualities of passion, curiosity, the ability to visualize knowledge, and clear thinking to guide us forward.”

While Pevsner is viewed as an expert in Leonardo da Vinci, his main profession and passion is research into the molecular basis of childhood and adult brain disorders in his lab at Kennedy Krieger Institute. His lab reported the mutation that causes Sturge-Weber syndrome, and ongoing studies include bipolar disorder, autism spectrum disorder and schizophrenia. He is the author of the textbook, Bioinformatics and Functional Genomics.

Exploring Leonardo da Vinci’s knowledge of the brain

NeuroServo’s portable EEG could become a better way to detect delirium

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by Amirah Al Idrus

When Nicolas Tremblay put three electroencephalogram (EEG) electrodes into a baseball cap, he was trying to build a tool to track focus in children with ADHD. He was pitching the device at a health hackathon last October when a nurse from the Montreal Heart Institute approached him with an idea: What if it could be modified for use in hospitals to diagnose patients with delirium?

Delirium—a sudden state of confusion characterized by reduced awareness of the sufferer’s environment—comes on suddenly and can last from hours to days. The American Delirium Society estimates the condition affects more than 7 million hospitalized Americans each year and, according to a Harvard Health report, delirium is the most common complication of hospitalization in people 65 and older.

Compared to hospitalized patients without delirium, those who suffer delirium tend to stay longer in the hospital and are more likely to develop dementia or other types of cognitive impairment and need long-term care after leaving hospital. Delirium is commonly detected via the Confusion Assessment Method, which helps health professionals identify problems with attention, memory, orientation and visual ability. Essentially, patients are asked a set of questions to assess their mental state. Though the method is standardized, it is not an objective test for the condition. What’s more, this approach doesn’t detect delirium early.

“Current methods are only able to detect delirium when the brain is already malfunctioning,” Tremblay said. “When delirium is detected at a later stage, it takes longer to bring the patient back. It costs a lot to the hospital because they have to keep the patient in hospital to revert delirium.”

NeuroServo set about creating a device to catch attention problems in hospitalized patients early, before these deficits manifest physically. Its educational tool, the electrode-fitted hat, measures electrical activity in the brain and signals attention—or lack thereof—via a built-in light that changes color. The device can also send EEG results via Bluetooth to a tablet app used by a teacher.

With input from doctors and nurses, NeuroServo developed a sterile version of the device, a disposable plastic strip holding three EEG electrodes that can be adhered to the patient’s forehead. It attaches to a portable EEG module that clips onto the patient’s jacket.

Using EEG to detect delirium isn’t a new concept; there is scientific proof that delirium can be found with EEG, Tremblay said. But using a traditional EEG on large numbers of patients just isn’t practical: The equipment is cumbersome, the process can require as many as 256 electrodes placed all over the scalp and a neurologist is needed to interpret the results.

NeuroServo’s device uses several algorithms specialized in a specific area of signal analysis, Tremblay said.

“The sum of these analyses is then used to return an easy-to-read graph and results to the nurse or caregiver,” he said.

As for the number of electrodes, NeuroServo’s electronics and algorithms are designed to obtain the best medical-grade EEG signal out of the forehead. ”This allows us to carefully track brain signals in the prefrontal cortex who is responsible for executive functions like attention control or cognitive flexibility,” Tremblay said.

He hopes to keep serving the educational market even as NeuroServo makes a push into the medtech sector. The company is still selling the cap for kids with ADHD, and the device is currently in a pilot study in France in children with autism spectrum disorder. As for its use as a delirium diagnostic tool, the Montreal Heart Institute is kicking off a pilot study this month. McGill University Health Centre will start a pilot later this year, and NeuroServo is working on a third study at a hospital in Boston.

What comes next depends on the outcome of those studies.

“We are waiting for the pilot results to be able to apply for approval from Health Canada, the FDA and so on,” Tremblay said.

NeuroServo is just one player working to make EEG possible for an area in which it has historically not been viable. Mountain View, California-based Ceribell came up with a portable device that quickly detects nonconvulsive seizures in ICU patients. Like NeuroServo’s device, Ceribell’s system doesn’t require a specialist to read its results—instead, it converts EEG signals into sound for a yes/no diagnosis within minutes.

https://www.fiercebiotech.com/biotech/neuroservo-s-portable-eeg-could-become-a-better-way-to-detect-delirium

Artificial intelligence singles out neurons faster than a human can

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Two-photon imaging shows neurons firing in a mouse brain. Recordings like this enable researchers to track which neurons are firing, and how they potentially correspond to different behaviors. The image is credited to Yiyang Gong, Duke University.

Summary: Convolutional neural network model significantly outperforms previous methods and is as accurate as humans in segmenting active and overlapping neurons.

Source: Duke University

Biomedical engineers at Duke University have developed an automated process that can trace the shapes of active neurons as accurately as human researchers can, but in a fraction of the time.

This new technique, based on using artificial intelligence to interpret video images, addresses a critical roadblock in neuron analysis, allowing researchers to rapidly gather and process neuronal signals for real-time behavioral studies.

The research appeared this week in the Proceedings of the National Academy of Sciences.

To measure neural activity, researchers typically use a process known as two-photon calcium imaging, which allows them to record the activity of individual neurons in the brains of live animals. These recordings enable researchers to track which neurons are firing, and how they potentially correspond to different behaviors.

While these measurements are useful for behavioral studies, identifying individual neurons in the recordings is a painstaking process. Currently, the most accurate method requires a human analyst to circle every ‘spark’ they see in the recording, often requiring them to stop and rewind the video until the targeted neurons are identified and saved. To further complicate the process, investigators are often interested in identifying only a small subset of active neurons that overlap in different layers within the thousands of neurons that are imaged.

This process, called segmentation, is fussy and slow. A researcher can spend anywhere from four to 24 hours segmenting neurons in a 30-minute video recording, and that’s assuming they’re fully focused for the duration and don’t take breaks to sleep, eat or use the bathroom.

In contrast, a new open source automated algorithm developed by image processing and neuroscience researchers in Duke’s Department of Biomedical Engineering can accurately identify and segment neurons in minutes.

“As a critical step towards complete mapping of brain activity, we were tasked with the formidable challenge of developing a fast automated algorithm that is as accurate as humans for segmenting a variety of active neurons imaged under different experimental settings,” said Sina Farsiu, the Paul Ruffin Scarborough Associate Professor of Engineering in Duke BME.

“The data analysis bottleneck has existed in neuroscience for a long time — data analysts have spent hours and hours processing minutes of data, but this algorithm can process a 30-minute video in 20 to 30 minutes,” said Yiyang Gong, an assistant professor in Duke BME. “We were also able to generalize its performance, so it can operate equally well if we need to segment neurons from another layer of the brain with different neuron size or densities.”

“Our deep learning-based algorithm is fast, and is demonstrated to be as accurate as (if not better than) human experts in segmenting active and overlapping neurons from two-photon microscopy recordings,” said Somayyeh Soltanian-Zadeh, a PhD student in Duke BME and first author on the paper.

Deep-learning algorithms allow researchers to quickly process large amounts of data by sending it through multiple layers of nonlinear processing units, which can be trained to identify different parts of a complex image. In their framework, this team created an algorithm that could process both spatial and timing information in the input videos. They then ‘trained’ the algorithm to mimic the segmentation of a human analyst while improving the accuracy.

The advance is a critical step towards allowing neuroscientists to track neural activity in real time. Because of their tool’s widespread usefulness, the team has made their software and annotated dataset available online.

Gong is already using the new method to more closely study the neural activity associated with different behaviors in mice. By better understanding which neurons fire for different activities, Gong hopes to learn how researchers can manipulate brain activity to modify behavior.

“This improved performance in active neuron detection should provide more information about the neural network and behavioral states, and open the door for accelerated progress in neuroscience experiments,” said Soltanian-Zadeh.

Artificial intelligence singles out neurons faster than a human can

Experimental PET scan detects abnormal tau protein in brains of living former NFL players

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CTE is a neurodegenerative disease that has been associated with a history of repetitive head impacts, including those that may or may not be associated with concussion symptoms in American football players. The image is in the public domain.

Summary: PET imaging of former NFL players who exhibited cognitive decline and psychiatric symptoms linked to CTE showed higher levels of tau in areas of the brain associated with the neurodegenerative disease. Using an experimental positron emission tomography (PET) scan, researchers have found elevated amounts of abnormal tau protein in brain regions affected by chronic traumatic encephalopathy (CTE) in a small group of living former National Football League (NFL) players with cognitive, mood and behavior symptoms. The study was published online in the New England Journal of Medicine.

Source: Boston University School of Medicine

The researchers also found the more years of tackle football played (across all levels of play), the higher the tau protein levels detected by the PET scan. However, there was no relationship between the tau PET levels and cognitive test performance or severity of mood and behavior symptoms.

“The results of this study provide initial support for the flortaucipir PET scan to detect abnormal tau from CTE during life. However, we’re not there yet,” cautioned corresponding author Robert Stern, PhD, professor of neurology, neurosurgery and anatomy and neurobiology at Boston University School of Medicine (BUSM). “These results do not mean that we can now diagnose CTE during life or that this experimental test is ready for use in the clinic.”

CTE is a neurodegenerative disease that has been associated with a history of repetitive head impacts, including those that may or may not be associated with concussion symptoms in American football players. At this time, CTE can only be diagnosed after death by a neuropathological examination, with the hallmark findings of the build-up of an abnormal form of tau protein in a specific pattern in the brain. Like Alzheimer’s disease (AD), CTE has been suggested to be associated with a progressive loss of brain cells. In contrast to AD, the diagnosis of CTE is based in part on the pattern of tau deposition and a relative lack of amyloid plaques.

The study was conducted in Boston and Arizona by a multidisciplinary group of researchers from BUSM, Banner Alzheimer’s Institute, Mayo Clinic Arizona, Brigham and Women’s Hospital and Avid Radiopharmaceuticals. Experimental flortaucipir PET scans were used to assess tau deposition and FDA-approved florbetapir PET scans were used to assess amyloid plaque deposition in the brains of 26 living former NFL players with cognitive, mood, and behavior symptoms (ages 40-69) and a control group of 31 same-age men without symptoms or history of traumatic brain injury. Results showed that the tau PET levels were significantly higher in the former NFL group than in the controls, and the tau was seen in the areas of the brain which have been shown to be affected in post-mortem cases of neuropathologically diagnosed CTE.

Interestingly, the former player and control groups did not differ in their amyloid PET measurements. Indeed, only one former player had amyloid PET measurements comparable to those seen in Alzheimer’s disease.

“Our findings suggest that mild cognitive, emotional, and behavioral symptoms observed in athletes with a history of repetitive impacts are not attributable to AD, and they provide a foundation for additional research studies to advance the scientific understanding, diagnosis, treatment, and prevention of CTE in living persons, said co-author, Eric Reiman, MD, Executive Director of Banner Alzheimer’s Institute in Phoenix, Arizona. “More research is needed to draw firm conclusions, and contact sports athletes, their families, and other stakeholders are waiting.

With support from NIH, the authors are working with additional researchers to conduct a longitudinal study called the DIAGNOSE CTE Research Project in former NFL players, former college football players, and persons without a history of contact sports play to help address these and other important questions. Initial results of that study are expected in early 2020.

Experimental PET scan detects abnormal tau protein in brains of living former NFL players

Your Blood Type May Help Protect You From Cognitive Decline

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Findings indicate that smaller volumes of grey matter are associated with non-‘O’ blood types. Image credit: The researchers.

A pioneering study conducted by leading researchers at the University of Sheffield has revealed blood types play a role in the development of the nervous system and may cause a higher risk of developing cognitive decline.

The research, carried out in collaboration with the IRCCS San Camillo Hospital Foundation in Venice, shows that people with an ‘O’ blood type have more grey matter in their brain, which helps to protect against diseases such as Alzheimer’s, than those with ‘A’, ‘B’ or ‘AB’ blood types.

Research fellow Matteo De Marco and Professor Annalena Venneri, from the University’s Department of Neuroscience, made the discovery after analysing the results of 189 Magnetic Resonance Imaging (MRI) scans from healthy volunteers.

The researchers calculated the volumes of grey matter within the brain and explored the differences between different blood types.

The results, published in The Brain Research Bulletin, show that individuals with an ‘O’ blood type have more grey matter in the posterior proportion of the cerebellum.

In comparison, those with ‘A’, ‘B’ or ‘AB’ blood types had smaller grey matter volumes in temporal and limbic regions of the brain, including the left hippocampus, which is one of the earliest part of the brain damaged by Alzheimer’s disease.

These findings indicate that smaller volumes of grey matter are associated with non-‘O’ blood types.

As we age a reduction of grey matter volumes is normally seen in the brain, but later in life this grey matter difference between blood types will intensify as a consequence of ageing.

“The findings seem to indicate that people who have an ‘O’ blood type are more protected against the diseases in which volumetric reduction is seen in temporal and mediotemporal regions of the brain like with Alzheimer’s disease for instance,” said Matteo DeMarco.

“However additional tests and further research are required as other biological mechanisms might be involved.”

Professor Annalena Venneri added: “What we know today is that a significant difference in volumes exists, and our findings confirm established clinical observations. In all likelihood the biology of blood types influences the development of the nervous system. We now have to understand how and why this occurs.”

Your Blood Type May Help Protect You From Cognitive Decline

Parkinson’s May Begin in Gut and Spread to the Brain Via the Vagus Nerve

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The research has presented strong evidence that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain. Many patients have also suffered from gastrointestinal symptoms before the Parkinson’s diagnosis is made. The image is for illustrative purposes only.

A major epidemiological registry-based study from Aarhus University and Aarhus University Hospital indicates that Parkinson’s disease begins in the gastrointestinal tract; the study is the largest in the field so far.

The chronic neurodegenerative Parkinson’s disease affects an increasing number of people. However, scientists still do not know why some people develop Parkinson’s disease. Now researchers from Aarhus University and Aarhus University Hospital have taken an important step towards a better understanding of the disease.

New research indicates that Parkinson’s disease may begin in the gastrointestinal tract and spread through the vagus nerve to the brain.

“We have conducted a registry study of almost 15,000 patients who have had the vagus nerve in their stomach severed. Between approximately 1970-1995 this procedure was a very common method of ulcer treatment. If it really is correct that Parkinson’s starts in the gut and spreads through the vagus nerve, then these vagotomy patients should naturally be protected against developing Parkinson’s disease,” explains postdoc at Aarhus University Elisabeth Svensson on the hypothesis behind the study.

A hypothesis that turned out to be correct:

“Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson’s disease. Their risk was halved after 20 years. However, patients who had only had a small part of the vagus nerve severed were not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain,” she says.

The research project has just been published in the internationally recognised journal Annals of Neurology.

The first clinical examination

The research has presented strong evidence that Parkinson’s disease begins in the gastrointestinal tract and spreads via the vagus nerve to the brain. Many patients have also suffered from gastrointestinal symptoms before the Parkinson’s diagnosis is made.

“Patients with Parkinson’s disease are often constipated many years before they receive the diagnosis, which may be an early marker of the link between neurologic and gastroenterologic pathology related to the vagus nerve ,” says Elisabeth Svensson.

Previous hypotheses about the relationship between Parkinson’s and the vagus nerve have led to animal studies and cell studies in the field. However, the current study is the first and largest epidemiological study in humans.

The research project is an important piece of the puzzle in terms of the causes of the disease. In the future the researchers expect to be able to use the new knowledge to identify risk factors for Parkinson’s disease and thus prevent the disease.

“Now that we have found an association between the vagus nerve and the development of Parkinson’s disease, it is important to carry out research into the factors that may trigger this neurological degeneration, so that we can prevent the development of the disease. To be able to do this will naturally be a major breakthrough,” says Elisabeth Svensson.

Parkinson’s May Begin in Gut and Spread to the Brain Via the Vagus Nerve

Empathy in rats shown with discovery of mirror neurons

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Summary: Study reports the anterior cingulate cortex of rats contain mirror neurons that respond to pain experienced by and observations of others.

Source: KNAW

Why is it that we can get sad when we see someone else crying? Why is it that we wince when a friend cuts his finger? Researchers from the Netherlands Institute for Neuroscience have found that the rat brain activates the same cells when they observe the pain of others as when they experience pain themselves. In addition, without the activity of these “mirror neurons”, the animals no longer share the pain of others. As many psychiatric disorders are characterized by a lack of empathy, finding the neural basis for sharing the emotions of others, and being able to modify how much an animal shares the emotions of others, is an exciting step towards understanding empathy and these disorders. The findings will be published in the leading journal Current Biology on April 11th.

Human neuroimaging studies have shown that when we experience pain ourselves, we activate a region of the brain called “the cingulate cortex”. When we see someone else in pain, we reactivate the same region.

On the basis of this, researchers formulated two speculations: (a) the cingulate cortex contains mirror neurons, i.e. neurons that trigger our own feeling of pain and are reactivated when we see the pain of others, and (b) that this is the reason why we wince and feel pain while seeing the pain of others. This intuitively plausible theory of empathy, however, remained untested because it is not possible to record the activity of individual brain cells in humans. Moreover, it is not possible to modulate brain activity in the human cingulate cortex to determine whether this brain region is responsible for empathy.

Rat shares emotions of others

For the first time, researchers at the Netherlands Institute for Neuroscience were able to test the theory of empathy in rats. They had rats look at other rats receiving an unpleasant stimulus (mild shock), and measured what happened with the brain and behavior of the observing rat. When rats are scared, their natural reaction is to freeze to avoid being detected by predators. The researchers found that the rat also froze when it observed another rat exposed to an unpleasant situation.

This finding suggests that the observing rat shared the emotion of the other rat. Corresponding recordings of the cingulate cortex, the very region thought to underpin empathy in humans, showed that the observing rats activated the very neurons in the cingulate cortex that also became active when the rat experienced pain himself in a separate experiment. Subsequently, the researchers suppressed the activity of cells in the cingulate cortex through the injection of a drug. They found that observing rats no longer froze without activity in this brain region.

Same region in rats and humans

This study shows that the brain makes us share the pain of others by activating the same cells that trigger our own pain. So far, this had never been shown for emotions – so-called mirror neurons had only been found in the motor system. In addition, this form of pain empathy can be suppressed by modifying activity in the cingulate cortex.

“What is most amazing”, says Prof. Christian Keysers, the lead author of the study, “is that this all happens in exactly the same brain region in rats as in humans. We had already found in humans, that brain activity of the cingulate cortex increases when we observe the pain of others unless we are talking about psychopathic criminals, who show a remarkable reduction of this activity.” The study thus sheds some light on these mysterious psychopathological disorders. “It also shows us that empathy, the ability to feel with the emotions of others, is deeply rooted in our evolution. We share the fundamental mechanisms of empathy with animals like rats. Rats had so far not always enjoyed the highest moral reputation. So next time, you are tempted to call someone “a rat”, it might be taken as a compliment…”

I feel you: Emotional mirror neurons found in the rat

If You Get the Chills From Music, You May Have a Unique Brain With Particularly Strong Ability to Experience Intense Emotions

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ummary: Researchers report on why some people experience more intense emotions while listening to music.

Source: USC.

When Alissa Der Sarkissian hears the song “Nude” by Radiohead, her body changes.

“I sort of feel that my breathing is going with the song, my heart is beating slower and I’m feeling just more aware of the song — both the emotions of the song and my body’s response to it,” said Der Sarkissian, a research assistant at USC’s Brain and Creativity Institute, based at the USC Dornsife College of Letters, Arts and Sciences.

Der Sarkissian is a friend of Matthew Sachs, a PhD student at USC who published a study last year investigating people like her, who get the chills from music.

The study, done while he was an undergraduate at Harvard University, found that people who get the chills from music actually have structural differences in the brain. They have a higher volume of fibers that connect their auditory cortex to the areas associated with emotional processing, which means the two areas communicate better.

“The idea being that more fibers and increased efficiency between two regions means that you have more efficient processing between them,” he said.

People who get the chills have an enhanced ability to experience intense emotions, Sachs said. Right now, that’s just applied to music because the study focused on the auditory cortex. But it could be studied in different ways down the line, Sachs pointed out.

Sachs studies psychology and neuroscience at USC’s Brain and Creativity Institute, where he’s working on various projects that involve music, emotions and the brain.

If You Get the Chills From Music, You May Have a Unique Brain

Chinese scientists have put human brain genes in monkeys—and yes, they may be smarter

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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/

Fecal Transplant Therapy in Kids Has Reduced Their Autism Severity by 47%

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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