Can we decode the language of our primate cousins?

The UNIGE team wanted to find out whether the frontal and orbitofrontal regions of our brain activate in the same way when faced with human and simian vocalizations.
Image Credit: © Leonardo Ceravolo

Are we able to differentiate between the vocal emissions of certain primates? A team from the University of Geneva (UNIGE) asked volunteers to categorize the vocalizations of three species of great apes (Hominidae) and humans. During each exposure to these "onomatopoeia", brain activity was measured. Unlike previous studies, the scientists reveal that phylogenetic proximity - or kinship - is not the only factor influencing our ability to identify these sounds. Acoustic proximity - the type of frequencies emitted - is also a determining factor. These results show how the human brain has evolved to process the vocal emissions of some of our closest cousins more efficiently. Find out more in the journal Cerebral Cortex Communications.

Our ability to process verbal language is not based solely on semantics, i.e. the meaning and combination of linguistic units. Other parameters come into play, such as prosody, which includes pauses, accentuation and intonation. Affective bursts - "Aaaah!" or ‘‘Oh!’’ for example - are also part of this, and we share these with our primate cousins. They contribute to the meaning and understanding of our vocal communications.

When such a vocal message is emitted, these sounds are processed by the frontal and orbitofrontal regions of our brain. The function of these two areas is, among other things, to integrate sensory and contextual information leading to a decision. Are they activated in the same way when we are exposed to the emotional vocalizations of our close cousins, the chimpanzees, macaques and bonobos? Are we able to differentiate between them?

AI screens for autism in the blink of an eye

Image Credit: Placidplace

With a single flash of light to the eye, artificial intelligence (AI) could deliver a faster and more accurate way to diagnose autism spectrum disorder (ASD) in children, according to new research from the University of South Australia and Flinders University.

Using an electroretinogram (ERG) - a diagnostic test that measures the electrical activity of the retina in response to a light stimulus – researchers have deployed AI to identify specific features to classify ASD.

Measuring retinal responses of 217 children aged 5-16 years (71 with diagnosed ASD and 146 children without an ASD diagnosis), researchers found that the retina generated a different retinal response in the children with ASD as compared to those who were neuro typical.

The team also found that the strongest biomarker was achieved from a single bright flash of light to the right eye, with AI processing significantly reducing the test time. The study found that higher frequency components of the retinal signal were reduced in ASD.

Conducted with University of Connecticut and University College London, the test could be further evaluated to see if these results could be used to screen for ASD among children aged 5 to 16 years with a high level of accuracy.

What Happens in the Brain While Daydreaming?

The findings provide a clue that daydreams may play a role in brain plasticity
Image Credit: Scientific Frontline 

You are sitting quietly, and suddenly your brain tunes out the world and wanders to something else entirely — perhaps a recent experience, or an old memory. You just had a daydream.

Yet despite the ubiquity of this experience, what is happening in the brain while daydreaming is a question that has largely eluded neuroscientists.

Now, a study in mice, published Dec. 13 in Nature, has brought a team led by researchers at Harvard Medical School one step closer to figuring it out.

The researchers tracked the activity of neurons in the visual cortex of the brains of mice while the animals remained in a quiet waking state. They found that occasionally these neurons fired in a pattern similar to one that occurred when a mouse looked at an actual image, suggesting that the mouse was thinking — or daydreaming — about the image. Moreover, the patterns of activity during a mouse’s first few daydreams of the day predicted how the brain’s response to the image would change over time.

The research provides tantalizing, if preliminary, evidence that daydreams can shape the brain’s future response to what it sees. This causal relationship needs to be confirmed in further research, the team cautioned, but the results offer an intriguing clue that daydreams during quiet waking may play a role in brain plasticity — the brain’s ability to remodel itself in response to new experiences.

Clues to preventing Alzheimer’s come from patient who, despite genetics, evaded disease

A woman who never developed Alzheimer's despite a strong genetic predisposition may hold the key to stopping the disease in its tracks. Studying the woman's unique complement of genetic mutations, researchers at Washington University School of Medicine in St. Louis have found clues that could help cut the link between the early, asymptomatic stage and the late stage, when cognitive decline sets in.
Image Credit: AartlistDesign

Alzheimer’s disease has plagued one large Colombian family for generations, striking down half of its members in the prime of life. But one member of that family evaded what had seemed would be fate: Despite inheriting the genetic defect that caused her relatives to develop dementia in their 40s, she stayed cognitively healthy into her 70s.

Researchers at Washington University School of Medicine in St. Louis now think they know why. A previous study had reported that, unlike her relatives, the woman carried two copies of a rare variant of the APOE gene known as the Christchurch mutation. In this study, researchers used genetically modified mice to show that the Christchurch mutation severs the link between the early phase of Alzheimer’s disease, when a protein called amyloid beta builds up in the brain, and the late phase, when another protein called tau accumulates and cognitive decline sets in. So the woman stayed mentally sharp for decades, even as her brain filled with massive amounts of amyloid. The findings, published in the journal Cell, suggest a new approach to preventing Alzheimer’s dementia.

Advanced MRI technology detects changes in the brain after COVID-19

Ida Blystad and her colleagues examine the brain using MRI. 
Photo Credit: Emma Busk Winquist

Researchers at LiU have examined the brains of 16 patients previously hospitalized for COVID-19 with persisting symptoms. They have found differences in brain tissue structure between patients with persisting symptoms after COVID-19 and healthy people. Their findings can bring insights into the underlying mechanisms of persisting neurological problems after COVID-19.

Several previous studies of persisting problems after COVID have involved MRI brain scanning. Although researchers have found differences compared with healthy brains, these differences are not specific to COVID-19.

“It can be frustrating for me as a doctor when I understand that the patients have problems, but I can’t find an explanation because there’s nothing in the MRI scan to explain it. To me, this underlines the importance of trying other examination technologies to understand what’s happening in the brain in patients with persisting symptoms after COVID-19,” says Ida Blystad, neuroradiologist in the Department of Radiology at Linköping University Hospital and researcher affiliated with the Department of Health, Medicine and Caring Sciences at Linköping University and the Centre for Medical Image Science and Visualization (CMIV).

Parkinson's: New hope when treatment options seem exhausted

Prof. Paul Lingor
Photo Credit: Courtesy of Technical University of Munich

As Parkinson's progresses, more invasive therapies are used that require brain surgery, for example. When these no longer deliver the desired results, physicians often conclude that treatment options are exhausted. A study led by researchers at the Technical University of Munich (TUM) now shows that such patients can still benefit from a change in treatment. So far, however, this option has only been used very rarely.

A team led by Prof. Paul Lingor has examined data from 22 German Parkinson's centers. The result: although there are several options for therapies in the late stages of the disease, rarely is more than one used - although those affected often benefit from them.

Parkinson's disease is the world’s second-most common neurodegenerative disease after Alzheimer's. So far it has proved incurable. Only the symptoms can be treated. In the early stages, tablets can generally provide relief from complaints. As the disease progresses, this is often no longer enough.

Molecular blueprint of circuits governing locomotor speed

Zebra fish
Photo Credit: Lars Bräutigam

Researchers at Karolinska Institutet, Sweden have uncovered the molecular logic underpinning the assembly of spinal circuits that control the speed of locomotion in adult zebrafish. The study has recently been published in Nature Neuroscience.

What does the study show?

A fundamental hallmark of motor actions is the flexibility of their timing, speed and strength that is central to rapid adaptation to the ever-changing world around us. This is particularly apparent during locomotion, a behavior that involves full-body coordination characterized by sudden changes in speed and strength.

“In this study, we used single-cell RNA sequencing in adult zebrafish to link the molecular diversity of motoneurons and interneurons with their modular circuit organization that is responsible for changes in locomotor speed” says Abdel El Manira, Professor at the Department of Neuroscience at Karolinska Institutet, and corresponding author of the article.

Brain health in over 50s deteriorated more rapidly during the pandemic

Photo Credit: Gabriel Porras

Brain health in over 50s deteriorated more rapidly during the pandemic, even if they didn’t have COVID-19, according to major new research linking the pandemic to sustained cognitive decline.

Researchers looked at results from computerized brain function tests from more than 3,000 participants of the online PROTECT study, who were aged between 50 and 90 and based in the UK. The remote study, led by teams at the University of Exeter and the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, and part-funded by NIHR Maudsley BRC, tested participants’ short-term memory and ability to complete complex tasks.

Through analyzing the results from this big dataset, researchers found that cognitive decline quickened significantly in the first year of the pandemic, when they found a 50 per cent change to the rate of decline across the study group. This figure was higher in those who already had mild cognitive decline before the pandemic, according to the research published in The Lancet Healthy Longevity.

What Happens When We Pass Out? Researchers ID New Brain and Heart Connections

An image of a heart labeled by vagal sensory neurons. In a new study published in the journal Nature, UC San Diego researchers and their colleagues found that these neurons trigger fainting, laying a foundation for addressing fainting-related disorders.
Image Credit: Augustine Lab, UC San Diego

Nearly 40 percent of people experience syncope, or fainting spells, at least once in their lives. These brief losses of consciousness, whether brought by pain, fear, heat, hyperventilation or other causes, account for a significant portion of hospital emergency room visits. Yet the exact root mechanisms at play when people “pass out” largely have remained a mystery.

Publishing a new report in Nature, University of California San Diego researchers, along with colleagues at The Scripps Research Institute and other institutions, have for the first time identified the genetic pathway between the heart and brain tied to fainting.

One of their unique approaches was to think of the heart as a sensory organ rather than the longstanding viewpoint that the brain sends out signals and the heart simply follows directions. School of Biological Sciences Assistant Professor Vineet Augustine, the paper’s senior author, applies a variety of approaches to better understand these neural connections between the heart and brain.

High metabolism is an early sign of Alzheimer’s disease

Illustration Credit: geralt

An early phase in the process of developing Alzheimer’s disease is a metabolic increase in a part of the brain called the hippocampus, report researchers from Karolinska Institutet in a study published in Molecular Psychiatry. The discovery opens up new potential methods of early intervention.

Alzheimer’s disease is the most common form of dementia and strikes about 20,000 people in Sweden every year. Researchers now show that a metabolic increase in the mitochondria, the cellular power plants, is an early indicator of the disease. 

The teams behind the study used mice that developed Alzheimer’s disease pathology in a similar way to humans. The increase in metabolism in young mice was followed by synaptic changes caused by disruption to the cellular recycling system (a process known as autophagy), a finding that was awarded the Nobel Prize in Physiology or Medicine in 2016. 

After a time, metabolism in the Alzheimer brain usually declines, which contributes to the degradation of synapses. This the researchers could also see in the older mice, which had had the disease for a longer time. 

Sets of neurons work in sync to track ‘time’ and ‘place,’ giving humans context for past, present and future

Illustration Credit: MasterTux

Two studies led by UCLA researchers offer new insights into the way neurons in the human brain represent time and space – the most basic ingredients of consciousness of human existence and the primary dimensions of experience that allow us to reconstruct the past and envision the future.

The new findings are based on recordings of the activity of single neurons in the brain, from studies led by Dr. Itzhak Fried, a neurosurgeon and researcher at the UCLA David Geffen School of Medicine, is the senior author of two articles in Cell Reports. Patients who had undergone surgical placement of special depth electrodes developed and implanted by Fried for surgical treatment of intractable epilepsy agreed to perform cognitive tasks while their brain cell activity is recorded for these studies.

Neurons that act as the brain’s GPS system – termed “place cells” and “grid cells” – were discovered initially in rodents, similar findings later described in humans by Fried and colleagues at UCLA in collaboration with Dr. Michael Kahana, professor of Psychology at the University of Pennsylvania and a co-senior author of one of the new studies. The brain’s clock cells, or “time cells,” were identified in more recent years.

New genes linked to ADHD identified potentially paving the way for new treatments

Image Credit: Braňo

Several new genes associated with conditions such as Attention-deficit hyperactivity disorder (ADHD) have been identified, unearthing a significant connection between these disorders and our immune system that could lead to new treatments. The research from the University of Surrey also confirms the role of gene ADGRL3 in conditions such as ADHD, giving scientists a greater understanding of its workings.

During this innovative study, scientists led by Dr Matt Parker from Surrey set out to understand more about ADGRL3, a gene closely linked to ADHD and other ‘externalizing’ disorders, in promoting behaviors such as substance abuse, which can be associated with the conditions. Through this work, scientists identified several new genes related to externalizing disorders, which could lead to the development of new medication to lessen the impact on individuals.

DNA organization influences the growth of deadly brain tumors in response to neuronal signals

Silvia Remeseiro
Photo Credit: Mattias Pettersson

A pioneering study at Umeå University, Sweden, has unveiled that the 3D organization of DNA can influence the progression of the aggressive brain tumor known as glioblastoma. Having identified the factors that glioblastoma uses to respond to neurons by growing and spreading, this discovery paves the way for further research into new treatments for brain tumors.

"We have now identified the most important factors behind how the tumor responds to nerve cells, thus becoming more dangerous. These findings offer hope in our long-term battle against this difficult-to-treat cancer, for which the prognosis has not improved in decades," comments Silvia Remeseiro, Wallenberg fellow at WCMM, Assistant Professor at Umeå University, and lead author of the study.

Glioblastoma is the most fatal type of brain tumor among adults and there is currently no curative treatment. Glioblastoma patients typically face a survival of roughly one-year post-diagnosis. Even following current treatment regimes, which include surgery, radiotherapy and chemotherapy, a mere four per cent of patients are still alive five years after diagnosis.

The brain may learn about the world the same way some computational models do

Two new MIT studies offer evidence supporting the idea that the brain uses a process similar to a machine-learning approach known as “self-supervised learning.”
Illustration Credit: geralt

To make our way through the world, our brain must develop an intuitive understanding of the physical world around us, which we then use to interpret sensory information coming into the brain.

How does the brain develop that intuitive understanding? Many scientists believe that it may use a process similar to what’s known as “self-supervised learning.” This type of machine learning, originally developed as a way to create more efficient models for computer vision, allows computational models to learn about visual scenes based solely on the similarities and differences between them, with no labels or other information.

A pair of studies from researchers at the K. Lisa Yang Integrative Computational Neuroscience (ICoN) Center at MIT offers new evidence supporting this hypothesis. The researchers found that when they trained models known as neural networks using a particular type of self-supervised learning, the resulting models generated activity patterns very similar to those seen in the brains of animals that were performing the same tasks as the models.

The findings suggest that these models are able to learn representations of the physical world that they can use to make accurate predictions about what will happen in that world, and that the mammalian brain may be using the same strategy, the researchers say.

An unexpected link between 2 schizophrenia risk proteins

The study findings suggest that when the proteins don’t bind properly, signaling among neurons, illustrated above, becomes imbalanced, which can lead to related negative behavioral symptoms.
 Image Credit: T. Ahmed, A. Buonanno, National institute of Child Health and Human Development

The discovery of a physical interaction between two proteins in brain cells that can be traced in mice to control of movement, anxiety and memory could one day open the door to development of new schizophrenia treatment strategies.

The research group is the first to determine that the two proteins, both among the dozens of proteins related to risk for the development of schizophrenia, bind to each other under normal conditions in multiple regions of the brain, and that their connection was found in mice to be key to maintaining normal movement, memory function and anxiety regulation.

When that connection doesn’t happen as it should, they found, behavior can be negatively affected – in mice, disruption to the proteins’ ability to interact increased hyperactivity, reduced risk avoidance and impaired memory. Though delusions and hallucinations are hallmark symptoms of schizophrenia, the condition also encompasses additional symptoms, including movement and memory problems. 

“These two proteins are seemingly unrelated, and our study has provided a link between them that wasn’t recognized before,” said lead author Chen Gu, associate professor of biological chemistry and pharmacology in The Ohio State University College of Medicine.  

First digital atlas of human fetal brain development published

Image Credit: Geralt

The first digital atlas showing how the human brain develops in the womb has been published by a global research team led by the University of Oxford.

A team of over 200 researchers around the world, involving multiple health and scientific institutions, led by the University of Oxford, has today published, in the journal Nature, the first digital atlas showing the dynamics of normative maturation of each hemisphere of the fetal brain between 14- and 31-weeks’ gestation - a critical period of human development.

The atlas was produced using over 2,500 3-dimensional ultrasound (3D US) brain scans that were acquired serially during pregnancy from 2,194 fetuses in the INTERGROWTH-21st Project, which is a large population-based study of healthy pregnant women living in eight diverse geographical regions of the world (including five in the Global South), whose children had satisfactory growth and neurodevelopment at 2 years of age.

The study is unique because, for the first time, an international dataset of 3D US scans, collected using standardized methods and equipment, has been analyzed with advanced artificial intelligence (AI) and image processing tools to construct a map showing how the fetal brain matures as pregnancy advances.

Brain implant at OHSU successfully controls both seizures and OCD

OHSU neurosurgeon Ahmed Raslan, M.D., and patient Amber Pearson.
Photo Credit: OHSU/Christine Torres Hicks

A patient at Oregon Health & Science University is the first in the world to benefit from a single stimulator implanted in the brain to effectively control two life-altering conditions: seizures caused by epilepsy and compulsive behavior caused by obsessive-compulsive disorder, or OCD.

Amber Pearson, 34, of Albany, said her seizures are under better control, but the relief from her psychiatric condition is profound.

“OCD is worse than having the seizures,” she said. “Epilepsy brings limitations to my life, but OCD controlled it.”

In the case study, published in the journal Neuron, co-authors from institutions across the country describe the interactive programming of the responsive neurostimulation system, or RNS, that now functions seamlessly to control the compulsions that once ruled her life.

“Before I started treatment with my RNS, I would wash my hands until they would bleed,” Pearson said. “My hands would be so dry that bending my fingers would crack the skin of my knuckles.”

Case report shows promising results using transcranial magnetic stimulation for post-stroke ataxia

Image Credit: UCLA| Health et al. Cerebellum. October 21, 2023

In a new case report, researchers at UCLA Health describe promising results using repetitive transcranial magnetic stimulation (rTMS) in the management of post-stroke cerebellar ataxia, a debilitating condition marked by impaired coordination and balance.

Cerebellar ataxia describes a group of neurological disorders that affect coordination, balance, and control of muscle movements. It results from damage or dysfunction of the cerebellum, a part of the brain responsible for coordinating voluntary movements. Ataxia can manifest as unsteady walking, difficulties with fine motor skills, and problems with speech, among other symptoms. The severity of ataxia can vary from mild to severe, and treatments often aim to manage symptoms and improve a person's quality of life as treatment options are limited.

Writing in The Cerebellum, researchers led by Evan Hy Einstein, Department of Psychiatry & Biobehavioral Sciences at the UCLA David Geffen School of Medicine, report on the case of a 58-year-old male who had experienced a cerebellar hemorrhage approximately 12 years previously. Despite intensive rehabilitation, symptoms such as slow and unsteady gait, balance issues, and urinary incontinence persisted over the years. The patient sought consultation for potential rTMS treatment. His primary complaints focused on his slow and unsteady gait, along with challenges related to balance and stability. The decision was made to employ bilateral cerebellar rTMS, representing an innovative approach to address the condition.

How Huntington’s Disease Begins Before Symptoms Appear

A microglia cell (shown in green) and corticostriatal synapses (purple) from a patient with Huntington’s disease.
Image Credit: Dan Wilton

A new study led by researchers at Boston Children’s Hospital and Harvard Medical School reveals how the process of Huntington’s disease begins well before symptoms appear — and shows that in mice, the process can be blocked to prevent cognitive problems related to Huntington’s.

If the findings hold true in humans, they raise the possibility of intervening early in the disease in people who carry the Huntington’s gene mutation.

The work, published in Nature Medicine, also could shed light on other neurodegenerative disorders.

The team found in patient tissue samples and mouse models that two players in the immune system — complement proteins and microglia — are activated very early in Huntington’s, leading to loss of synapses in the brain before cognitive and motor symptoms emerge. The researchers revealed how and where the synapses are lost.

The findings corroborate a potential treatment that’s currently in clinical trials for the disease.

The study was led by senior author Beth Stevens, HMS associate professor of neurology at Boston Children’s, and first author Dan Wilton, HMS research fellow in neurology in the Stevens lab.

UConn Health Researchers Find that Youthful Proteins Help Nerves Regrow

Three sections of optic nerve were injured by crushing (the white diamond on the far left of each nerve marks the crush point.) The lower two nerves each express genes (Rpl7 or Rpl7a) newly identified by the Trakhtenberg lab as promoting nerve axon regeneration. The axons carry the bright green dye. The insets to the right show how much more axon regrowth is occurring in the nerves that express the regeneration genes, and how no regrowth happens in the normal control (top).
Image Credit: Courtesy of Trakhtenberg Lab/UConn Health

Damaged nerves of the brain, eye, and spinal cord cannot grow back. But specific gene therapies might be able to change this, leading to treatments for paralysis and other forms of nerve damage, UConn Health researchers report in the October issue of Experimental Neurology.

Axons are the long arms of nerve cells that reach from our extremities to our spinal cord, and from our eye to our brain. Injuries that smash or sever axons—and often the large bundles of axons that we commonly call nerves—can cause paralysis, blindness, lack of sexual function, or other devastating outcomes. Most of the time, these central nervous system axons don’t repair themselves, and we have no good treatments for this.

Axons fail to regenerate for several reasons. Some of them have to do with the environment the axon grows in, but another reason is that the ability to grow is lost as the nervous system matures during and after birth. The loss of key proteins prevents regrowth once an organism matures, reports a team of researchers at UConn School of Medicine.