TL;DR
- By tuning into a subset of brain waves, researchers have dramatically reduced the power requirements of neural interfaces while improving their accuracy — a discovery that could lead to long-lasting brain implants that can both treat neurological diseases and enable mind-controlled prosthetics and machines.
- The scientists who developed the first 3D multicellular brain organoid with a functional blood brain barrier now report that the model could be a promising platform to screen drugs that could work to control inflammation, which is at the center of many neurological conditions, like ischemic stroke.
- What if we were able to modify the negative effect of a returning memory that makes us afraid? A research group from the University of Bologna succeeded in this and developed a new non-invasive experimental protocol.
- A new study has shown that humans, mice and flies share the same fundamental genetic mechanisms that regulate the formation and function of brain areas involved in attention and movement control.
- Our brains have an upper limit on how much they can process at once due to a constant but limited energy supply, according to a new study using a brain imaging method that measures cellular metabolism.
- Researchers sought to determine whether a comprehensive and personalized program, designed to mitigate risk factors of Alzheimer’s disease could improve cognitive and metabolic function in individuals experiencing cognitive decline. Findings provided evidence that this approach can improve risk factor scores and stabilize cognitive function.
- Children who suffer trauma from abuse or violence early in life show biological signs of aging faster than children who have never experienced adversity, according to new research. The study examined three different signs of biological aging — early puberty, cellular aging and changes in brain structure — and found that trauma exposure was associated with all three.
- When we say someone has a quick mind, it may be in part thanks to our expanded cerebellum that distinguishes human brains from those of macaque monkeys, for example. High-resolution imaging shows the cerebellum is 80 percent of the area of the cortex, indicating it has grown as human behavior and cognition evolved.
- “Julich-Brain” is the name of the first 3D-atlas of the human brain that reflects the variability of the brain’s structure with microscopic resolution. The atlas features close to 250 structurally distinct areas, each one based on the analysis of 10 brains. German researchers led by Prof. Katrin Amunts have now presented the new brain atlas in the renowned journal Science.
- An early blood test could detect which babies deprived of oxygen at birth are at risk of serious neurodisabilities like cerebral palsy and epilepsy.
- Music training does not have a positive impact on children’s cognitive skills, such as memory, and academic achievement, such as maths, reading or writing, according to a study published in Memory & Cognition.
- Common green apple flavorant farnesene enhances nicotine reward in mouse models. The flavorant is also rewarding on its own. Researchers say with or without nicotine, flavored vapes, especially those containing farnesene, pose potential neurological risks, including addiction.
- …And more!
Neuroscience market
The global neuroscience market size was valued at USD 28.4 billion in 2016 and it is expected to reach USD 38.9 billion by 2027.
Latest researches
A low-power band of neuronal spiking activity dominated by local single units improves the performance of brain-machine interfaces
by Nason et al. in Nature Biomedical Engineering
By tuning into a subset of brain waves, University of Michigan researchers have dramatically reduced the power requirements of neural interfaces while improving their accuracy — a discovery that could lead to long-lasting brain implants that can both treat neurological diseases and enable mind-controlled prosthetics and machines.
The team, led by Cynthia Chestek, associate professor of biomedical engineering and core faculty at the Robotics Institute, estimated a 90% drop in power consumption of neural interfaces by utilizing their approach.
“Currently, interpreting brain signals into someone’s intentions requires computers as tall as people and lots of electrical power — several car batteries worth,” said Samuel Nason, first author of the study and a Ph.D. candidate in Chestek’s Cortical Neural Prosthetics Laboratory. “Reducing the amount of electrical power by an order of magnitude will eventually allow for at-home brain-machine interfaces.”
Neurons, the cells in our brains that relay information and action around the body, are noisy transmitters. The computers and electrodes used to gather neuron data are listening to a radio stuck in between stations. They must decipher actual content amongst the brain’s buzzing. Complicating this task, the brain is a firehose of this data, which increases the power and processing beyond the limits of safe implantable devices.
Currently, to predict complex behaviors such as grasping an item in a hand from neuron activity, scientists can use transcutaneous electrodes, or direct wiring through the skin to the brain. This is achievable with 100 electrodes that capture 20,000 signals per second, and enables feats such as reenabling an arm that was paralyzed or allowing someone with a prosthetic hand to feel how hard or soft an object is. But not only is this approach impractical outside of the lab environment, it also carries a risk of infection.
Some wireless implants, created using highly efficient, application-specific integrated circuits, can achieve almost equal performance as the transcutaneous systems. These chips can gather and transmit about 16,000 signals per second. However, they have yet to achieve consistent operation and their custom-built nature is a roadblock in getting approval as safe implants compared to industrial-made chips.
“This is a big leap forward,” Chestek said. “To get the high bandwidth signals we currently need for brain machine interfaces out wirelessly would be completely impossible given the power supplies of existing pacemaker-style devices.”
To reduce power and data needs, researchers compress the brain signals. Focusing on neural activity spikes that cross a certain threshold of power, called threshold crossing rate or TCR, means less data needs to be processed while still being able to predict firing neurons. However, TCR requires listening to the full firehose of neuron activity to determine when a threshold is crossed, and the threshold itself can change not only from one brain to another but in the same brain on different days. This requires tuning the threshold, and additional hardware, battery and time to do so.
Compressing the data in another way, Chestek’s lab dialed in to a specific feature of neuron data: spiking-band power. SBP is an integrated set of frequencies from multiple neurons, between 300 and 1,000 Hz. By listening only to this range of frequencies and ignoring others, taking in data from a straw as opposed to a hose, the team found a highly accurate prediction of behavior with dramatically lower power needs.
Compared to transcutaneous systems, the team found the SBP technique to be just as accurate while taking in one-tenth as many signals, 2,000 versus 20,000 signals per second. Compared to other methods such as using a threshold crossing rate, the team’s approach not only requires much less raw data, but is also more accurate at predicting neuron firing, even among noise, and does not require tuning a threshold.
The team’s SBP method solves another problem limiting an implant’s useful life. Over time, an interfaces’ electrodes fail to read the signals among noise. However, because the technique performs just as well when a signal is half of what is required from other techniques like threshold crossings, implants could be left in place and used longer.
While new brain-machine interfaces can be developed to take advantage of the team’s method, their work also unlocks new capabilities for many existing devices by reducing the technical requirements to translate neurons to intentions.
Multicellular 3D Neurovascular Unit Model for Assessing Hypoxia and Neuroinflammation Induced Blood-Brain Barrier Dysfunction
by Goodwell Nzou, Robert T. Wicks, Nicole R. VanOstrand, Gehad A. Mekky, Stephanie A. Seale, Aya EL-Taibany, Elizabeth E. Wicks, Carl M. Nechtman, Eric J. Marotte, Vishruti S. Makani, Sean V. Murphy, M. C. Seeds, John D. Jackson, Anthony J. Atala in Scientific Reports
The scientists who developed the first 3D multicellular brain organoid with a functional blood brain barrier now report that the model could be a promising platform to screen drugs that could work to control inflammation, which is at the center of many neurological conditions, like ischemic stroke.
Wake Forest Institute for Regenerative Medicine (WFIRM) scientists first published in 2018 that they had developed the 3D brain organoid — the first engineered tissue equivalent to closely resemble normal human brain anatomy containing all six major cell types found in normal organs including neurons and immune cells. They reported that the organoids promoted the formation of a fully cell-based, natural and functional barrier — the blood brain barrier — that mimics normal human anatomy. The blood brain barrier (BBB) is a semipermeable membrane that separates the circulating blood from the brain, protecting it from foreign substances that could cause injury.
“It is well known that inflammation is at the center of many neurological conditions,” said Goodwell Nzou, PhD., a co-author of the study. “Our results here implicate inflammation as one of the causes of blood brain barrier dysfunction. These organoids can help us gain understanding of some of the brain physiological changes that happen as the result of a stroke.”
For this study, the 3D brain organoid was used to model the effects of oxygen deprivation and inflammation on blood brain barrier function to better understand what is happening in a human brain during an ischemic stroke. The team evaluated the expression levels of proteins critical in BBB maintenance, basement membrane proteins, tight junction proteins, and BBB transport proteins, finding significant changes that may contribute to BBB dysfunction. The research shows how the BBB becomes leaky and allows blood-born components to easily cross the barrier.
“The work demonstrates how important this model is to further understanding of disease mechanisms at the BBB, the passage of drugs through the barrier, and the effects of drugs once they cross the barrier,” said Anthony Atala, MD, senior author and director of WFIRM. “We can also optimize the model for personalized medicine. An organoid containing patient derived cells to identify therapeutic targets that are specific to the individual could be tested with different drugs to determine efficacy which will result in better outcomes for patients.”
Hypoxia induced permeability and cell death. (A) Zo-1 staining around the organoid showing complete BBB coverage around the organoids. Cell viability was assessed using calcein AM (green- live cells) and ethidium homodimer 1 (red- dead cells) (B). The number of cells per organoid under both normoxic and hypoxic condition was determined by pooling 24 organoids into an eppendorf tube. Cell suspensions were obtained by dissociating the organoids with dispase. The cells were subsequently counted, and the data is shown in ©. Protein levels for six groups containing 80 organoids each were obtained from six randomly chosen plates and total protein levels were determined by BCA assay in (D). In (E), 10 organoids were used in each group and 5 randomly chosen organoids were imaged. The results show increased permeability of labeled albumin (red) and FITC labeled IgG (green) into organoids post hypoxic culture conditions compared to no penetration of these proteins under normoxic conditions. Pre-hypoxia represents organoids from the same batch that were pooled and assessed for albumin and IgG permeability prior to culturing under hypoxic condition. Images shown are middle slices of the z-stack confocal image. Fluorescence of albumin was quantified in 4 organoids under normoxic condition and post hypoxia as illustrated in F. (G) Shows the individual slices across the organoid and (H) the quantification of fluorescent albumin density from (E) within the organoid of each slice. Student T-Test, two tailed hypotheses, *P < 0.05. Data represented as mean ±SEM. Scale bars 200 μm.
State-Dependent TMS over Prefrontal Cortex Disrupts Fear-Memory Reconsolidation and Prevents the Return of Fear
by Borgomaneri, S., Battaglia, S., Garofalo, S., Tortora, F., Avenanti, A., & Pellegrino, G. di. in Current Biology
What if we were able to modify the negative effect of a returning memory that makes us afraid? A research group from the University of Bologna succeeded in this and developed a new non-invasive experimental protocol. The result of this study (to be found in the journal Current Biology) is an innovative protocol that combines fear conditioning — a stimulus associated with something unpleasant, that induces a negative memory — and the neurostimulation of a specific site of the prefrontal cortex.
This process alters the perception of an unpleasant (aversive) event so that it will no longer induce fear. “This experimental protocol combining transcranial stimulation and memory reconsolidation allowed us to modify an aversive memory that the participants had learned the day before”, explains Sara Borgomaneri, researcher at the University of Bologna and first author of the study. “This result has relevant repercussions for understanding how memory works. It might even lead to the development of new therapies to deal with traumatic memories”.
The primary focus of the research group is the process of reconsolidation. This process maintains, strengthens, and alters those events that are already stored in our long-term memory. “Every time an event is recalled in our memory, there is a limited period of time in which it can be altered”, explains Simone Battaglia, researcher and co-author of this study. “The protocol we developed exploits this short time window and can, therefore, interfere with the reconsolidation process of learned aversive memories”.
Researchers used TMS (Transcranial Magnetic Stimulation) to “erase” the fear induced by a negative memory. With an electromagnetic coil placed on the head of the participant, TMS creates magnetic fields that can alter the neural activity of specific brain areas. TMS is a non-invasive procedure that does not require surgery or any action on the participant and for this reason is widespread in research as well as in clinic and rehabilitation programmes.
“With TMS, we could alter the functioning of the prefrontal cortex, which proved to be fundamental in the reconsolidation process of aversive memories” says Sara Borgomaneri. “Thanks to this procedure, we obtained results that, until now, were only possible by delivering drugs to patients”.
The research group developed this protocol through a trial involving 98 healthy people. Every participant had learned an aversive memory and the next day underwent a TMS session over the prefrontal cortex.
“First, we created the aversive memory by combining an unpleasant stimulation with some images”, explains Borgomaneri. “The day after, we presented a group of participants with the same stimulus, which, in their memory, was recorded as aversive. Using TMS immediately afterwards, we interfered with their prefrontal cortex activity”.
To test the effectiveness of the protocol, other groups of participants underwent TMS without their aversive memory to be recalled (no reconsolidation was triggered), and some other groups were stimulated with TMS in control brain areas, not involved in memory reconsolidation.
At that point, the only thing left to do for researchers was to evaluate the effectiveness of TMS. They waited for another day and once again tested how the participants reacted when the aversive memory was recalled. And they obtained encouraging results. Participants who had their prefrontal cortex activity inhibited by TMS showed a reduced psycho-physiological response to the unpleasant stimulus. They remembered the event (explicit memory) but its negative effect was substantially reduced.
Ancestral regulatory mechanisms specify conserved midbrain circuitry in arthropods and vertebrates
by Bridi et al. in PNAS
A new study led by researchers from King’s College London has shown that humans, mice and flies share the same fundamental genetic mechanisms that regulate the formation and function of brain areas involved in attention and movement control.
With these new findings scientists can potentially better understand the subtle changes that can occur in genes and brain circuits that can lead to mental health disorders such as anxiety and autism spectrum disorders.
Although physically very different, research has found that the brains of flies, mice and humans are similar in how they form and how they function. Data has shown that the genetic mechanisms that underlie the brain development of insects and mammals are very similar but this can be interpreted in two different ways, where some believe it provides evidence of one single ancestor for both mammals and insects and others think it could support the theory that brains evolved multiple times independently.
“To my knowledge this is the first study that provides evidence of the source of similarities between human and fly brains, how they form and how they function,” said senior author on the study, Dr Frank Hirth from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN), King’s College London.
He continued, “Our research shows that the brain circuits essential for coordinated behaviour are put in place by similar mechanisms in humans, flies and mice. This indicates that the evolution of their very different brains can be traced back to a common ancestral brain more than a half billion years ago.”
This collaborative study between King’s College London, University of Arizona, University of Leuven and Leibniz Institute DSMZ has provided strong evidence that the mechanisms that regulate genetic activity required for the formation of brain areas important to control behavior, is the same for insects and mammals.
Most strikingly they have demonstrated that when these regulatory mechanisms are inhibited or impaired in insects and mammals they experience very similar behavioral problems. This indicates that the same building blocks that control the activity of genes are essential to both the formation of brain circuits and the behavior-related functions they perform. According to the researchers this provides evidence that these mechanisms have been established in one common ancestor.
“The jigsaw puzzle of how the brain evolved still lacks an image on the box, but the pieces currently being added suggest a very early origin of essential circuits that, over an immense span of time have been maintained, albeit with modification, across the great diversity of brains we see today,” said Nicholas Strausfeld, Regents Professor of Neuroscience at the University of Arizona and a co-author on the study.
The study focused on those areas of the brain known as the deutocerebral-tritocerebral boundary (DTB) in flies and the midbrain-hindbrain boundary (MHB) in vertebrates including humans. Using genomic data, researchers identified the genes that play a major role in the formation of the brain circuits that are responsible for basic motion in the DTB in flies and MHB in humans. They then ascertained the parts of the genome that control when and where these genes are expressed, otherwise known as cis-regulatory elements.
The researchers found that these cis-regulatory elements are very similar in flies, mice and humans, indicating that they share the same fundamental genetic mechanism by which these brain areas develop. By manipulating the relevant genomic regions in flies so they no longer regulate the genes appropriately, the researchers showed a subsequent impairment in behavior. This corresponds to findings from research with people where mutations in gene regulatory sequences or the regulated genes themselves have been associated with behavioral problems including anxiety and autism spectrum disorders.
“For many years researchers have been trying to find the mechanistic basis behind behaviour and I would say that we have discovered a crucial part of the jigsaw puzzle by identifying these basic genetic regulatory mechanisms required for midbrain circuit formation and function,” said Hirth.
“If we can understand these very small, very basic building blocks, how they form and function, this will help find answers to what happens when things go wrong at a genetic level to cause these disorders.”
Attention and capacity limits in perception: A cellular metabolism account
by Merit Bruckmaier, Ilias Tachtsidis, Phong Phan, Nilli Lavie in The Journal of Neuroscience
Our brains have an upper limit on how much they can process at once due to a constant but limited energy supply, according to a new study using a brain imaging method that measures cellular metabolism.
The study, published in the Journal of Neuroscience, found that paying attention can change how the brain allocates its limited energy; as the brain uses more energy in processing what we attend to, less energy is supplied to processing outside our attention focus.
Explaining the research, senior author Professor Nilli Lavie (UCL Institute of Cognitive Neuroscience) said:
“It takes a lot of energy to run the human brain. We know that the brain constantly uses around 20% of our metabolic energy, even while we rest our mind, and yet it’s widely believed that this constant but limited supply of energy does not increase when there is more for our mind to process.
“If there’s a hard limit on energy supply to the brain, we suspected that the brain may handle challenging tasks by diverting energy away from other functions, and prioritising the focus of our attention.
“Our findings suggest that the brain does indeed allocate less energy to the neurons that respond to information outside the focus of our attention when our task becomes harder. This explains why we experience inattentional blindness and deafness even to critical information that we really want to be aware of.”
The research team of cognitive neuroscientists and biomedical engineers measured cerebral metabolism with a non-invasive optical imaging method. In this way they could see how much energy brain regions use as people focus attention on a task, and how that changes when the task becomes more mentally demanding. They used broadband near-infrared spectroscopy to measure the oxidation levels of an enzyme involved in energy metabolism in brain cells’ mitochondria, the energy generators that power each cell’s biochemical reactions.
The researchers employed their technique to measure brain metabolism in different regions of the visual cortex in the brains of 18 people as they carried out visual search tasks that were either complex or simple, while sometimes also presented with a visual distraction that was irrelevant to the task.
They identified elevated cellular metabolism in the brain areas responsive to the attended task stimuli as the task was more complex, and these increases were directly mirrored with reduced cellular metabolism levels in areas responding to unattended stimuli. This push-pull pattern was closely synchronised, showing a trade-off of limited energy supply between attended and unattended processing.
Co-author Professor Ilias Tachtsidis (UCL Medical Physics & Biomedical Engineering) said: “By using our in-house developed broadband near-infrared spectroscopy, an optical brain monitoring technology we developed at UCL, we were better able to measure an enzyme in the mitochondria (the power factory of the cells) that plays an integral part in metabolism.”
A Comprehensive, Multi-Modal Strategy to Mitigate Alzheimer’s Disease Risk Factors Improves Aspects of Metabolism and Offsets Cognitive Decline in Individuals with Cognitive Impairment
by Ginger Schechter, Gajendra Kumar Azad, Rammohan Rao, Allison McKeany, Matthew Matulaitis, Denise M. Kalos, Brian K. Kennedy in Journal of Alzheimer’s Disease Reports
Researchers sought to determine whether a comprehensive and personalized program, designed to mitigate risk factors of Alzheimer’s disease could improve cognitive and metabolic function in individuals experiencing cognitive decline. Findings provided evidence that this approach can improve risk factor scores and stabilize cognitive function.
Affirmativ Health sought to determine whether a comprehensive and personalized program, designed to mitigate risk factors of Alzheimer’s disease could improve cognitive and metabolic function in individuals experiencing cognitive decline. Findings provided evidence that this approach can improve risk factor scores and stabilize cognitive function.
July 31, 2020/Sonoma, CA Cognitive decline is a major concern of the aging population. Already, Alzheimer’s disease affects approximately 5.4 million Americans and 30 million people globally. Without effective prevention and treatment, the prospects for the future are bleak. By 2050, it is estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer’s disease is on the rise — recent estimates suggest that Alzheimer’s disease has become the third leading cause of death in the United States behind cardiovascular disease and cancer. Since its first description over 100 years ago, Alzheimer’s disease has been without effective treatment. While researchers continue to seek out a cure, it is becoming clear that there are effective treatment options. More and more research supports the conclusion that Alzheimer’s disease is not a disease of only Beta Amyloid plaques and Tao tangles but a complex and systemic disease. In this study of patients with varying levels of cognitive decline, it is demonstrated how a precision and personalized approach results in either stabilization or improvement in memory.
Interventions to stop the progression of Alzheimer’s disease have been marginally successful at best. This study uses a more comprehensive, personalized approach addressing each participant’s unique risk factors. “The findings, are encouraging and indicate that a more extensive clinical study is warranted,” said Brian Kennedy, PhD, Director of The Centre for Healthy Aging, National University Health System, Singapore and Chief Scientific Officer, Affirmativ Health.
The Affirmativ Health scientific team, after thorough review of published research, has developed a comprehensive approach to addressing scientifically supported risk factors that have been rigorously defined as interventions to promote prevention, increased resiliency, and stabilization of brain function in the realm of AD and dementia. Utilizing cutting edge technology in concert with in-person coaching and consultation, we are demonstrating that a multi-modal and personalized approach promotes an improved resiliency and restoration of optimal brain function. The personalized therapeutic program includes genetics, an extensive blood panel, medical history and lifestyle data to evaluate relevant metabolic risk factors and nutrient levels associated with cognitive health. “Target laboratory levels differ from standard laboratory ranges as the goal is to reach optimized levels for cognitive health,” Ginger Schechter, MD, Chief Medical Officer, Affirmativ Health
The study approach considers more than 35 factors known to contribute to cognitive decline. Results demonstrate that certain of those factors are more affected than others again demonstrating the need for a more precise treatment plan. “This study supports the need for an approach that focuses on a one-size fits one, not a one-size fits all, approach that comprehensively assesses all involved risk factors affecting memory loss,” Denise M Kalos, CEO Affirmativ Health.
The human cerebellum has almost 80% of the surface area of the neocortex
by Martin I. Sereno, Jörn Diedrichsen, Mohamed Tachrount, Guilherme Testa-Silva, Helen d’Arceuil, Chris De Zeeuw in Proceedings of the National Academy of Sciences
When we say someone has a quick mind, it may be in part thanks to our expanded cerebellum that distinguishes human brains from those of macaque monkeys, for example. High-resolution imaging shows the cerebellum is 80 percent of the area of the cortex, indicating it has grown as human behavior and cognition evolved.
Sometimes referred to by its Latin translation as the ‘“little brain”’, the cerebellum is located close to the brainstem and sits under the cortex in the hindbrain. New research at San Diego State University, however, calls the “little” terminology into question.
The cerebellum plays a versatile role, contributing to our five senses as well as pain, movements, thought, and emotion.
It’s essentially a flat sheet with the thickness of a crepe, crinkled into hundreds of folds to make it fit into a compact volume about one-eighth the volume of the cerebral cortex. For this reason, the surface area of the cerebellum was thought to be considerably smaller than that of the cerebral cortex.
By using an ultra-high-field 9.4 Tesla MRI machine to scan the brain and custom software to process the resulting images, an SDSU neuroimaging expert discovered the tightly packed folds actually contain a surface area equal to 80% of the cerebral cortex’s surface area. In comparison, the macaque’s cerebellum is about 30% the size of its cortex.
“The fact that it has such a large surface area speaks to the evolution of distinctively human behaviors and cognition,” said Martin Sereno, psychology professor, cognitive neuroscientist and director of the SDSU MRI Imaging Center. “It has expanded so much that the folding patterns are very complex.”
Unprecedented insights
Collaborating with imaging and cerebellum experts from the United Kingdom, Netherlands and Canada, Sereno used customized open source FreeSurfer software that he originally developed with colleagues while at the University of California San Diego to computationally reconstruct the folded surface of the cerebellum. The software also unfolds and flattens the cerebellar cortex so as to visualize it to the level of each individual folia — or thin leaf like fold.
A pioneer in brain imaging who has leveraged functional MRI to uncover visual maps in the brain, Sereno found that when the cerebellum is completely unfolded, it forms a strange “crepe” four inches wide by three feet long. The findings were published this week in a study in PNAS (Proceedings of the National Academy of Sciences).
“Until now we only had crude models of what it looked like,” Sereno said. “We now have a complete map or surface representation of the cerebellum, much like cities, counties, and states.”
Puzzle pieces
Previous research discovered that while there were many similarities between the cortex and the cerebellum, there was one key difference. In the cerebral cortex, regions representing different parts of the body are arranged roughly like they are in the actual body: juxtaposed and orderly. But in the cerebellum, they were placed more randomly.
“You get a little chunk of the lip, next to a chunk of the shoulder or face, like jumbled puzzle pieces,” Sereno explained.
Those parts of the cerebellum are therefore set up to pull in and coordinate information from disparate parts of the body.
It is intriguing to think that there might be analogs of ‘“fractured somatotopy”’ in the cognitive parts of the cerebellum that could help support highly complex, sophisticated cognitive functions, such as language or abstract reasoning, Sereno said.
“When you think of the cognition required to write a scientific paper or explain a concept, you have to pull in information from many different sources. And that’s just how the cerebellum is set up.”
Until now, the cerebellum was thought to be involved mainly in basic functions like movement, but its expansion over time and its new inputs from cortical areas involved in cognition suggest that it can also process advanced concepts like mathematical equations.
“Now that we have the first high resolution base map of the human cerebellum, there are many possibilities for researchers to start filling in what is certain to be a complex quilt of inputs, from many different parts of the cerebral cortex in more detail than ever before,” Sereno said.
For instance, there is some recent evidence that people who suffer cerebellum damage have difficulty processing emotion.
“The ‘little brain’ is quite the jack of all trades,” Sereno said. “Mapping the cerebellum will be an interesting new frontier for the next decade.”
Julich-Brain: A 3D probabilistic atlas of the human brain’s cytoarchitecture
by Amunts, K., Mohlberg, H., Bludau, S., & Zilles, K. in Science
“Julich-Brain” is the name of the first 3D-atlas of the human brain that reflects the variability of the brain’s structure with microscopic resolution. The atlas features close to 250 structurally distinct areas, each one based on the analysis of 10 brains. German researchers led by Prof. Katrin Amunts have now presented the new brain atlas in the renowned journal Science.
“Julich-Brain” is the name of the first 3D-atlas of the human brain that reflects the variability of the brain’s structure with microscopic resolution. The atlas features close to 250 structurally distinct areas, each one based on the analysis of 10 brains. More than 24000 extremely thin brain sections were digitized, assembled in 3D and mapped by experts. As part of the new EBRAINS infrastructure of the European Human Brain Project, the atlas serves as an interface to link different information about the brain in a spatially precise way. German researchers led by Prof. Katrin Amunts have now presented the new brain atlas in the renowned journal Science.
Under the microscope, it can be seen that the human brain is not uniformly structured, but divided into clearly distinguishable areas. They differ in the distribution and density of nerve cells and in function. With the Julich-Brain, researchers led by Katrin Amunts now present the most comprehensive digital map of the cellular architecture and make it available worldwide via the EBRAINS research infrastructure.
“On the one hand, the digital brain atlas will help to interpret the results of neuroimaging studies, for example of patients, more accurately”, says Katrin Amunts, Director at the German Research Center Juelich and Professor at the University of Duesseldorf. “On the other hand, it is becoming the basis for a kind of ‘Google Earth’ of the brain — because the cellular level is the best interface for linking data about very different facets of the brain.
A Google Earth of the Brain
In this way, the researchers are making a significant contribution to the Human Brain Project (HBP), for which the European Commission just approved 150 million Euro until 2023. “Together with many partners in this project, we are building EBRAINS as a novel high-tech research infrastructure for the neurosciences,” says Amunts, who is also the Scientific Research Director of the project.
More than a quarter century of research has gone into the 3D atlas. Dozens of experts have used image analysis and mathematical algorithms to evaluate the tissue sections over the years and determine the boundaries between brain areas, which together make up a length of almost 2000 meters.
Regions vary in their difference
Mapping showed that areas vary between different brains, for example in terms of size and location. The Julich-Brain therefore displays the position and shape of individual regions as “probability maps”. The researchers found particularly large differences in the Broca region, which is involved in language. In contrast, the primary visual area appeared much more uniform.
As part of EBRAINS, the Julich Brain Atlas is the starting point for bringing structure and function together. The atlas is already helping to link data on gene expression, connectivity and functional activity, for example, to better understand brain functions and the mechanisms of diseases. “EBRAINS also enables us to use the maps for simulations or to apply artificial intelligence to explore the division of labor between brain areas. The huge amounts of data generated from this are processed using the EBRAINS computing platform.” The computational power comes from the new European supercomputing network FENIX, which is formed by five leading centres for High Performance Computing, including the Julich Supercomputing Centre (JSC).
Digital brain science
“It is exciting to see how far the combination of brain research and digital technologies has progressed,” says Amunts. “Many of these developments converge in the Julich-Brain-Atlas and on EBRAINS. They help us — and more and more researchers worldwide — to better understand the complex organization of the brain and to jointly uncover how things are connected.”
Biological Aging in Childhood and Adolescence Following Experiences of Threat and Deprivation: A Systematic Review and Meta-Analysis
by Natalie Colich, Eileen S. Williams, Maya Rosen and Katie McLaughlin in Psychological Bulletin
Children who suffer trauma from abuse or violence early in life show biological signs of aging faster than children who have never experienced adversity, according to new research. The study examined three different signs of biological aging — early puberty, cellular aging and changes in brain structure — and found that trauma exposure was associated with all three.
“Exposure to adversity in childhood is a powerful predictor of health outcomes later in life — not only mental health outcomes like depression and anxiety, but also physical health outcomes like cardiovascular disease, diabetes and cancer,” said Katie McLaughlin, PhD, an associate professor of psychology at Harvard University and senior author of the study published in the journal Psychological Bulletin. “Our study suggests that experiencing violence can make the body age more quickly at a biological level, which may help to explain that connection.”
Previous research found mixed evidence on whether childhood adversity is always linked to accelerated aging. However, those studies looked at many different types of adversity — abuse, neglect, poverty and more — and at several different measures of biological aging. To disentangle the results, McLaughlin and her colleagues decided to look separately at two categories of adversity: threat-related adversity, such as abuse and violence, and deprivation-related adversity, such as physical or emotional neglect or poverty.
The researchers performed a meta-analysis of almost 80 studies, with more than 116,000 total participants. They found that children who suffered threat-related trauma such as violence or abuse were more likely to enter puberty early and also showed signs of accelerated aging on a cellular level-including shortened telomeres, the protective caps at the ends of our strands of DNA that wear down as we age. However, children who experienced poverty or neglect did not show either of those signs of early aging.
In a second analysis, McLaughlin and her colleagues systematically reviewed 25 studies with more than 3,253 participants that examined how early-life adversity affects brain development. They found that adversity was associated with reduced cortical thickness — a sign of aging because the cortex thins as people age. However, different types of adversity were associated with cortical thinning in different parts of the brain. Trauma and violence were associated with thinning in the ventromedial prefrontal cortex, which is involved in social and emotional processing, while deprivation was more often associated with thinning in the frontoparietal, default mode and visual networks, which are involved in sensory and cognitive processing.
These types of accelerated aging might originally have descended from useful evolutionary adaptations, according to McLaughlin. In a violent and threat-filled environment, for example, reaching puberty earlier could make people more likely to be able to reproduce before they die. And faster development of brain regions that play a role in emotion processing could help children identify and respond to threats, keeping them safer in dangerous environments. But these once-useful adaptations may have grave health and mental health consequences in adulthood.
The new research underscores the need for early interventions to help avoid those consequences. All of the studies looked at accelerated aging in children and adolescents under age 18. “The fact that we see such consistent evidence for faster aging at such a young age suggests that the biological mechanisms that contribute to health disparities are set in motion very early in life. This means that efforts to prevent these health disparities must also begin during childhood,” McLaughlin said.
There are numerous evidence-based treatments that can improve mental health in children who have experienced trauma, McLaughlin said. “A critical next step is determining whether these psychosocial interventions might also be able to slow down this pattern of accelerated biological aging. If this is possible, we may be able to prevent many of the long-term health consequences of early-life adversity,” she says.
Cognitive and academic benefits of music training with children: A multilevel meta-analysis
by Sala and Gobet m in Memory & Cognition
Music training does not have a positive impact on children’s cognitive skills, such as memory, and academic achievement, such as maths, reading or writing, according to a study published in Memory & Cognition.
Previous research trials, carried out to examine a potential causal link between music training and improved cognitive and academic performance, have reached inconsistent conclusions, with some suggesting that there may be a link between music training and better cognitive and academic performance and others finding little effect.
Researchers Giovanni Sala at Fujita Health University, Japan and Fernand Gobet at the London School of Economics and Political Science, UK examined existing experimental evidence regarding the impact of music training on children’s non-music cognitive skills and academic achievement.
The authors re-analyzed data from 54 previous studies conducted between 1986 and 2019, including a total of 6,984 children. They found that music training appeared to be ineffective at enhancing cognitive or academic skills, regardless of the type of skill (such as verbal, non-verbal, speed-related and so on), participants’ age, and duration of music training.
When comparing between the individual studies included in their meta-analysis, the authors found that studies with high-quality study design, such as those which used a group of active controls — children who did not learn music, but instead learned a different skill, such as dance or sports — showed no effect of music education on cognitive or academic performance. Small effects were found in studies that did not include controls or which did not randomize participants into control groups (ones that received different or no training) and intervention groups (ones that received music training).
Giovanni Sala, the lead author said: “Our study shows that the common idea that ‘music makes children smarter’ is incorrect. On the practical side, this means that teaching music with the sole intent of enhancing a child’s cognitive or academic skills may be pointless. While the brain can be trained in such a way that if you play music, you get better at music, these benefits do not generalize in such a way that if you learn music, you also get better at maths. Researchers’ optimism about the benefits of music training appears to be unjustified and may stem from misinterpretation of previous empirical data.”
Fernand Gobet, the corresponding author added: “Music training may nonetheless be beneficial for children, for example by improving social skills or self-esteem. Certain elements of music instruction, such as arithmetical music notation could be used to facilitate learning in other disciplines.”
The authors caution that too few studies have been conducted to reach a definitive conclusion about possible positive effects of music education on non-academic or cognitive characteristics. Alternative potential avenues involving music activities may be worth exploring.
Transcriptomic profile of adverse neurodevelopmental outcomes after neonatal encephalopathy
by Paolo Montaldo, Aubrey Cunnington, Vania Oliveira, Ravi Swamy, Prathik Bandya, Stuti Pant, Peter J. Lally, Phoebe Ivain, Josephine Mendoza, Gaurav Atreja, Vadakepat Padmesh, Mythili Baburaj, Monica Sebastian, et al. in Scientific Reports
An early blood test could detect which babies deprived of oxygen at birth are at risk of serious neurodisabilities like cerebral palsy and epilepsy.
The prototype test looks for certain genes being switched on and off that are linked to long-term neurological issues. Further investigations of these genes may provide new targets for treating the brain damage before it becomes permanent.
The team behind the test, led by Imperial College London researchers in collaboration with groups in India, Italy and the USA, have published their findings today in the journal Scientific Reports.
The research was conducted in Indian hospitals, where there are around 0.5–1.0 million cases of birth asphyxia (oxygen deprivation) per year. Babies can suffer oxygen deprivation at birth for a number of reasons, including when the mother has too little oxygen in her blood, infection, or through complications with the umbilical cord during birth.
Following oxygen deprivation at birth, brain injury can develop over hours to months and affect different regions of the brain, resulting in a variety of potential neurodisabilities such as cerebral palsy, epilepsy, deafness or blindness.
This makes it hard to determine which babies are most at risk of complications and to design interventions that can prevent the worst outcomes.
Now, in preliminary study of 45 babies that experienced oxygen deprivation at birth, researchers have identified changes to a raft of genes in their blood that could identify those that go on to develop neurodisabilities.
The babies had their blood taken within six hours after birth and were followed up after 18 months old to see which had developed neurodisabilities. The blood was examined with next-generation sequencing to determine any difference in gene expression — the ‘switching on or off’ of genes — between those babies that developed neurodisabilities and those that didn’t.
The team found 855 genes were expressed differently between the two groups, with two showing the most significant difference.
Examining these two genes in particular, and what processes their expression causes within cells, could lead to a deeper understanding of the causes of neurodisabilities prompted by oxygen deprivation, and potentially how to disrupt them, improving outcomes.
Lead author Dr Paolo Montaldo, from the Centre for Perinatal Neuroscience at Imperial, said: “We know that early intervention is key to preventing the worst outcomes in babies following oxygen deprivation, but knowing which babies need this help, and how best to help them, remains a challenge.”
Senior author Professor Sudhin Thayyil, from the Centre for Perinatal Neuroscience at Imperial, said: “The results from these blood tests will allow us to gain more insight into disease mechanisms that are responsible for brain injury and allow us to develop new therapeutic interventions or improve those which are already available.”
The babies were part of a trial called Hypothermia for Encephalopathy in Low and middle-income countries (HELIX), which also examines the use of hypothermia (extreme cooling) on babies to prevent brain injuries developing following oxygen deprivation.
In higher-income countries this is known to reduce the chances of babies developing neurodisabilities, but in lower income settings cooling may not be feasible, and even with cooling 30 percent of babies still have adverse outcomes, so new therapies are still needed.
Green Apple E-Cigarette Flavorant Farnesene Triggers Reward-Related Behavior by Promoting High-Sensitivity nAChRs in the Ventral Tegmental Area
by Skylar Y. Cooper, Austin T. Akers and Brandon J. Henderson in eNeuro
Common green apple flavorant farnesene enhances nicotine reward in mouse models. The flavorant is also rewarding on its own. Researchers say with or without nicotine, flavored vapes, especially those containing farnesene, pose potential neurological risks, including addiction.
Vaping entices adolescents into nicotine use with fun flavors like green apple and cotton candy. Nicotine-free flavored vapes have also gained popularity. But of the over 7000 available flavor chemicals, only a handful have been studied. With or without nicotine, flavored vapes pose potential risks for the brain, including addiction.
To continue unravelling these risks, Cooper et al. gave mice either nicotine, the green apple flavorant farnesene, or both in one chamber and a saline solution in another. Farnesene was rewarding by itself, as mice chose the farnesene chamber over the saline chamber. But farnesene also enhanced reward when combined with nicotine.
The research team next measured how farnesene changed nicotine receptor expression and neuron activation. Alone, farnesene partially activated nicotinic receptors, meaning it may increase nicotine’s receptor activation when both substances are present. Farnesene also increased the proportion of high- to low-sensitivity receptors. A greater proportion of high-sensitivity receptors increases the effects of a standard nicotine dose, which could heighten reward and drug-seeking behavior. Despite their marketing, vape flavors are not risk-free and may exacerbate the effects of nicotine.
From Volume 23 Issue 8, August 2020 of Nature Neuroscience:
Citation count has become one of the most important methods to evaluate a scientist’s contributions. In an extensive analysis of citations from a number of leading neuroscience journals, Dworkin and colleagues find evidence of gender bias in citation practices that can have an adverse impact on women’s careers.
Extra neural ensemble disrupts memory recall
Poll and colleagues examined the historical activity of hippocampal CA1 neurons during learning and memory recall using longitudinal two-photon in vivo imaging, providing evidence that extra neural ensemble activity disrupts memory recall in a mouse model of early Alzheimer’s disease.
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