Modern Media Publishing is pleased to announce the inaugural issue of the Wits Journal of Neuroscience*, a new academic journal aiming to connect those in the field of neuroscience and broaden its horizons in South Africa.
The new publication will feature articles from clinician researchers in the fields of neurosurgery, neurology, ophthalmology and ears, nose and throat (ENT). The journal features original research and case reports and MMed articles selected by its distinguished editorial board. It also reports on local neuroscience news and events as well as international research highlights. Readers also get a peek behind the curtain at upcoming research.
Professor John R. Ouma, Head of Department of Neuroscience at Wits said, “The aim of this new journal is to fill a gap that has been existing, wherein there has not hitherto been a common platform for academicians and others interested in neurosciences to come together and share ideas as well as generate new science.
“This journal will be widely circulated within the Neuroscience community of this University and its associated hospitals, and then further afield to sister Universities, hospitals and entities to ensure that the ideas generated and expressed in it achieve the widest exposure and impact.
“We hope you enjoy it, both now, and in future editions.”
*The Wits Journal of Neuroscience is Produced and Distributed on behalf of the Wits Dept of Neuroscience by Modern Media Publishing (Pty) Ltd. They can be contacted on 011-326-4171 or by email on info@modernmedia.co.za
Problems with the brain’s ability to ‘prune’ itself of unnecessary connections may underlie a wide range of mental health disorders that begin during adolescence, according to research published in Nature Medicine.
The findings, from an international collaboration, led by researchers in the UK, China and Germany, may help explain why people are often affected by more than one mental health disorder, and may in future help identify those at greatest risk.
One in seven adolescents (aged 10-19 years old) worldwide experiences mental health disorders, according to the World Health Organization (WHO). Depression, anxiety and behavioural disorders, such as attention deficit hyperactivity disorder (ADHD), are among the leading causes of illness and disability among young people, and adolescents will commonly have more than one mental health disorder.
Many mental health problems emerge during adolescence, such as depression and anxiety, which manifest as ‘internalising’ symptoms, including low mood and worrying. Other conditions such as attention deficit hyperactivity disorder (ADHD) manifest as ‘externalising’ symptoms, such as impulsive behaviour.
Professor Barbara Sahakian from the Department of Psychiatry at the University of Cambridge said: “Young people often experience multiple mental health disorders, beginning in adolescence and continuing – and often transforming – into adult life. This suggests that there’s a common brain mechanism that could explain the onset of these mental health disorders during this critical time of brain development.”
In the study, the researchers say they have identified a characteristic pattern of brain activity among these adolescents, which they have termed the ‘neuropsychopathological factor’, or NP factor for short.
The team examined data from 1,750 adolescents, aged 14 years, from the IMAGEN cohort, a European research project examining how biological, psychological, and environmental factors during adolescence may influence brain development and mental health. In particular, they examined imaging data from brain scans taken while participants took part in cognitive tasks, looking for patterns of brain connectivity – in other words, how different regions of the brain communicate with each other.
Adolescents who experienced mental health problems – regardless of whether their disorder was one of internalising or externalising symptoms, or whether they experienced multiple disorders – showed similar patterns of brain activity. These patterns – the NP factor – were largely apparent in the frontal lobes, the area at the front of the brain responsible for executive function which, among other functions, controls flexible thinking, self-control and emotional behaviour.
The researchers confirmed their findings by replicating them in 1799 participants from the ABCD Study in the USA, a long-term study of brain development and child health, and by studying patients who had received psychiatric diagnoses.
When the team looked at genetic data from the IMAGEN cohort, they found that the NP factor was strongest in individuals who carried a particular variant of the gene IGSF11 that has been previously associated with multiple mental health disorders. This gene is known to play an important role in synaptic pruning, a process whereby unnecessary brain connections – synapses – are discarded. Problems with pruning may particularly affect the frontal lobes, since these regions are the last brain areas to complete development in adolescents and young adults.
Dr Tianye Jia from the Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China and the Institute of Psychiatry, Psychology & Neuroscience, King’s College London, London, UK said: “As we grow up, our brains make more and more connections. This is a normal part of our development. But too many connections risk making the brain inefficient. Synaptic pruning helps ensure that brain activity doesn’t get drowned out in ‘white noise’.
“Our research suggests that when this important pruning process is disrupted, it affects how brain regions talk to each other. As this impact is seen most in the frontal lobes, this then has implications for mental health.”
The researchers say that the discovery of the NP factor could help identify those young people at greatest risk of compounding mental health problems.
Professor Jianfeng Feng from Fudan University in Shanghai, China, and the University of Warwick, UK, said: “We know that many mental health disorders begin in adolescence and that individuals who develop one disorder are at increased risk of developing other disorders, too. By examining brain activity and looking for this NP factor, we might be able to detect those at greatest risk sooner, offering us more opportunity to intervene and reduce this risk.”
A new study suggests that notion of the body and mind being inextricably intertwined is more than mere abstraction: parts of the brain area that control movement are plugged into networks involved in thinking and planning, and in control of involuntary bodily functions such as blood pressure and heartbeat. The findings represent a literal linkage of body and mind in the very structure of the brain, overturning decades of interpretations.
The research, published in the journal Nature, could help explain some baffling phenomena, such as why anxiety causes people to pace; why stimulating the vagus nerve, which regulates internal organ functions such as digestion and heart rate, may alleviate depression; and why people who exercise regularly report a more positive outlook on life.
“People who meditate say that by calming your body with, say, breathing exercises, you also calm your mind,” said first author Evan M. Gordon, PhD, an assistant professor of radiology at Washington University School of Medicine in St. Louis. “Those sorts of practices can be really helpful for people with anxiety, for example, but so far, there hasn’t been much scientific evidence for how it works. But now we’ve found a connection. We’ve found the place where the highly active, goal-oriented ‘go, go, go’ part of your mind connects to the parts of the brain that control breathing and heart rate. If you calm one down, it absolutely should have feedback effects on the other.”
Gordon and senior author Nico Dosenbach, MD, PhD, an associate professor of neurology, did not set out to answer age-old philosophical questions about the relationship between the body and the mind. They set out to verify the long-established map of the areas of the brain that control movement, using modern brain-imaging techniques.
In the 1930s, neurosurgeon Wilder Penfield, MD, mapped such motor areas of the brain by applying small jolts of electricity to the exposed brains of people undergoing brain surgery, and noting their responses. He discovered that stimulating a narrow strip of tissue on each half of the brain causes specific body parts to twitch. Moreover, the control areas in the brain are arranged in the same order as the body parts they direct, with the toes at one end of each strip and the face at the other. Penfield’s map of the motor regions of the brain – depicted as a homunculus, or “little man” – has become a staple of neuroscience textbooks.
Gordon, Dosenbach and colleagues set about replicating Penfield’s work with functional magnetic resonance imaging (fMRI). They recruited seven healthy adults to undergo hours of fMRI brain scanning while resting or performing tasks. From this high-density dataset, they built individualized brain maps for each participant. Then, they validated their results using three large, publicly available fMRI datasets – the Human Connectome Project, the Adolescent Brain Cognitive Development Study and the UK Biobank – which together contain brain scans from about 50 000 people.
To their surprise, they discovered that Penfield’s map wasn’t quite right. Control of the feet was in the spot Penfield had identified. Same for the hands and the face. But interspersed with those three key areas were another three areas that did not seem to be directly involved in movement at all, even though they lay in the brain’s motor area.
Moreover, the nonmovement areas looked different than the movement areas. They appeared thinner and were strongly connected to each other and to other parts of the brain involved in thinking, planning, mental arousal, pain, and control of internal organs and functions such as blood pressure and heart rate. Further imaging experiments showed that while the nonmovement areas did not become active during movement, they did become active when the person thought about moving.
“All of these connections make sense if you think about what the brain is really for,” Dosenbach said. “The brain is for successfully behaving in the environment so you can achieve your goals without hurting or killing yourself. You move your body for a reason. Of course, the motor areas must be connected to executive function and control of basic bodily processes, like blood pressure and pain. Pain is the most powerful feedback, right? You do something, and it hurts, and you think, ‘I’m not doing that again.'”
Dosenbach and Gordon named their newly identified network the Somato (body)-Cognitive (mind) Action Network, or SCAN. To understand how the network developed and evolved, they scanned the brains of a newborn, a 1-year-old and a 9-year-old. They also analysed data that had been previously collected on 9 monkeys. The network was not detectable in the newborn, but it was clearly evident in the 1-year-old and nearly adult-like in the 9-year-old. The monkeys had a smaller, more rudimentary system without the extensive connections seen in humans.
“This may have started as a simpler system to integrate movement with physiology so that we don’t pass out, for example, when we stand up,” Gordon said. “But as we evolved into organisms that do much more complex thinking and planning, the system has been upgraded to plug in a lot of very complex cognitive elements.”
Clues to the existence of a mind-body network have been around for a long time, scattered in isolated papers and inexplicable observations.
“Penfield was brilliant, and his ideas have been dominant for 90 years, and it created a blind spot in the field,” said Dosenbach, who is also an associate professor of biomedical engineering, of paediatrics, occupational therapy, radiology, and psychological & brain sciences. “Once we started looking for it, we found lots of published data that didn’t quite jibe with his ideas, and alternative interpretations that had been ignored. We pulled together a lot of different data in addition to our own observations, and zoomed out and synthesised it, and came up with a new way of thinking about how the body and the mind are tied together.”
Example of 3D imaging of segmented granule cells shown in green and orange, with nuclei in blue and purple respectively, and mitochondria in yellow. A thin connection can be seen between the two cells in blue, with subcompartments attached to the tube containing the mitochondria, shown in pink. Credit: Diego Cordero / Membrane Traffic and Pathogenesis Unit, Institut Pasteur
Over a hundred years after the discovery of the neuron by neuroanatomist Santiago Ramón y Cajal, scientists continue to deepen their knowledge of the brain and its development. Now, scientists detail novel insights into how cells in the outer layers of the brain interact immediately after birth during formation of the cerebellum, the brain region towards the back of the skull. Publishing their results in in Science Advances, the scientists demonstrated a novel type of connection between neural precursor cells via nanotubes, even before synapses form.
In 2009, Chiara Zurzolo’s team from the Institut Pasteur identified a novel mechanism for direct communication between neuronal cells in culture via nanoscopic tunnels, known as tunnelling nanotubes. These are involved in the spread of various toxic proteins that accumulate in the brain during neurodegenerative diseases – but may also be tapped for the treatment of diseases or cancers.
In this new study, the researchers discovered nanoscopic tunnels that connect precursor cells in the brain, more specifically the cerebellum – an area that develops after birth and is important for making postural adjustments to maintain balance – as they mature into neurons. These tunnels, although similar in size, vary in shape from one to another: some contain branches while others don’t, some are enveloped by the cells they connect while others are exposed to their local environment. The authors believe these intercellular connections (ICs) may enable the exchange of molecules that help pre-neuronal cells physically migrate across various layers and reach their final destination as the brain develops.
Intriguingly, ICs share anatomical similarities with bridges formed when cells finish dividing. “ICs could derive from cellular division but persist during cell migration, so this study could shed light on the mechanisms allowing coordination between cell division and migration implicated in brain development. On the other hand, ICs established between cells post mitotically could allow direct exchange between cells beyond the usual synaptic connections, representing a revolution in our understanding of brain connectivity. We show that there are not only synapses allowing communication between cells in the brain, there are also nanotubes,” says Dr Zurzolo, senior author and head of the Membrane Traffic and Pathogenesis Unit (Institut Pasteur/CNRS).
To achieve these discoveries, the researchers used a three-dimensional (3D) electron microscopy method and brain cells from mouse models to study how the brain regions communicate between each other. Very high resolution neural network maps could thus be reconstructed. The 3D cerebellum volume produced and used for the study contains over 2000 cells. “If you really want to understand how cells behave in a three-dimensional environment, and map the location and distribution of these tunnels, you have to reconstruct an entire ecosystem of the brain, which requires extraordinary effort with twenty or so people involved over 4 years,” said the article’s first author Diego Cordero.
To meet the challenges of working with the wide range of cell types the brain contains, the authors used an AI tool to automatically distinguish cortical layers. Furthermore, they developed an open-source program called CellWalker to characterise morphological features of 3D segments. The tissue block was reconstructed from brain section images. This program being made freely available will enable scientists to quickly and easily analyse the complex anatomical information embedded in these types of microscope images.
The next step will be to identify the biological function of these cellular tunnels to understand their role in the development of the central nervous system and in other brain regions, and their function in communication between brain cells in neurodegenerative diseases and cancers.
Dopamine, long associated with pleasure, motivation and reward-seeking, also appears to play an important role in why exercise and other physical efforts feel ‘easy’ to some people and exhausting to others. These are the findings of of a study of people with Parkinson’s disease, which is published in NPG Parkinson’s Disease. Parkinson’s disease is marked by a loss of dopamine-producing cells in the brain over time.
According to the researchers, the findings might eventually lead to more effective ways to help people establish and stick with exercise regimens, new treatments for fatigue associated with depression and many other conditions, and a better understanding of Parkinson’s disease.
“Researchers have long been trying to understand why some people find physical effort easier than others,” says study leader Vikram Chib, Ph.D., associate professor in the Department of Biomedical Engineering at the Johns Hopkins University School of Medicine and research scientist at the Kennedy Krieger Institute. “This study’s results suggest that the amount of dopamine availability in the brain is a key factor.”
Chib explains that after a bout of physical activity, people’s perception and self-reports of the effort they expended varies, and also guides their decisions about undertaking future exertions. Previous studies have shown that people with increased dopamine are more willing to exert physical effort for rewards, but the current study focuses on dopamine’s role in people’s self-assessment of effort needed for a physical task, without the promise of a reward.
For the study, Chib and his colleagues from Johns Hopkins Medicine and the Kennedy Krieger Institute recruited 19 adults diagnosed with Parkinson’s disease, a condition in which neurons in the brain that produce dopamine gradually die off, causing unintended and uncontrollable movements such as tremors, fatigue, stiffness and trouble with balance or coordination.
In Chib’s lab, 10 male volunteers and nine female volunteers with an average age of 67 were asked to perform the same physical task, that of squeezing a hand grip equipped with a sensor, on two different days within four weeks of each other. On one of the days, the patients were asked to take their standard, daily synthetic dopamine medication as they normally would. On the other, they were asked not to take their medication for at least 12 hours prior to performing the squeeze test.
On both days, the patients were initially taught to squeeze a grip sensor at various levels of defined effort, and then were asked to squeeze and report how many units of effort they put forth.
When the participants had taken their regular synthetic dopamine medication, their self-assessments of units of effort expended were more accurate than when they hadn’t taken the drug. They also had less variability in their efforts, showing accurate squeezes when the researchers cued them to squeeze at different levels of effort.
In contrast, when the patients hadn’t taken the medication, they consistently over-reported their efforts, meaning they perceived the task to be physically harder, and had significantly more variability among grips after being cued.
In another experiment, the patients were given a choice between a sure option of squeezing with a relatively low amount of effort on the grip sensor or flipping a coin and taking a chance on having to perform either no effort or a very high level of effort. When these volunteers had taken their medication, they were more willing to take a chance on having to perform a higher amount of effort than when they didn’t take their medication.
A third experiment offered participants the choice between getting a small amount of guaranteed money or, getting either nothing or a higher amount of money on a coin flip. Results showed no difference in the subjects on days when they took their medication and when they did not. This result, researchers say, suggests that dopamine’s influence on risk-taking preferences is specific to physical effort-based decision-making.
Together, Chib says, these findings suggest that dopamine level is a critical factor in helping people accurately assess how much effort a physical task requires, which can significantly affect how much effort they’re willing to put forth for future tasks. For example, if someone perceives that a physical task will take an extraordinary amount of effort, they may be less motivated to do it.
Understanding more about the chemistry and biology of motivation could advance ways to motivate exercise and physical therapy regimens, Chib says. In addition, inefficient dopamine signalling could help explain the pervasive fatigue present in conditions such as depression and long COVID, and during cancer treatments. Currently, he and his colleagues are studying dopamine’s role in clinical fatigue.
University of Helsinki and Taiwanese researchers have found a new way to remove waste from the brain after haemorrhage, using a protein called cerebral dopamine neurotrophic factor (CDNF).
Intracerebral haemorrhage, and bleeding into the brain tissue, is a devastating neurological condition affecting millions of people annually. It has a high mortality rate, with long-term neurological deficits experienced by many survivors. To date, no medication has been identified that supports brain recovery following haemorrhage.
In an international collaboration, researchers from the Brain Repair laboratory, University of Helsinki, together with their Taiwanese colleagues investigated whether CDNF, a protein being currently tested for Parkinson’s disease treatment, could be a potential treatment for brain haemorrhage.
Research suggests that CDBF also has therapeutic effects and enhances immune cell’s response after brain haemorrhage. The authors found that the administration of cerebral dopamine neurotrophic factor accelerates haemorrhagic lesion resolution, reduces brain swelling, and improves functional outcomes in an animal model of brain haemorrhage.
“Surprisingly, we found that cerebral dopamine neurotrophic factor acts on immune cells in the bleeding brain, by increasing anti-inflammatory mediators and suppressing the production of the pro-inflammatory cytokines that are responsible for cell signalling. This is a significant step towards the treatment of injuries caused by brain haemorrhage, for which we currently have no cure,” says Professor Mikko Airavaara, from University of Helsinki.
Dr.Vassileios Stratoulias from the Brain Repair laboratory comments, “It’s interesting to note that after a bleeding episode, the brain contains a lot of waste and debris. Cerebral dopamine neurotrophic factor encourages immune cells in the brain to consume and remove the waste and debris, which is essential for the brain’s recovery!.”
The administration of cerebral dopamine neurotrophic factor also resulted in the alleviation of cell stress in the area that surrounds the haematoma.
Finally, the researchers demonstrated that systemic administration of cerebral dopamine neurotrophic factor promotes scavenging by the brain’s immune cells after brain haemorrhage and has beneficial effects in an animal model of brain haemorrhage.
Over the past fifty years, there have been remarkable claims about the effects of Wolfgang Amadeus Mozart’s music. Reports about alleged symptom-alleviating effects of listening to Mozart’s Sonata KV448 in epilepsy attracted a lot of public attention. However, the empirical validity of the underlying scientific evidence has remained unclear. Now, University of Vienna psychologists Sandra Oberleiter and Jakob Pietschnig show in a new study published in the journal Nature Scientific Reports that there is no evidence for a positive effect of Mozart’s melody on epilepsy.
In the past, Mozart’s music has been associated with numerous ostensibly positive effects on humans, animals, and even microorganisms. For instance, listening to his sonata has been said to increase the intelligence of adults, children, or foetuses in the womb. Even cows were said to produce more milk, and bacteria in sewage treatment plants were said to work better when they heard Mozart’s composition.
However, most of these alleged effects have no scientific basis. The origin of these ideas can be traced back to the long-disproven observation of a temporary increase in spatial reasoning test performance among students after listening to the first movement allegro con spirito of Mozart’s sonata KV448 in D major.
More recently, the Mozart effect experienced a further variation: Some studies reported symptom relief in epilepsy patients after they had listened to KV448. However, a new comprehensive research synthesis by Sandra Oberleiter and Jakob Pietschnig from the University of Vienna, based on all available scientific literature on this topic, showed that there is no reliable evidence for such a beneficial effect of Mozart’s music on epilepsy. They found that this alleged Mozart effect can be mainly attributed to selective reporting, small sample sizes, and inadequate research practices in this corpus of literature. “Mozart’s music is beautiful, but unfortunately, we cannot expect relief from epilepsy symptoms from it” conclude the researchers.
Researchers at Massachusetts General Hospital have discovered a novel molecular mechanism behind the most common forms of acquired hydrocephalus – which could lead to the first non-surgical treatments for the life-threatening disease. Research in animal models uncovered a pathway through which infection or bleeding in the brain triggers inflammation, causing increased production of cerebrospinal fluid (CSF) by the choroid plexus and lead to swelling of the brain ventricles.
“Finding a nonsurgical treatment for hydrocephalus, given the fact neurosurgery is fraught with tremendous morbidity and complications, has been the holy grail for our field,” says Kristopher Kahle, MD, PhD, a paediatric neurosurgeon at MGH and senior author of the study in the journal Cell. “We’ve identified through a genome-wide analytical approach the mechanism that underlies the swelling of the ventricles which occurs after a brain bleed or brain infection in acquired hydrocephalus. We’re hopeful these findings will pave the way for approval of an anti-inflammatory drug to treat hydrocephalus, which could be a game-changer for populations in the US and around the world that don’t have access to surgery.”
Occurring in about 0.2% of births, acquired hydrocephalus is the most common cause of brain surgery in children, though it can affect people at any age. In underdeveloped regions where bacterial infection is the most prevalent form, hydrocephalus is often deadly for children due to the lack of surgical intervention. Brain surgery, where a shunt is implanted to drain fluid from the brain, is the only known treatment. But about half of all shunts in paediatric patients fail within two years of placement, according to the Hydrocephalus Association, requiring repeat neurosurgical operations and a lifetime of brain surgeries.
Pivotal to the process is the choroid plexus, the brain structure that routinely pumps cerebrospinal fluid into the four ventricles of the brain to keep the organ buoyant and injury-free within the skull. An infection or brain bleed, however, can create a dangerous neuroinflammatory response where the choroid plexus floods the ventricles with cerebral spinal fluid and immune cells from the periphery of the brain in a cytokine storm, swelling the brain ventricles.
“Scientists in the past thought that entirely different mechanisms were involved in hydrocephalus from infection and from haemorrhage in the brain,” explains co-author Bob Carter, MD, PhD, chair of the Department of Neurosurgery at MGH. “Dr Kahle’s lab found that the same pathway was involved in both types and that it can be targeted with immunomodulators like rapamycin, a drug that’s been approved by the US Food and Drug Administration for transplant patients who need to suppress their immune system to prevent organ rejection.”
MGH researchers are continuing to explore how rapamycin and other drugs which quell the inflammation seen in acquired hydrocephalus could be repurposed. “What has me most excited is that this noninvasive therapy could provide a way to help young patients who don’t have access to neurosurgeons or shunts,” says Kahle. “No longer would a diagnosis of hydrocephalus be fatal for these children.”
Typically developing infants perceive audio-video synchrony better than high-risk for autism infants, according to new research published in the European Journal of Pediatrics. The research from Rutgers University might enable far earlier autism diagnoses.
If follow-up research demonstrates that most infants who miss unmatched audio and video develop autism spectrum disorder (ASD), physicians may be able to diagnose the condition years earlier – a potentially important step as early treatment strongly predicts better outcomes.
“We’re a long way from validating this as a diagnostic tool, but the results definitely suggest it could be a diagnostic tool,” said senior author Michael Lewis, professor at Rutgers Robert Wood Johnson Medical School.
Lewis and other researchers have long known children with ASD struggle to perceive audio-visual speech as a unified event, and they’ve hypothesised that this difficulty may contribute to social impairments and language deficits in such children.
To study whether these difficulties arise before it’s currently possible to diagnose ASD, generally around age 3, the researchers assembled two groups of infants ages 4 to 24 months, one comprising children whose developmental delays indicate an elevated risk of ASD and the other comprising typically developing children.
The researchers showed that participants from both groups two types of videos with progressively longer time separation between image and sound. The first videos featured a ball making noises as it bounced against a wall. The second showed a woman talking.
When watching videos of the ball, the two groups performed similarly. When watching videos of the woman, however, the differences were stark. Typically, developing children perceive audio-visual gaps that are, on average, a tenth of a second smaller than those perceived by the kids with developmental delays.
Although this result confirmed the researchers’ initial hypothesis, some findings were surprising. The ability to perceive audio-visual mismatch wasn’t associated with vocabulary size in children old enough to have a vocabulary.
If a high percentage of the children who were slowest to identify mismatched audio and video go on to be diagnosed with autism – and the findings are repeated with far more children than the 88 who participated in this study – audio-visual tests might prove a revolutionary diagnostic tool for a condition that’s becoming far more common, Lewis said.
However, scientific validation is just the first step to adoption, he said. Insurers would need to pay for tests, and paediatricians would need to embrace them before they could be used to begin providing support services to children in need.
“Earlier diagnosis won’t allow us to cure ASD anytime soon, but it will allow for the earlier provision of support services that can help such children in areas of weakness and direct them toward areas of strength,” Lewis said. “The goal is to create happy people whose schooling and, eventually, careers are well suited to them, and that’s certainly an achievable goal for most.”
A “biocomputer” powered by human brain cells could be developed within our lifetime, according to an article in the journal Frontiers in Science. The Johns Hopkins University researchers expect such “organoid intelligence” technology to exponentially expand the capabilities of modern computing and create novel fields of study, as well as yielding insights into neurodegenerative diseases.
“Computing and artificial intelligence have been driving the technology revolution but they are reaching a ceiling,” said Thomas Hartung, a professor of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health and Whiting School of Engineering who is spearheading the work. “Biocomputing is an enormous effort of compacting computational power and increasing its efficiency to push past our current technological limits.”
For nearly two decades scientists have used tiny organoids, lab-grown tissue resembling fully grown organs, to experiment on kidneys, lungs, and other organs without resorting to human or animal testing. More recently Hartung and colleagues at Johns Hopkins have been working with brain organoids, orbs the size of a pen dot with neurons and other features that promise to sustain basic functions like learning and remembering.
“This opens up research on how the human brain works,” Hartung said. “Because you can start manipulating the system, doing things you cannot ethically do with human brains.”
Hartung began to grow and assemble brain cells into functional organoids in 2012 using cells from human skin samples reprogrammed into an embryonic stem cell-like state. Each organoid contains about 50 000 cells, about the size of a fruit fly’s nervous system. He now envisions building a futuristic computer with such brain organoids.
Computers that run on this “biological hardware” could in the next decade begin to alleviate energy-consumption demands of supercomputing that are becoming increasingly unsustainable, Hartung said. Even though computers process calculations involving numbers and data faster than humans, brains are much smarter in making complex logical decisions, like telling a dog from a cat.
“The brain is still unmatched by modern computers,” Hartung said. “Frontier, the latest supercomputer in Kentucky, is a $600 million, 6,800-square-feet installation. Only in June of last year, it exceeded for the first time the computational capacity of a single human brain – but using a million times more energy.”
It might take decades before organoid intelligence can power a system as smart as a mouse, Hartung said. But by scaling up production of brain organoids and training them with artificial intelligence, he foresees a future where biocomputers support superior computing speed, processing power, data efficiency, and storage capabilities.
“It will take decades before we achieve the goal of something comparable to any type of computer,” Hartung said. “But if we don’t start creating funding programs for this, it will be much more difficult.”
Medical applications
Organoid intelligence could also revolutionise drug testing research for neurodevelopmental disorders and neurodegeneration, said Lena Smirnova, a Johns Hopkins assistant professor of environmental health and engineering who co-leads the investigations.
“We want to compare brain organoids from typically developed donors versus brain organoids from donors with autism,” Smirnova said. “The tools we are developing towards biological computing are the same tools that will allow us to understand changes in neuronal networks specific for autism, without having to use animals or to access patients, so we can understand the underlying mechanisms of why patients have these cognition issues and impairments.”
To assess the ethical implications of working with organoid intelligence, a diverse consortium of scientists, bioethicists, and members of the public have been embedded within the team.
