Keep Forgetting Things? Neuroscience Says This Simple Food Boosts Your Brain and Improves Memory Inc.
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Keep Forgetting Things? Neuroscience Says This Simple Food Boosts Your Brain and Improves Memory - Inc.
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George Bloom, PhD, researches Alzheimer's disease at the University of Virginia.
Credit: Dan Addison | University Communications
University of Virginia Alzheimers researchers have discovered how harmful tau proteins damage the essential operating instructions for our brain cells, a finding which could lead to new treatments.
The toxic protein, the researchers found, warps the shape of the nuclei of nerve cells, or neurons. This alters the function of genes contained inside and reprograms the cells to make more tau.
While the protein has long been a prime suspect in Alzheimers and other neurodegenerative tauopathies, the new research from UVAs George Bloom, Ph.D.; his recently graduated student Xuehan Sun, Ph.D.; and collaborators is among the first to identify concrete physical harms that tau causes to neurons. As such, it offers researchers exciting leads as they work to develop new treatments for Alzheimers disease and tauopathies, which are now untreatable.
A lot of fantastic research has been done by other labs to learn how toxic tau spreads from neuron to neuron in the brain, but very little is known about exactly how this toxic tau damages neurons, and that question is the motivation for our new paper, said Bloom, of UVAs Departments of Biology, Cell Biology andNeuroscience, as well as the UVA Brain Institute, the Virginia Alzheimers Disease Center and UVAs Program in Fundamental Neuroscience. The toxic tau described here is actually released from neurons, so if we can figure out how to intercept it when its floating around in the brain outside of neurons, using antibodies or other drugs, it might be possible to slow or halt progression of Alzheimers disease and other tauopathies.
Tauopathies are characterized by the buildup of tau inside the brain. Alzheimers disease is well known, but there are many other tauopathies, including frontotemporal lobar degeneration, progressive supranuclear palsy and chronic traumatic encephalopathy. These diseases typically present as dementia, personality changes and/or movement problems. There are no treatments available for non-Alzheimers tauopathies, so the UVA researchers were eager to better understand what is happening, so that scientists can find ways to prevent or treat it.
Bloom and his team discovered that tau oligomers assemblages of multiple tau proteins can have dramatic effects on the normally smooth shape of neuronal nuclei. The oligomers cause the nuclei to fold in on themselves, or invaginate, disrupting the genetic material contained within. The physical location and arrangement of genes affects how they work, so this unnatural rearrangement can have dire effects.
Our discovery that tau oligomers alter the shape of the nucleus drove us to the next step testing the idea that changes in gene expression are caused by the nuclear shape change, Bloom said. Thats exactly what we saw for many genes, and the biggest change is that the gene for tau itself increases its expression almost three-fold. So bad tau might cause more bad tau to be made by neurons that would be like a snowball rolling downhill.
The researchers found that patients with Alzheimers disease had twice as many invaginated nuclei as people without the condition. Increases were also seen in lab mice used as models of Alzheimers and another tauopathy.
The researchers say that additional research into how this process happens could open the door to new ways to prevent and treat Alzheimers and other tauopathies.
The researchers have published their findings in the scientific journal Alzheimers & Dementia. The article is open access, meaning it is free to read. The research team consisted of Xuehan Sun, Guillermo Eastman, Yu Shi, Subhi Saibaba, Ana K. Oliveira, John R. Lukens, Andrs Norambuena, Joseph A. Thompson, Michael D. Purdy, Kelly Dryden, Evelyn Pardo, James W. Mandell and Bloom. The researchers have no financial interest in the work.
The research was supported by the National Institutes of Health, grant RF1 AG051085; the Owens Family Foundation; the Cure Alzheimers Fund; Rick Sharp Alzheimers Foundation; Webb and Tate Wilson; and the NanoString nCounter Grant Program.
To keep up with the latest medical research news from UVA, subscribe to theMaking of Medicineblog.
Alzheimer s & Dementia
9-Dec-2023
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Alzheimers discovery reveals dire effect of - EurekAlert
Summary: Researchers uncovered the protective effects of physical and social activities on brain health in older adults.
Analyzing data from a 12-year longitudinal study, researchers focused on the entorhinal cortex, vital for learning and memory and vulnerable in Alzheimers disease. They found that increased physical and social activity slowed the thinning of the entorhinal cortex and, consequently, memory decline over seven years.
This research underscores the importance of an active lifestyle in preserving brain health and cognitive function in old age.
Key Facts:
Source: University of Zurich
Physical exercise is associated with a variety of positive health aspects. Numerous studies have shown that regular physical activity has a preventive effect on cardiovascular diseases, diabetes, cancer, high blood pressure and obesity.
But how do various leisure activities physical, social and cognitive affect brain health in old age?
A team of researchers from the University Research Priority Program Dynamics of Healthy Aging and from the Healthy Longevity Center of the University of Zurich (UZH) decided to investigate this question.
To this end, they examined data from a comprehensive longitudinal study on brain development and behavior in old age. The longitudinal study was set in motion 12 years ago by Lutz Jncke, meanwhile professor emeritus at UZH, who continues to supervise the project together with co-lead Susan Mrillat.
The aim of the current research was to investigate the relationships between the thickness of the entorhinal cortex, memory performance and leisure activities in cognitively healthy adults over the age of 65, for a period of seven years.
Exercise and social activity slow down neurodegeneration
The entorhinal cortex, approximately 3.5 millimeters thick, is part of the cerebral cortex in the inner part of the temporal lobe and plays a key role in learning and memory. It is also one of the brain regions that is affected early on in the development of Alzheimers disease.
Our findings show that in people who were more physically and socially active at the beginning of the study, the thickness of their entorhinal cortex decreased less over the seven-year period, says neuropsychologist Jncke.
The researchers also found that the thickness of the entorhinal cortex is closely linked to memory performance. The less the thickness of this brain structure decreased over the course of the study, the less memory performance was reduced.
Physical exercise and an active social life with friends and family are therefore important for brain health and can prevent neurodegeneration in later life, says Jncke.
Brain can be trained like a muscle
It was also shown that higher memory performance at the beginning of the study was associated with a lower decline in memory performance over the course of the study.
These findings support the idea that we have a cognitive reserve, and that the brain can be trained throughout our lives like a muscle to counteract age-related decline, says Isabel Hotz, one of the two first authors alongside Pascal Deschwanden.
In other words, it pays to be physically, mentally and socially active throughout our lives, including in later life.
Fortunately, many older people in Switzerland already seem to be living by this credo: according to the Swiss Health Survey conducted by the Swiss Federal Statistical Office in 2022, around three quarters of people over 65 get the recommended amount of physical exercise in their daily lives.
Author: Kurt Bodenmueller Source: University of Zurich Contact: Kurt Bodenmueller University of Zurich Image: The image is credited to Neuroscience News
Original Research: Open access. Associations between white matter hyperintensities, lacunes, entorhinal cortex thickness, declarative memory and leisure activity in cognitively healthy older adults: A 7-year study by Lutz Jncke et al. NeuroImage
Abstract
Associations between white matter hyperintensities, lacunes, entorhinal cortex thickness, declarative memory and leisure activity in cognitively healthy older adults: A 7-year study
Cerebral small vessel disease (cSVD) is a growing epidemic that affects brain health and cognition. Therefore, a more profound understanding of the interplay between cSVD, brain atrophy, and cognition in healthy aging is of great importance.
In this study, we examined the association between white matter hyperintensities (WMH) volume, number of lacunes, entorhinal cortex (EC) thickness, and declarative memory in cognitively healthy older adults over a seven-year period, controlling for possible confounding factors.
Because there is no cure for cSVD to date, the neuroprotective potential of an active lifestyle has been suggested. Supporting evidence, however, is scarce. Therefore, a second objective of this study is to examine the relationship between leisure activities, cSVD, EC thickness, and declarative memory.
We used a longitudinal dataset, which consisted of five measurement time points of structural MRI and psychometric cognitive ability and survey data, collected from a sample of healthy older adults (baselineN=231, age range: 6487 years, ageM=70.8 years), to investigate associations between cSVD MRI markers, EC thickness and verbal and figural memory performance.
Further, we computed physical, social, and cognitive leisure activity scores from survey-based assessments and examined their associations with brain structure and declarative memory. To provide more accurate estimates of the trajectories and cross-domain correlations, we applied latent growth curve models controlling for potential confounders.
Less age-related thinning of the right (=0.92,p<.05) and left EC (=0.82,p<.05) was related to less declarative memory decline; and a thicker EC at baseline predicted less declarative memory loss (=0.54,p<.05). Higher baseline levels of physical (=0.24,p<.05), and social leisure activity (=0.27,p<.01) predicted less thinning of right EC. No relation was found between WMH or lacunes and declarative memory or between leisure activity and declarative memory.
Higher education was initially related to more physical activity (=0.16,p<.05) and better declarative memory (=0.23,p<.001), which, however, declined steeper in participants with higher education (=.35,p<.05). Obese participants were less physically (=.18,p<.01) and socially active (=.13,p<.05) and had thinner left EC (=.14,p<.05) at baseline.
Antihypertensive medication use (=.26,p<.05), and light-to-moderate alcohol consumption (=.40,p<.001) were associated with a smaller increase in the number of lacunes whereas a larger increase in the number of lacunes was observed in current smokers (=0.30,p<.05).
Our results suggest complex relationships between cSVD MRI markers (total WMH, number of lacunes, right and left EC thickness), declarative memory, and confounding factors such as antihypertensive medication, obesity, and leisure activity.
Thus, leisure activities and having good cognitive reserve counteracting this neurodegeneration. Several confounding factors seem to contribute to the extent or progression/decline of cSVD, which needs further investigation in the future.
Since there is still no cure for cSVD, modifiable confounding factors should be studied more intensively in the future to maintain or promote brain health and thus cognitive abilities in older adults.
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Active Aging: Exercise and Social Life Shield Brain Health - Neuroscience News
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May-Britt Moser, Soledad Gonzalo Cogno and Edvard Moser. Photo: Kavli Institute for Systems Neuroscience, NTNU
Credit: Photo: Kavli Institute for Systems Neuroscience, NTNU
Scientists at NTNUs Kavli Institute for Systems Neuroscience in Norway have discovered a pattern of activity in the brain that can serveas a template for building sequential experiences.
I believe we have found one of the brains prototypes for building sequences says Professor Edvard Moser.He describes the activity pattern as a fundamental algorithm that is intrinsic to the brain and independent of experience.
The breakthrough discovery was published in Nature 20. December 2023.
The ability to organise elements into sequences is a fundamental biological function essential for our survival. Without it, we would not be able to communicate, to keep track of time, to find our way, or even remember what we are in the process of doing. The world would cease to present itself to us in meaningful experiences, as every event would be fragmented into an erratic series of random happenings.The NTNU researchers discovery of a rigid sequence pattern in the brain provides new insights into how we organise experiences into a temporal order.
Have you ever heard memories described as snapshots? That is not a very faithful description, according to Professor Edvard Moser. It is more helpful to think of memories as videos, he says.All your experiences in the world extend over time, says Professor May-Britt Moser. One thing happens, then another thing, then a third.Your brain has the remarkable ability to mentally capture and organise selected events into the chronological order in which they occurred, and to link them together as meaningful experiences. This sequence building activity takes place on the timescale in which you interact in the situation. When you recall this memory, the process of reliving the sequence of events in your mind also takes time.How is the brain able to generate and store all these unique and lengthy sequences of information on the fly?, asks Edvard Moser. There has to exist a foundational mechanism for sequence formation there.There is a mismatch in neuroscience between the timescales at which brain activity is typically studied, in the millisecond regime, and the timescales at which many of our most important brain functions occur, in the tens of seconds to several minutes range, says Soledad Gonzalo Cogno, Kavli Research Group Leader and first author of the paper, expanding on the motivation behind this study.The team set out to identify this fundamental mechanism for sequence formation, which occurs on very slow timescales, like most of our brain functions do.
To uncover how neurons coordinate at the slow timescales at which many of our brain functions unfold, the Kavli researchers focused on the medial entorhinal cortex (MEC), a brain area that supports brain functions that depend on sequence formation, such as navigation and episodic memory, which unfold very slowly in time.The sheer volume of information about the outside world being processed in the brain at any one time posed a challenge to the pursuit. Any baseline signal from structured and recurrent neural algorithms would risk drowning in the noise of incoming experience.To get around this, the researchers created an experimental environment that was almost devoid of sensory inputs. They let a mouse run in complete darkness, with no task to complete and no reward to earn. The mouse could run or rest as it pleased, for as long as the session lasted.At the same time, the researchers recorded what was happening in the entorhinal cortex of the mouses brain while its orchestra of nerve cells remained in this soft-spoken standby position.
This is what we found, says Soledad Gonzalo Cogno, pointing to a zebra-striped figure in front of her.The pattern is made up of thousands of dots clustered together. Each dot is a neural signal. We can see that the neural activity moves through all the cells from bottom to top along the Y-axis as time progresses along the X-axis. The clustering tells us that the activity is coordinated as waves running through the network, like rhythms in a symphony. The sequences are ultra-slow, meaning that it takes two minutes for the wave to travel through the neural network, before the whole process repeats again, sometimes for as long as the duration of the test session, over periods of up to an hour.The figure shows several hundred mouse entorhinal cortex neurons oscillating at ultra-slow frequencies, spanning time windows ranging from tens of seconds to several minutes. The dynamic that excited the researchers even more is that as each cell oscillates, the cells also organise themselves into sequences, with cell A firing before cell B, cell B firing before cell C, and so on, until they have completed a full loop and return to cell A, where the cycle repeats. This highly structured activity overlaps with the timescale of events that we encode into our memories and provides the perfect template for building the sequential structure that forms the basis of episodic memories.These waves of coordinated activity did not travel in a straight line from one end of the brain tissue to the other. Instead, the waves travel along the thin synaptic connections between cells that talk to each other in the network. Cells can talk to other cells far away as well as to their nearest neighbours. The anatomical tangle makes it difficult to see coordinated activity with the naked eye without first having located the cells from the raster plot.
This video illustrates this.
The zebra-striped raster plot shows the slow waves of activity through the whole network over a period of time.If you fold the raster plot into a tube, so that the top and the bottom of the figure overlap, you will see that the diagonal stripes connect to form a coherent spiral, explains May-Britt Moser. The spiral represents the network activity over time.If you rotate the spiral by 90 degrees, you will see a ring. All the cells in the network have their set time to fire, distributed across the surface of this ring. The signal travels through the entire ring structure before returning to the same cell.This ring is a signature for coordination patterns in the form of repetitive sequences, which is what we found in the MEC, says Soledad Gonzalo Cogno. Other brain areas have different coordination patterns.Your brain may already be equipped with this ring before you experience anything in this world. It is acquired through evolution and may be specified in our genesWhat excites me most about this discovery is the prospect that these sequences may open up for new ways of understanding the brain, says Gonzalo Cogno. The discoveries that follow may challenge the way we think about coordination throughout the brain. Cells that are so different still seem to be coordinated and work together on different timescales.
Experimental study
Animals
Minute-scale oscillatory sequences in medial entorhinal cortex
20-Dec-2023
The authors declare that they have no competing financial interests.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
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A framework in your brain for organising the order of things - EurekAlert
Summary: Researchers uncovered how Alzheimers Disease (AD) impacts COVID-19 outcomes through changes in the olfactory mucosal cells. Their study focused on individuals with AD who experienced exacerbated COVID-19 symptoms.
Using an advanced 3D in vitro model of the olfactory mucosa, the research revealed that while initial infection rates were similar between healthy individuals and those with AD, the latter showed altered gene activities post-infection, indicating heightened oxidative stress and immune response changes.
This study provides crucial insights into the interplay between COVID-19 and AD, particularly through the olfactory system.
Key Facts:
Source: University of Eastern Finland
A new study identifies alterations in the transcriptomic signatures in human olfactory mucosal cells of individuals with Alzheimers disease following SARS-CoV-2 infection, potentially contributing to exacerbated COVID-19 outcomes.
The study was conducted at the University of Eastern Finland in collaboration with the University of Helsinki and published inJournal of Neuroinflammation.
The study was prompted by concerns about the impact of COVID-19 on individuals with pre-existing conditions such as Alzheimers disease (AD). Olfactory dysfunction, characterized by an impaired sense of smell, is commonly associated with COVID-19 and is also observed in persons with AD.
Exploring the olfactory mucosa as a direct interface between the external environment and the brain, the research aimed to investigate the interaction between SARS-CoV-2 infection and AD within the olfactory mucosa , assessing the potential for this tissue to serve as a plausible entry route for the virus into the brain.
Employing an innovative 3D in vitro model of the olfactory mucosa, the study utilized primary cells obtained from voluntary donors, including both cognitively healthy individuals and those diagnosed with AD.
These cells were cultivated at the air-liquid interface (ALI), a technique providing a controlled environment that closely mimics physiological conditions. The collection of olfactory mucosal biopsies was conducted collaboratively with Kuopio University Hospital.
This multidisciplinary research integrated expertise from molecular and cellular biology, neurology, and virology to investigate the effects of various SARS-CoV-2 variants on the olfactory mucosa.
Distinct immune responses after infection between AD patients and healthy individuals
Contrary to expectations, cells derived from healthy individuals and those with AD exhibited comparable susceptibility to infection by SARS-CoV-2 virus, indicating no significant difference in initial infection rates between the two groups.
However, a significant contrast emerged in the gene activity of infected cells from individuals with AD. Their cells displayed heightened oxidative stress, altered immune responses, and substantial changes in genes related to olfaction when compared to olfactory mucosal cells from cognitively healthy individuals.
The results suggest a plausible scenario where individuals affected by AD might face potentially more severe COVID-19 outcomes due to pre-existing inflammation in the olfactory mucosa, says Ali Shahbaz, a doctoral researcher in Professor Katja Kanninens research group at the University of Eastern Finland and the first author of the study.
The present study represents a pivotal advancement in understanding the intricate interplay between COVID-19 and AD.
Funding: The study was funded by the Academy of Finland.
Author: Ulla Kaltiala Source: University of Eastern Finland Contact: Ulla Kaltiala University of Eastern Finland Image: The image is credited to Neuroscience News
Original Research: Open access. Human-derived airliquid interface cultures decipher Alzheimers diseaseSARS-CoV-2 crosstalk in the olfactory mucosa by Katja Kanninen et al. Journal of Neuroinflammation
Abstract
Human-derived airliquid interface cultures decipher Alzheimers diseaseSARS-CoV-2 crosstalk in the olfactory mucosa
The neurological effects of the coronavirus disease of 2019 (COVID-19) raise concerns about potential long-term consequences, such as an increased risk of Alzheimers disease (AD). Neuroinflammation and other AD-associated pathologies are also suggested to increase the risk of serious SARS-CoV-2 infection. Anosmia is a common neurological symptom reported in COVID-19 and in early AD. The olfactory mucosa (OM) is important for the perception of smell and a proposed site of viral entry to the brain. However, little is known about SARS-CoV-2 infection at the OM of individuals with AD.
To address this gap, we established a 3D in vitro model of the OM from primary cells derived from cognitively healthy and AD individuals. We cultured the cells at the airliquid interface (ALI) to study SARS-CoV-2 infection under controlled experimental conditions. Primary OM cells in ALI expressed angiotensin-converting enzyme 2 (ACE-2), neuropilin-1 (NRP-1), and several other known SARS-CoV-2 receptor and were highly vulnerable to infection. Infection was determined by secreted viral RNA content and confirmed with SARS-CoV-2 nucleocapsid protein (NP) in the infected cells by immunocytochemistry. Differential responses of healthy and AD individuals-derived OM cells to SARS-CoV-2 were determined by RNA sequencing.
Results indicate that cells derived from cognitively healthy donors and individuals with AD do not differ in susceptibility to infection with the wild-type SARS-CoV-2 virus. However, transcriptomic signatures in cells from individuals with AD are highly distinct. Specifically, the cells from AD patients that were infected with the virus showed increased levels of oxidative stress, desensitized inflammation and immune responses, and alterations to genes associated with olfaction. These results imply that individuals with AD may be at a greater risk of experiencing severe outcomes from the infection, potentially driven by pre-existing neuroinflammation.
The study sheds light on the interplay between AD pathology and SARS-CoV-2 infection. Altered transcriptomic signatures in AD cells may contribute to unique symptoms and a more severe disease course, with a notable involvement of neuroinflammation. Furthermore, the research emphasizes the need for targeted interventions to enhance outcomes for AD patients with viral infection. The study is crucial to better comprehend the relationship between AD, COVID-19, and anosmia. It highlights the importance of ongoing research to develop more effective treatments for those at high risk of severe SARS-CoV-2 infection.
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Alzheimers Alters COVID-19 Response in Olfactory Cells - Neuroscience News
Computational models that mimic the structure and function of the human auditory system could help researchers design better hearing aids, cochlear implants, and brain-machine interfaces. A new study from MIT has found that modern computational models derived from machine learning are moving closer to this goal.
In the largest study yet of deep neural networks that have been trained to perform auditory tasks, the MIT team showed that most of these models generate internal representations that share properties of representations seen in the human brain when people are listening to the same sounds.
The study also offers insight into how to best train this type of model: The researchers found that models trained on auditory input including background noise more closely mimic the activation patterns of the human auditory cortex.
What sets this study apart is it is the most comprehensive comparison of these kinds of models to the auditory system so far. The study suggests that models that are derived from machine learning are a step in the right direction, and it gives us some clues as to what tends to make them better models of the brain, says Josh McDermott, an associate professor of brain and cognitive sciences at MIT, a member of MITs McGovern Institute for Brain Research and Center for Brains, Minds, and Machines, and the senior author of the study.
MIT graduate student Greta Tuckute and Jenelle Feather PhD 22 are the lead authors of the open-accesspaper, which appears today inPLOS Biology.
Deep neural networks are computational models that consists of many layers of information-processing units that can be trained on huge volumes of data to perform specific tasks. This type of model has become widely used in many applications, and neuroscientists have begun to explore the possibility that these systems can also be used to describe how the human brain performs certain tasks.
These models that are built with machine learning are able to mediate behaviors on a scale that really wasnt possible with previous types of models, and that has led to interest in whether or not the representations in the models might capture things that are happening in the brain, Tuckute says.
When a neural network is performing a task, its processing units generate activation patterns in response to each audio input it receives, such as a word or other type of sound. Those model representations of the input can be compared to the activation patterns seen in fMRI brain scans of people listening to the same input.
In 2018, McDermott and then-graduate student Alexander Kellreportedthat when they trained a neural network to perform auditory tasks (such as recognizing words from an audio signal), the internal representations generated by the model showed similarity to those seen in fMRI scans of people listening to the same sounds.
Since then, these types of models have become widely used, so McDermotts research group set out to evaluate a larger set of models, to see if the ability to approximate the neural representations seen in the human brain is a general trait of these models.
For this study, the researchers analyzed nine publicly available deep neural network models that had been trained to perform auditory tasks, and they also created 14 models of their own, based on two different architectures. Most of these models were trained to perform a single task recognizing words, identifying the speaker, recognizing environmental sounds, and identifying musical genre while two of them were trained to perform multiple tasks.
When the researchers presented these models with natural sounds that had been used as stimuli in human fMRI experiments, they found that the internal model representations tended to exhibit similarity with those generated by the human brain. The models whose representations were most similar to those seen in the brain were models that had been trained on more than one task and had been trained on auditory input that included background noise.
If you train models in noise, they give better brain predictions than if you dont, which is intuitively reasonable because a lot of real-world hearing involves hearing in noise, and thats plausibly something the auditory system is adapted to, Feather says.
The new study also supports the idea that the human auditory cortex has some degree of hierarchical organization, in which processing is divided into stages that support distinct computational functions. As in the 2018 study, the researchers found that representations generated in earlier stages of the model most closely resemble those seen in the primary auditory cortex, while representations generated in later model stages more closely resemble those generated in brain regions beyond the primary cortex.
Additionally, the researchers found that models that had been trained on different tasks were better at replicating different aspects of audition. For example, models trained on a speech-related task more closely resembled speech-selective areas.
Even though the model has seen the exact same training data and the architecture is the same, when you optimize for one particular task, you can see that it selectively explains specific tuning properties in the brain, Tuckute says.
McDermotts lab now plans to make use of their findings to try to develop models that are even more successful at reproducing human brain responses. In addition to helping scientists learn more about how the brain may be organized, such models could also be used to help develop better hearing aids, cochlear implants, and brain-machine interfaces.
A goal of our field is to end up with a computer model that can predict brain responses and behavior. We think that if we are successful in reaching that goal, it will open a lot of doors, McDermott says.
The research was funded by the National Institutes of Health, an Amazon Fellowship from the Science Hub, an International Doctoral Fellowship from the American Association of University Women, an MIT Friends of McGovern Institute Fellowship, a fellowship from theK. Lisa Yang Integrative Computational Neuroscience (ICoN) Center at MIT,and a Department of Energy Computational Science Graduate Fellowship.
Republished with permission ofMIT News. Read theoriginal article.
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Deep neural networks show promise as models of human hearing - Freethink
image:
Large chains of migrating cells forming braided streams break down into a shower of young migrating neurons that continue to integrate into the entorhinal cortex and neighboring regions until 2-3 years of age.
Credit: Lab of Shawn Sorrell/Pitt
The human brain continues to be built after we are born for far longer than previously recognized, suggests research by Shawn Sorrells, assistant professor of neuroscience inthe Kenneth P. Dietrich School of Arts andSciences. Sorrellss research on postnatal brain development, published today inthe journalNature, shines light on fundamental processes that contribute to the development of important brain functions, such as learning, memory and spatial navigation.
The new research suggests that a subset of inhibitory neurons within the entorhinal cortex, or EC -- an area of the brain essential for forming memories -- continue to migrate into this region where they build new neuronal connections from birth through toddlerhood. The study suggests that extensive postnatal neuronal migration across the EC might underlie critical neuroplasticity periods during which the brain is especially receptive to changes and adaptations. The discovery also points to a possible reason why EC neurons are more susceptible to neurodegeneration, since other recent studies have found that this same type of neuron is impacted early in Alzheimers disease.
By analyzing brain samples that were provided, in part, by the epilepsy tissue bank at UPMC Childrens Hospital and the Neuropathology Department at UPMC Presbyterian Hospital, Sorrells' research team was first to show that, unlike what was previously thought, neuronal migration of such scale and duration is extensive within regions that control thoughts and emotions. The discovery offers an explanation for how the human brain makes billions of new neurons over a very short time span through a mechanism that allows neurons to continue arriving after birth.
It is generally thought that the brain is done recruiting neurons by the time an individual is born, said Sorrells. We were incredibly excited to learn that not only does large-scale neuronal migration continue into specific brain regions, but that this process also continues into ages when children are crawling and beginning to walk.
Imaging analysis
Human tissue samples
Protracted Neuronal Recruitment in the Temporal Lobe of Young Children
20-Dec-2023
A.A.B is a co-founder and is on the Scientific Advisory Board of Neurona Therapeutics. C.J.Y is a Scientific Advisory Board member for and holds equity in Related Sciences and ImmunAI, a consultant for and holds equity in Maze Therapeutics, and a consultant for TReX Bio. C.J.Y. has received research support from Chan Zuckerberg Initiative, Chan Zuckerberg Biohub, and Genentech
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
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Integrating research and clinical care to uncover secrets of brain development - EurekAlert
Fanta has collaborated with TikTok to release the #FantaTikTokExperience an entertaining and innovative experience combining flavour, fun, and cutting-edge technology for TikTok Creators.
The adventure is rooted in fascinating neuroscientific findings that unravel how our senses may influence our perceptions of flavour. Could watching a TikTok video change the perception of the taste of a Fanta flavour? That's precisely what the Fanta set out to discover with this experiment.
"Through our innovative collaboration with TikTok, we have delved into intriguing new facets of sensory perception," says Zainab Mohamed, Fanta senior brand director at Coca-Cola Africa. "The compelling dynamics between our senses have never been more apparent. The power of visuals and sounds may transform the taste experience a revelation that adds a whole new layer of excitement to enjoying Fanta. With TikTok's pulsating platform, we have been able to bring this sensory adventure to life, providing an engaging, immersive, and truly unique experience for our influencers."
To test this phenomenon, TikTok Creators were invited to scan a QR code on limited-edition Fanta cans. Fanta launched a WebAR platform, guiding users through TikTok videos which the creators watched while consuming a limited-edition Fanta beverage, offering a fun and interactive experience. As the creators sipped their Fanta beverage, they were presented with the opportunity to test if they could sense the flavour shifting from fruity to tangy, or even bitter, based on the video they watched.
Prolonging the thrill, an unforgettable live spectacle was hosted at Cape Town's Zeitz MOCAA on 20 December 2023. It took the neuroscientific experiment a step further by serving influencers the limited-edition Fanta beverage, set against a backdrop of distinct sounds and eye-catching visuals.
The event also featured "Reaction Booths", fitted with cameras to record the spontaneous responses of creators as they viewed TikTok videos while savoring the #FantaTikTokExperience. The #FantaTikTokExperience is a testament to Fanta's commitment to providing unique, creative and playful experiences to their audiences. This unique blend of technology, creativity, and sensory exploration breaks new ground, adding a playful twist to enjoying Fanta.
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Fanta and TikTok collaborate to challenge tastebuds with neuroscience experiment - Bizcommunity.com
Revolutionizing Our Understanding of the Brain
In a significant technological breakthrough, a supercomputer capable of simulating the entire human brain is set to be switched on in 2024. This incredible innovation, named the DeepSouth supercomputer, is expected to revolutionize our understanding of the brain and its functions. The project, spearheaded by Western Sydney University, aims to create a digital replica of the human brain, providing researchers with a groundbreaking tool to study neurological disorders and develop new treatments.
The DeepSouth supercomputer uses a neuromorphic system that emulates biological processes, simulating large networks of spiking neurons at 228 trillion synaptic operations per second. This remarkable system is purpose-built to operate like networks of neurons, requiring less power and enabling greater efficiencies. The supercomputer, to be based at Western Sydney University, is expected to be operational by April 2024.
The implications and potential applications of this technology are vast. It is anticipated that this supercomputer will significantly advance smart devices, sensors for manufacturing and agriculture, and smarter AI applications. Furthermore, the DeepSouth supercomputer will allow researchers to better understand how brains can process massive amounts of information using such little power. This knowledge could potentially lead to the creation of a cyborg brain vastly more powerful than our own, revolutionizing our understanding of how our brains work.
The development of the worlds first human brain-scale supercomputer is considered a game changer for the study of neuroscience. There is widespread interest from researchers studying neuroscience and those who want to prototype new engineering solutions in the AI space. If successful, this project could lead to significant advancements in neuroscience and medical technology, marking a major milestone in the fields of neuroscience and artificial intelligence.
In conclusion, the DeepSouth supercomputer represents a significant leap in our quest to understand and replicate the complex workings of the human brain. The potential benefits of this technology range from a deeper understanding of neurological disorders to advancements in AI applications. As we eagerly await the launch of this supercomputer in 2024, we can only imagine the wealth of insights and breakthroughs that lie ahead in the field of neuroscience and beyond.
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DeepSouth Supercomputer: Revolutionizing Our Understanding of the Brain - Medriva
Wireless Communication Between Neurons: A Game-Changer in Neuroscience
In a breakthrough for neuroscience research, scientists have uncovered a novel form of communication between neurons a wireless, or non-synaptic, mode of interaction. This revolutionary discovery challenges the traditional understanding of synaptic communication, where neurons connect via axons and dendrites with neurotransmitters bridging a minuscule gap between them. Synaptic communication, akin to a wired internet connection, maintains a degree of privacy, while this newfound wireless communication allows chemical messengers to traverse more extended distances through the intercellular space, potentially risking message interception.
Contributing significantly to our comprehension of neural communication is the nematode Caenorhabditis elegans (C. elegans). Possessing just over 300 neurons, C. elegans has been fundamental in mapping the connections between neurons, known as the connectome. The first comprehensive connectome was published back in 1986, and most recently, researchers have published an inventory of all wireless connections within C. elegans, particularly those utilizing neuropeptides as chemical messengers.
One research group predicted the wireless connection map based on gene expression within neurons, while another employed optogenetics to examine the impact of activating or deactivating nerve cells on their neighboring cells. These findings suggest a profound departure of the wireless communication network from the synaptic network, underscoring the complexity of the neural communication matrix.
The implications of these findings are far-reaching. They offer a fresh perspective on the functioning of the human nervous system and how diseases or medications might influence it, potentially revolutionizing treatments for neurological disorders and the design of brain-computer interfaces (BCIs). BCIs, systems that enable direct communication between the brain and an external device or computer system, have immense potential in medicine, rehabilitation, and human augmentation. BCIs harness the power of real-time recordings of brain activity for communication and control, allowing individuals to interact with devices using only their thoughts.
Future applications of this research could include the treatment of neurological diseases such as Attention Deficit Hyperactivity Disorder (ADHD), ALS, epilepsy, and stroke, as well as advancements in functional brain mapping and consciousness assessment. As we continue to unravel the mysteries of the brain and its complex communication networks, the possibilities seem endless.
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Revolution in Neuroscience: Wireless Neuron Communication - BNN Breaking