Last week, 10 graduate students took to the stage to compete in Dals annual 3 Minute Thesis (3MT) competition, with medical neuroscience PhD student Reynaldo Popoli earning this years winning title with his presentation on improving the quality of life for patients living with the neurological disorder ALS.
The 3MT finals, held Tuesday, March 19 in the Dalhousie Student Union Building, challenged competitors to present their research to a non-specialist audience in three engaging minutes or less, using only one static PowerPoint slide as a visual aid.
Five masters and five PhD students shared their research, representing the Faculties of Medicine, Science and Health.
Along with taking home the title of Dals newest 3MT champion after winning over the judging panel, Popoli won a cash prize of $1,000 and the opportunity to represent Dalhousie at the Eastern 3MT regionals at the Institut national de la recherche scientifique in Quebec this June.
I feel incredibly grateful, especially to my colleagues that allowed me to practice my presentation and provided invaluable feedback, he says.
Faculty of Graduate Studies Dean Marty Leonard with Popoli.
Popolis presentation called attention to the devastating impacts of ALS a disease that affects the cells in our bodies that control our muscles. These cells originate in the brain and spinal cord and travel to the muscles, forming connections called neuromuscular junctions. In ALS, the cells withdraw from the muscles, and these connections are left non-functional.
The goal of my research is to understand some of the changes that occur in ALS. More precisely, in the connections between the cells that control our movements and their respective muscles. By understanding these changes, we hope we can use different therapeutic approaches to slow down disease progression and improve symptoms, he says.
Popolis research looks at drugs that help regulate and maintain the integrity of the neuromuscular junction. He has shown that the use of these drugs in ALS make symptoms progress much slower and maintain neuromuscular junctions for longer, allowing for a 10 per cent increase in life expectancy and better quality of life for patients.
My work is far from over, but Im hopeful that with this novel research, well be able to find new treatments for this devastating disease.
Pooyan Moradi, another PhD student in medical neuroscience, and Kaela Trumble, a masters student in rehabilitation research, were also selected as top finalists by the judging panel.
Moradi earned second place and a $500 prize, presenting on the use of artificial intelligence to detect seizures in animals and how this model can be applied to better predict epilepsy in humans who have suffered head injuries.
Pooyan Moradi.
Trumble placed third in the competition and won $250 with a presentation covering the differences in how people develop health problems as they age in relation to heart disease.
Kaela Trumble.
The remaining eight finalists each earned $100 prizes for their inspiring presentations.
Also receiving the most votes for the Peoples Choice Award, biochemistry and molecular biology masters student Dina Rogers captivated the crowd when describing a biological recycling process by which PET plastic can be repurposed into new materials by protein engineering to combat climate change. The award, valued at $500, was generously sponsored by Estelle Joubert, assistant dean of the Faculty of Graduate Studies, and entrepreneur Paul Doerwald.
Dina Rogers.
Recommended reading:Where experience meets impact: Introducing Dalhousies 2023 Top Coop Students of the Year
This year's 3MT finals opened with a traditional Mi'kma'ki welcome with Elder Ann LaBillois. The event was enthusiastically hosted by CBC reporter and video journalist Brett Ruskin for a sixth time.
Judges for the competition were Dr. Frank Harvey, Dal's provost and vice-president academic, Grace Jefferies-Aldridge, Dals vice-president, people and culture, and Kristan Hines, senior vice-president of corporate and public affairs at NATIONAL Public Relations.
Organized by the Faculty of Graduate Studies, the event served as an opportunity for members of the Dal community and beyond to learn about the impactful work the universitys graduate students are engaged in.
For many of us, the 3 Minute Thesis competition is the highlight of the year at Dalhousie, says Dr. Marty Leonard, dean of the Faculty of Graduate Studies. It challenges students to take what could be very technologically or theoretically complex research or better yet, both and make it accessible and interesting to anyone.
Dalhousie President Dr. Kim Brooks invited the crowd to relish the opportunity to celebrate the extraordinary research happening on campus.
Dal President Kim Brooks.
If you have the privilege of spending time in a university, one of the things you get to do often in your academic life is trace an idea back to its origins, she says. And almost every time you find a new idea, a unique contribution, and you trace it back to its origins, you find a graduate student.
3MT finalists.
Dina Rogers, MSc, Biochemistry and Molecular Biology
Proteins vs. Pollution: A Biochemical Solution to a Brighter Future
Kateryna Rudenko, MES, Environmental Studies
Weaving Mikmaki from Stories We Share
Joy Liu, MSc, Statistics
From Approximate to Accurate: Improving Sea Scallop Meat Weight Estimates in the Bay of Fundy through Statistical Modeling
Reynaldo Popoli, PhD, Medical Neuroscience
How a life changes forever in just 12 months
Kaela Trumble, MSc, Rehabilitation Research
How will your heart age?
Eniko Zsoldos, PhD, Chemistry
Improving Battery Sustainability by Limiting Charging
Divya Rathore, PhD, Physics and Atmospheric Science
Many Shades of Green
Sophie Inkpen, MSc, Kinesiology
Taking Action Through Activity: A Program for Patients with Acquired Brain Injury
Pooyan Moradi, PhD, Medical Neuroscience
Cloudy with a Chance of Epilepsy
Fatemeh Mahdizadeh Karizaki, PhD in Health
Promoting Health and Wellbeing: Access and Inclusion to Childcare and Early Learning for Children with Disabilities in Nova Scotia
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Big research, little time: Medical neuroscience student wins 3 Minute Thesis finals - Dal News
Summary: Researchers illuminated the pivotal role of the protein MEIS2 in brain development, particularly in the differentiation of inhibitory projection neurons, crucial for motion control and decision-making. This protein, in conjunction with DLX5, activates specific genes that guide the development of these neurons.
A mutation in MEIS2, linked to intellectual disabilities in patients, hampers this process, underscoring the proteins significance in neurodevelopment. The study enriches our understanding of the genetic orchestration behind neuron diversity and highlights the intricate relationship between gene activation and neuronal fate, offering new insights into the genetic underpinnings of neurodevelopmental disorders.
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Source: Max Planck Institute
Brain development is a highly orchestrated process involving numerous parallel and sequential steps. Many of these steps depend on the activation of specific genes.
A team led by Christian Mayer at the Max Planck Institute for Biological Intelligence discovered that a protein called MEIS2 plays a crucial role in this process: it activates genes necessary for the formation of inhibitory projection neurons.
These neurons are vital for motion control and decision-making. A MEIS2 mutation, known from patients with severe intellectual disability, was found to disrupt these processes.
The study provides valuable insights into brain development and consequences of genetic mutations.
Nerve cells are a prime example for interwoven family relations. The specialized cells that form the brain come in hundreds of different types, all of which develop from a limited set of generalized progenitor cells their immature parents. During development, only a specific set of genes is activated in a single progenitor cell.
The precise timing and combination of activated genes decide which developmental path the cell will take. In some cases, apparently identical precursor cells develop into strikingly different neurons. In others, different precursors give rise to the same nerve cell type.
The complexity is mind-blowing and not easy to disentangle in the lab. Christian Mayer and his team set out to do so nevertheless (Diversity research in the brain). Together with colleagues in Munich and Madrid, they now added another puzzle piece to our understanding of neuron development.
The scientists studied the formation of inhibitory neurons that produce the neurotransmitter GABA cells, which are known to display a broad range of diversity. In the adult brain, inhibitory neurons can act locally, or they can extend long-range axons to remote brain areas.
Locally connected interneurons are an integral part of the cortical circuit, reciprocally linking cortical neurons. Long-range projection neurons, on the other hand, primarily populate subcortical regions. They contribute to motivated behavior, reward learning and decision-making.
Both types, interneurons and projection neurons, originate in the same area of the developing brain. From here, the newborn neurons migrate to their final locations in the brain.
Using abarcoding approach, Christian Mayer and his team followed the family relationships between precursor cells and young inhibitory neurons. They discovered that a protein called MEIS2 plays an important role when a precursor cell decides whether it should turn into an interneuron or into a projection neuron: MEIS2 assists the cellular machinery to activate the genes that are required for a precursor cell to become a projection neuron.
To advance this development, MEIS2 works together with another protein, known as DLX5. When MEIS2 is missing or doesnt function correctly, the development of projection neurons is stalled and a larger fraction of precursor cells turns into interneurons instead. However, MEIS2 cant do the job by itself.
Our experiments show that MEIS2 and DLX5 have to come together at the same time, and in the same cells, explains Christian Mayer.
Only the combination of the two will fully activate the genes that drive projection neuron development.
The importance of this process is underscored by previous reports on a MEIS2 variant that was found in patients with intellectual disabilities and a delayed development. Due to a small change in the MEIS2 gene, a slightly different protein is produced.
The team around Christian Mayer tested this MEIS2 variant in their experiments and found that it leads to a failure to induce the specific genes needed to form projection neurons.
The inability of MEIS2 to activate the genes essential for the formation of projection neurons may contribute to neurodevelopmental disorders, such as those observed in patients with mutations in the gene encoding this protein, says Christian Mayer.
Intrigued by this discovery, the researchers delved into the mechanism by which MEIS2 activates projection neuron specific genes.
Patients with mutations in MEIS2 suffer from a diverse range of effects, like irregularities in digits, impaired lung to brain development, or intellectual disabilities. At a first look, these symptoms have nothing in common, relates Christian Mayer.
This shows, how important it is to understand that genes often have very different roles in different parts of the body.
The genome has millions of non-coding regulatory elements like enhancers, promoters, and insulators. These elements dont actually code for proteins themselves, but they act like switches, controlling when and where genes turn on and off.
Enhancers, which are part of the genome, are like interpreters in the cell. If MEIS2 and DLX5 are present together, a specific set of enhancers becomes active. It is this specific set of enhancers that induces projection neuron genes in the brain. In other parts of the body, MEIS2 interacts with other proteins to induce different sets of enhancers, explains Christian Mayer.
Recent large-scale whole exome sequencing studies in patients have provided a systematic and highly reliable identification of risk genes for neurodevelopmental disorders.
Future studies focusing on the molecular interactions between the proteins encoded by these risk genes, such as MEIS2, will pave the way for a comprehensive understanding of the biological mechanisms underlying neurodevelopmental disorders.
Author: Marius Bruer Source: Max Planck Institute Contact: Marius Bruer Max Planck Institute Image: The image is credited to Neuroscience News
Original Research: Open access. Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development by Christian Mayer et al. Nature Neuroscience
Abstract
Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development
The mammalian telencephalon contains distinct GABAergic projection neuron and interneuron types, originating in the germinal zone of the embryonic basal ganglia. How genetic information in the germinal zone determines cell types is unclear.
Here we use a combination of in vivo CRISPR perturbation, lineage tracing and ChIPsequencing analyses and show that the transcription factor MEIS2 favors the development of projection neurons by binding enhancer regions in projection-neuron-specific genes during mouse embryonic development.
MEIS2 requires the presence of the homeodomain transcription factor DLX5 to direct its functional activity toward the appropriate binding sites.
In interneuron precursors, the transcription factor LHX6 represses the MEIS2DLX5-dependent activation of projection-neuron-specific enhancers. Mutations ofMeis2result in decreased activation of regulatory enhancers, affecting GABAergic differentiation.
We propose a differential binding model where the binding of transcription factors atcis-regulatory elements determines differential gene expression programs regulating cell fate specification in the mouse ganglionic eminence.
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The Genetic Secrets of Neuron Formation - Neuroscience News
After several decades of developments in AI, has the inspiration that can be drawn from neuroscience been exhausted? Recent initiatives make the case for taking a fresh look at the intersection between the two fields.
The effects of neuroscience on artificial intelligence (AI), and the mutual influence of the two fields, have been discussed and debated in the past few decades. Not long after the seminal workshop at Dartmouth College in 1956, which launched the field of AI, artificial neural networks called perceptrons were introduced by Rosenblatt. He studied them as simple models of brain-inspired systems following earlier work, including from McCulloch and Pitts, who introduced formal models of biological neurons, and from Hebb, who postulated the conditions under which the connection strengths of biological neurons change. Research on hierarchical processing in the visual system in the 1960s inspired the development of convolutional neural networks in the 1980s. However, as AI research has evolved at a fast pace, progress over recent years has stirred a divergence from this original neuroscience inspiration. The pursuit of more powerful artificial neural systems in leading AI research labs, particularly those affiliated with tech companies, is currently focussed on engineering. This pursuit emphasizes further scaling up of complex architectures such as transformers, rather than integrating insights from neuroscience.
Credit: [Vertigo3d]/[E+]/Getty
A recent panel discussing the role of neuroscience in contemporary AI research and the extent of their mutual influence was convened at COSYNE, the leading computational and systems neuroscience conference. The panel involved Anthony Zador (Cold Spring Harbor Laboratory), Alexandre Pouget (University of Geneva), Blaise Aguera y Arcas (Google), Kim Stachenfeld (Google DeepMind and Columbia University), Jonathan Pillow (Princeton University) and Eva Dyer (Georgia Institute of Technology), with Paul Middlebrooks (host of the Brain-Inspired podcast) moderating.
Interestingly, the panellists did not seem to agree on the extent to which neuroscience currently influences and is influenced by AI research. For example, Aguera y Arcas believes that, historically, progress has resulted at times of convergence between the two fields and that, even though this does not seem to be the case now, in the future we might discover parallels between transformers and brain computation. This optimism was echoed by Zador, who argued that neuroscience has provided key insights for AI. He stated that the missing piece in current AI methods may come from basic research in neuroscience. By contrast, Pouget stated that although neuroscience labs are pushing hard to discover fundamental principles that can be incorporated into AI, nothing especially convincing has emerged in the past three decades, whereas, in contrast, neuroscience research has been profoundly influenced by recent developments in AI. This seems to be confirmed by Stachenfelds comment that the use of AI methods in brain research is a low-hanging fruit that has influenced the way neuroscience research is pursued at Google DeepMind. Dyer noted that with the shift of AI towards transformers and other complex architectures, the field seems to have moved away from its neural-inspired roots; however, AI may still look towards neuroscience for help in understanding complex information processing systems.
The COSYNE panel forms part of a recent coalition of initiatives around NeuroAI, a push to identify fresh ideas at the intersection between neuroscience and AI. For example, Neuromatch, a platform facilitating global collaboration in computational sciences, has developed a NeuroAI course scheduled for July 2024 on the common principles of natural and artificial intelligence. Other programs that promote interdisciplinary collaboration include the Cold Spring Harbor NeuroAI program, which will hold its third conference From neuroscience to artificially intelligent systems in autumn 2024. Academic institutions are embracing NeuroAI, as evidenced by NeuroAI and Intelligent Systems at Princeton University and UCL NeuroAI at University College London, which encourage collaboration between the neuroscience and AI communities.
Scientific meetings such as COSYNE have a crucial role in convening researchers drawn to ideas that transcend traditional academic boundaries. In a perspective article on the origins of COSYNE1, Zador highlights how such meetings create and nurture communities, such as theoretical and experimental neuroscientists, while facilitating the exchange of scientific languages. During the Q&A session of the COSYNE panel discussion, Pouget emphasized the roles of neuroscience, cognitive science and AI in understanding the brain, and expressed concerns about the limited representation of contributions from cognitive science and cognitive neuroscience at the conference. This frustration prompted researchers in these fields to establish the Cognitive and Computational Neuroscience Conference (CCN), which organized its first meeting in 2017. Although distinct, CCN and COSYNE complement one another, offering intriguing prospects for exploring how the different approaches systems neuroscience versus cognitive science and cognitive neuroscience shape and are shaped by AI.
Overall, the extent of the role of neuroscience in AI research, and that of AI in neuroscience research, remain open questions for the future. However, these two fields are deeply linked, and the exchange of ideas between them continues to evolve. The upcoming generation of scientists will need to possess fluency in both domains, making interdisciplinary programs such as Neuromatch and conferences such as COSYNE and CNN indispensable. The (re)emergence of NeuroAI will prompt researchers to explore the crucial questions necessary for uncovering some of the brains computational principles that have remained elusive, paving the way for the development of more intelligent machines.
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The new NeuroAI - Nature.com
Summary: Researchers reviewed 50 studies to deepen our understanding of aphantasia, a phenomenon where individuals cant visualize mentally. The research reveals aphantasias diverse impact, from reduced autobiographical memory and face recognition to broader implications in music imagination and occupation choices, suggesting a spectrum rather than a binary condition.
Additionally, the review highlights genetic predispositions and familial patterns, offering a glimpse into the physiological and neural underpinnings of both aphantasia and its opposite, hyperphantasia. This exploration not only clarifies the range of human cognitive experience but also challenges misconceptions about imagination and visual thinking.
Key Facts:
Source: University of Exeter
People who cannot bring to mind visual imagery are also less likely to experience imagery of other kinds, like imagining music, according to new research by the academic who first discovered the phenomenon.
Professor Adam Zeman, of the University of Exeter, first coined the term aphantasia in 2015, to describe those who cant visualise. Since then, tens of thousands of people worldwide have identified with the description.
Many say they knew they processed information differently to others but were unable to describe how. Some of them expressed shock on discovering that other people can conjure up an image in their minds eye.
Now, Professor Zeman has conducted a review of around 50 recent studies, published inTrends in Cognitive Sciences, to summarise findings in a field that has emerged since his first publication. Research indicates that aphantasia is not a single entity but has subtypes.
For example, not everyone with aphantasia has a poor autobiographical memory or difficulty in recognising faces, and in a minority of people, aphantasia appeared to be linked to autism. People who cannot visualise are more likely to have scientific occupations. Unexpectedly, although people with aphantasia cant visualise at will, they often dream visually.
Professor Zemans review provides evidence that whether people have aphantasia or hyperphantasia a particularly vivid visual imagination is linked to variations in their physiology and neural connectivity in the brain, as well as in behaviour.
For example, listening to scary stories alters skin conductance in those with imagery, meaning people sweat but this does not occur in people with aphantasia.
Aphantasia is thought to affect around one percent of the population, while three percent are hyperphantasic. These figures rise to around five and 10 percent with more generous criteria for inclusion. Both aphantasia and hyperphantasia often run in families, hinting at the possibility of a genetic basis.
Professor Zeman, who now holds honorary contracts at the universities of Exeter and Edinburgh, said: Coining the term aphantasia has unexpectedly opened a window on a neglected aspect of human experience. It is very gratifying that people who lack imagery have found the term helpful, while a substantial surge of research is shedding light on the implications of aphantasia.
Despite the profound contrast in subjective experience between aphantasia and hyperphantasia, effects on everyday functioning are subtle lack of imagery does not imply lack of imagination. Indeed, the consensus among researchers is that neither aphantasia nor hyperphantasia is a disorder.
These are variations in human experience with roughly balanced advantages and disadvantages. Further work should help to spell these out in greater detail.
I struggle to fully immerse myself in role-play with my children
Solicitor Mary Wathens frustration that she struggled to engage in role playing games with her two young children, when she found all other engagement with her children so fulfilling, was her sign that she had aphantasia, meaning she cannot visualise imagery.
The 43-year-old, from Newent near Cheltenham, said: One of my friends said that he uses the images in his head to enhance role play. When I asked him to explain this in more detail it became clear that he and everyone else in the room could easily create an image in their head and use that as the backdrop for the role play.
This was totally mind-blowing to me. I just cannot understand what they really mean where is this image and what does it look like? To me, unless you can see something with your eyes, its not there.
Marys shock intensified when she realised her husband, has such vivid visual imagery that he is probably hyperphantasic. He thinks in moving pictures, like movies sometimes to the point that he can mistake those thoughts for memories. To me, thats unfathomable.
Mary has come to realise that her lack of visual imagery may well account for her difficulties with memory. She said: I can comprehend and retain concepts and principles really well but Im unable to recall facts and figures. I cant recreate something in my head or re see something that is not actually there in that moment.
Ive found it quite saddening to learn that other people can call to mind an image of their children when theyre not there. Id love to be able to do that, but I just cant but Ive learned to compensate by taking plenty of photos, so that I can relive those memories through those images.
Whilst Im sure there are wonderful advantages to being able to think in pictures, I think its important to remind myself that there are advantages to having aphantasia too.
Im a really good written and verbal communicator I think thats because Im not caught up with any pictures, so I just focus on the power of the word. Im also a deeply emotional person and perhaps thats my brains way of overcompensating; I feel things as a way of experiencing them, rather than seeing them.
I think its really important to raise awareness that some people just dont have this ability particularly as using visual imagination is a key way that young children are taught to learn and engage.
Primary teachers need to know that some children just wont be able to visualise and that could be why theyre not engaging in those kinds of activities. We need to ensure we cater for everyone and encourage other ways of learning and engaging.
Author: Louise Vennells Source: University of Exeter Contact: Louise Vennells University of Exeter Image: The image is credited to Neuroscience News
Original Research: Open access. Aphantasia and hyperphantasia exploring imagery vividness extremes by Adam Zeman et al. Trends in Cognitive Sciences
Abstract
Aphantasia and hyperphantasia exploring imagery vividness extremes
The vividness of imagery varies between individuals. However, the existence of people in whom conscious, wakeful imagery is markedly reduced, or absent entirely, was neglected by psychology until the recent coinage of aphantasia to describe this phenomenon.
Hyperphantasia denotes the converse imagery whose vividness rivals perceptual experience. Around 1% and 3% of the population experience extreme aphantasia and hyperphantasia, respectively.
Aphantasia runs in families, often affects imagery across several sense modalities, and is variably associated with reduced autobiographical memory, face recognition difficulty, and autism. Visual dreaming is often preserved.
Subtypes of extreme imagery appear to be likely but are not yet well defined. Initial results suggest that alterations in connectivity between the frontoparietal and visual networks may provide the neural substrate for visual imagery extremes.
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Exploring Aphantasia: The Mind Without a Mental Picture - Neuroscience News
Summary: A global study involving 131 researchers from 105 labs across seven countries has found altered brain pH and lactate levels across various animal models of neuropsychiatric and neurodegenerative disorders. This large-scale research reveals a common endophenotype involving energy metabolism dysfunction as a hallmark in disorders such as schizophrenia, autism, and Alzheimers.
The study demonstrates that about 30% of the examined animal models showed significant alterations in brain pH and lactate levels, linking these metabolic changes to impaired working memory and suggesting intrinsic disease characteristics rather than effects of medication. These findings open new avenues for understanding the transdiagnostic characteristics of cognitive impairments and developing targeted treatment strategies.
Key Facts:
Source: Fujita Health University
A global collaborative research group comprising 131 researchers from 105 laboratories across seven countries announces a groundbreaking research paper submitted toLife.
Titled Large-scale Animal Model Study Uncovers Altered Brain pH and Lactate Levels as a Transdiagnostic Endophenotype of Neuropsychiatric Disorders Involving Cognitive Impairment, the study identifies brain energy metabolism dysfunction leading to altered pH and lactate levels as common hallmarks in numerous animal models of neuropsychiatric and neurodegenerative disorders, such as intellectual disability, autism spectrum disorders, schizophrenia, bipolar disorder, depressive disorders, and Alzheimers disease.
At the forefront of neuroscience research, the research group sheds light on altered energy metabolism as a key factor in various neuropsychiatric and neurodegenerative disorders. While considered controversial, an elevated lactate level and the resulting decrease in pH is now also proposed as a potential primary component of these diseases.
Unlike previous assumptions associating these changes with external factors like medication, the research groups previous findings suggest that they may be intrinsic to the disorders.
This conclusion was drawn from five animal models of schizophrenia/developmental disorders, bipolar disorder, and autism, which are exempt from such confounding factors.
However, research on brain pH and lactate levels in animal models of other neuropsychiatric and neurological disorders has been limited. Until now, it was unclear whether such changes in the brain were a common phenomenon.
Additionally, the relationship between alterations in brain pH and lactate levels and specific behavioral abnormalities had not been clearly established.
This study, encompassing 109 strains/conditions of mice, rats, and chicks, including animal models related to neuropsychiatric conditions, reveals that changes in brain pH and lactate levels are a common feature in a diverse range of animal models of disorders, including schizophrenia/developmental disorders, bipolar disorder, autism, as well as models of depression, epilepsy, and Alzheimers disease. This studys significant insights include:
I.Common Phenomenon Across Disorders: About 30% of the 109 types of animal models exhibited significant changes in brain pH and lactate levels, emphasizing the widespread occurrence of energy metabolism changes in the brain across various neuropsychiatric conditions.
II.Environmental Factors as a Cause: Models simulating depression through psychological stress, and those induced to develop diabetes or colitis, which have a high comorbidity risk for depression, showed decreased brain pH and increased lactate levels. Various acquired environmental factors could contribute to these changes.
III.Cognitive Impairment Link: A comprehensive analysis integrating behavioral test data revealed a predominant association between increased brain lactate levels and impaired working memory, illuminating an aspect of cognitive dysfunction.
IV.Confirmation in Independent Cohort: These associations, particularly between higher brain lactate levels and poor working memory performance, were validated in an independent cohort of animal models, reinforcing the initial findings.
V.Autism Spectrum Complexity: Variable responses were noted in autism models, with some showing increased pH and decreased lactate levels, suggesting subpopulations within the autism spectrum with diverse metabolic patterns.
This is the first and largest systematic study evaluating brain pH and lactate levels across a range of animal models for neuropsychiatric and neurodegenerative disorders.
Our findings may lay the groundwork for new approaches to develop the transdiagnostic characterization of different disorders involving cognitive impairment, states Dr. Hideo Hagihara, the studys lead author.
Professor Tsuyoshi Miyakawa, the corresponding author, explains, This research could be a stepping stone towards identifying shared therapeutic targets in various neuropsychiatric disorders.
Future studies will center on uncovering treatment strategies that are effective across diverse animal models with brain pH changes. This could significantly contribute to developing tailored treatments for patient subgroups characterized by specific alterations in brain energy metabolism.
In this paper, the mechanistic insights into the reduction in pH and the increase in lactate levels remain elusive. However, it is known that lactate production increases in response to neural hyperactivity to meet the energy demand, and the authors seem to think this might be the underlying reason.
Author: Hisatsugu Koshimizu Source: Fujita Health University Contact: Hisatsugu Koshimizu Fujita Health University Image: The image is credited to Neuroscience News
Original Research: Open access. Large-scale animal model study uncovers altered brain pH and lactate levels as a transdiagnostic endophenotype of neuropsychiatric disorders involving cognitive impairment by Hideo Hagihara et al. eLife
Abstract
Large-scale animal model study uncovers altered brain pH and lactate levels as a transdiagnostic endophenotype of neuropsychiatric disorders involving cognitive impairment
Increased levels of lactate, an end-product of glycolysis, have been proposed as a potential surrogate marker for metabolic changes during neuronal excitation. These changes in lactate levels can result in decreased brain pH, which has been implicated in patients with various neuropsychiatric disorders.
We previously demonstrated that such alterations are commonly observed in five mouse models of schizophrenia, bipolar disorder, and autism, suggesting a shared endophenotype among these disorders rather than mere artifacts due to medications or agonal state.
However, there is still limited research on this phenomenon in animal models, leaving its generality across other disease animal models uncertain. Moreover, the association between changes in brain lactate levels and specific behavioral abnormalities remains unclear.
To address these gaps, the International Brain pH Project Consortium investigated brain pH and lactate levels in 109 strains/conditions of 2294 animals with genetic and other experimental manipulations relevant to neuropsychiatric disorders.
Systematic analysis revealed that decreased brain pH and increased lactate levels were common features observed in multiple models of depression, epilepsy, Alzheimers disease, and some additional schizophrenia models.
While certain autism models also exhibited decreased pH and increased lactate levels, others showed the opposite pattern, potentially reflecting subpopulations within the autism spectrum.
Furthermore, utilizing large-scale behavioral test battery, a multivariate cross-validated prediction analysis demonstrated that poor working memory performance was predominantly associated with increased brain lactate levels. Importantly, this association was confirmed in an independent cohort of animal models.
Collectively, these findings suggest that altered brain pH and lactate levels, which could be attributed to dysregulated excitation/inhibition balance, may serve as transdiagnostic endophenotypes of debilitating neuropsychiatric disorders characterized by cognitive impairment, irrespective of their beneficial or detrimental nature.
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Altered Brain pH Linked to Cognitive Disorders - Neuroscience News
Summary: Researchers challenge the notion that rational thinking is the only path to good decision-making. Highlighting the limited role of rationality in our choices, the researchers emphasize the profound influence of emotions, as demonstrated in his wine tasting study where perceived value affected enjoyment. This revelation not only questions our reliance on logic but also underscores the importance of emotional engagement in ensuring decision confidence. They advocate for a balanced approach, integrating instinct and intuition into our decision-making processes.
Key Facts:
Source: Stanford
Rational, analytical thinking is often seen as the gold standard when it comes to decision-making.
Yet according to Professor Baba Shiv, cool, level-headed intellect isnt the only game in town. Is a good decision based on reason? he asks. Or is it based on emotion?
Shivis the Sanwa Bank, Limited, Professor of Marketing at Stanford Graduate School of Business. Throughout his career, hes researched how brain structures related to emotion and motivation affect the choices we make.
In exploring the complex neurology that leads people to choose one course of action over another, he has uncovered insights that challenge our prevailing ideas about reason and rationality. Shiv explores how we can use our emotions and instincts to make meaningful decisions instead of relying on our rational brains alone.
Post-Enlightenment Western thought is infused with the assumption that rationality is at the core of properly functioning individuals and, by extension, properly functioning societies.
We have this embedded in our minds from childhood, Shiv says. If youre making consequential decisions, be as rational as possible.
Its an idea that Shiv traces from Aristotle to Descartes to the present, but one that forgets that we have evolved with emotion. If emotion were irrelevant, we would have evolved very differently.
According to Shiv, the rational brain is only responsible for about 5 to 10% of our decision-making. Emotions have a profound influence on our decisions and we arent aware of it, he says.
Shiv demonstrated this in a study involving wine drinkers and the neural processes used to distinguish different vintages. Subjects were told that they would be trying five different cabernet sauvignons, each identified by price.
In fact, only three wines were used two were poured twice, and each was marked with a fake price ranging from $5 to $90. As the participants tasted each wine, Shiv monitored their brain activity.
What intrigued me was that people swore that the more expensive the wine is, the better it tastes, Shiv says.
And the question I had was: Is this just a figment of our imagination? Or is the brain extracting more pleasure when the wine is more expensive?
That is exactly what his results found: The area of the brain that codes for pleasure shows greater activation when the brain thinks it is tasting a higher-priced wine than when its tasting a lower-priced wine, even though subjects tasted the same wine.
In addition to helping us make decisions, emotions play a critical role in helping us commit to the choices that we make. To move forward with a decision, we need what Shiv calls decision confidence, the conviction that our choice is the correct one.
If you emerge from the decision with doubts, youre more likely to give up too early and not persist in the course of action that you adopted, he says.
You need to emerge from the decision feeling absolutely confident. Its not making the right decision but making the decision right.
Much of society, especially business, places a premium on rational thinking, but Shiv encourages us to embrace our instincts and intuitions. If we want to make better decisions, then we need to think more like an artist.
Author: Baba Shiv Source: Stanford Contact: Baba Shiv Stanford Image: The image is credited to Neuroscience News
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Emotion vs. Reason: Rethinking Decision-Making - Neuroscience News
Summary: Researchers unveiled a groundbreaking discovery that DNA damage and brain inflammation are vital processes for forming long-term memories, particularly within the brains hippocampus.
Contrary to previous beliefs associating inflammation with neurological diseases, this study highlights inflammations critical role in memory formation through the activation of the Toll-Like Receptor 9 (TLR9) pathway following DNA damage in hippocampal neurons.
These findings not only challenge conventional views on brain inflammation but also caution against indiscriminate inhibition of the TLR9 pathway, given its importance in memory encoding and the potential risks of genomic instability.
Key Facts:
Source: Albert Einstein College of Medicine
Just as you cant make an omelet without breaking eggs, scientists atAlbert Einstein College of Medicinehave found that you cant make long-term memories without DNA damage and brain inflammation.
Their surprising findings were published online today in the journalNature.
Inflammation of brain neurons is usually considered to be a bad thing, since it can lead to neurological problems such as Alzheimers and Parkinsons disease, said study leaderJelena Radulovic, M.D., Ph.D., professor in theDominick P. Purpura Department of Neuroscience, professor of psychiatry and behavioral sciences, and the Sylvia and Robert S. Olnick Chair in Neuroscience at Einstein.
But our findings suggest that inflammation in certain neurons in the brains hippocampal region is essential for making long-lasting memories.
The hippocampus has long been known as the brains memory center. Dr. Radulovic and her colleagues found that a stimulus sets off a cycle of DNA damage and repair within certain hippocampal neurons that leads to stable memory assembliesclusters of brain cells that represent our past experiences. Elizabeth Wood, a Ph.D. student, and Ana Cicvaric, a postdoc in the Radulovic lab, were the studys first authors at Einstein.
From Shocks to Stable Memories
The researchers discovered this memory-forming mechanism by giving mice brief, mild shocks sufficient to form a memory of the shock event (episodic memory). They then analyzed neurons in the hippocampal region and found that genes participating in an important inflammatory signaling pathway had been activated.
We observed strong activation of genes involved in the Toll-Like Receptor 9 (TLR9) pathway, said Dr. Radulovic, who is also director of thePsychiatry Research Institute at Montefiore Einstein(PRIME).
This inflammatory pathway is best known for triggering immune responses by detecting small fragments of pathogen DNA. So at first we assumed the TLR9 pathway was activated because the mice had an infection. But looking more closely, we found, to our surprise, that TLR9 was activated only in clusters of hippocampal cells that showed DNA damage.
Brain activity routinely induces small breaks in DNA that are repaired within minutes. But in this population of hippocampal neurons, the DNA damage appeared to be more substantial and sustained.
Triggering Inflammation to Make Memories
Further analysis showed that DNA fragments, along with other molecules resulting from the DNA damage, were released from the nucleus, after which the neurons TLR9 inflammatory pathway was activated; this pathway in turn stimulated DNA repair complexes to form at an unusual location: the centrosomes.
These organelles are present in the cytoplasm of most animal cells and are essential for coordinating cell division. But in neuronswhich dont dividethe stimulated centrosomes participated in cycles of DNA repair that appeared to organize individual neurons into memory assemblies.
Cell division and the immune response have been highly conserved in animal life over millions of years, enabling life to continue while providing protection from foreign pathogens, Dr. Radulovic said.
It seems likely that over the course of evolution, hippocampal neurons have adopted this immune-based memory mechanism by combining the immune responses DNA-sensing TLR9 pathway with a DNA repair centrosome function to form memories without progressing to cell division.
Resisting Inputs of Extraneous Information
During the week required to complete the inflammatory process, the mouse memory-encoding neurons were found to have changed in various ways, including becoming more resistant to new or similar environmental stimuli.
This is noteworthy, said Dr. Radulovic, because were constantly flooded by information, and the neurons that encode memories need to preserve the information theyve already acquired and not be distracted by new inputs.
Importantly, the researchers found that blocking the TLR9 inflammatory pathway in hippocampal neurons not only prevented mice from forming long-term memories but also caused profound genomic instability, i.e, a high frequency of DNA damage in these neurons.
Genomic instability is considered a hallmark of accelerated aging as well as cancer and psychiatric and neurodegenerative disorders such as Alzheimers, Dr. Radulovic said.
Drugs that inhibit the TLR9 pathway have been proposed for relieving the symptoms of long COVID. But caution needs to be shown because fully inhibiting the TLR9 pathway may pose significant health risks.
The study is titled Formation of memory assemblies through the DNA sensing TLR9 pathway. Other Einstein authors are: Hui Zhang, Ph.D., Zorica Petrovic, B.A., Anna Carboncino, Ph.D., Kendra K. Parker, B.A., Thomas E. Bassett, Ph.D., Xusheng Zhang, M.S.
The other contributors are: co-first author Vladimir Jovasevic, Ph.D., at Northwestern University, Chicago, IL; Maria Moltesen, Ph.D., Naoki Yamawaki, Ph.D., Hande Login, Ph.D., Joanna Kalucka, Ph.D., all at Aarhus University, Aarhus, Denmark; Farahnaz Sananbenesi, and Andre Fischer, Ph.D., at University Medical Center, Gttingen, Germany.
Author: Elaine Iandoli Source: Albert Einstein College of Medicine Contact: Elaine Iandoli Albert Einstein College of Medicine Image: The image is credited to Neuroscience News
Original Research: Open access. Formation of memory assemblies through the DNA sensing TLR9 pathway byJelena Radulovic et al. Nature
Abstract
Formation of memory assemblies through the DNA sensing TLR9 pathway
As hippocampal neurons respond to diverse types of information, a subset assembles into microcircuits representing a memory. Those neurons typically undergo energy-intensive molecular adaptations, occasionally resulting in transient DNA damage.
Here we found discrete clusters of excitatory hippocampal CA1 neurons with persistent double-stranded DNA (dsDNA) breaks, nuclear envelope ruptures and perinuclear release of histone and dsDNA fragments hours after learning.
Following these early events, some neurons acquired an inflammatory phenotype involving activation of TLR9 signalling and accumulation of centrosomal DNA damage repair complexes.
Neuron-specific knockdown ofTlr9impaired memory while blunting contextual fear conditioning-induced changes of gene expression in specific clusters of excitatory CA1 neurons.
Notably, TLR9 had an essential role in centrosome function, including DNA damage repair, ciliogenesis and build-up of perineuronal nets.
We demonstrate a novel cascade of learning-induced molecular events in discrete neuronal clusters undergoing dsDNA damage and TLR9-mediated repair, resulting in their recruitment to memory circuits.
With compromised TLR9 function, this fundamental memory mechanism becomes a gateway to genomic instability and cognitive impairments implicated in accelerated senescence, psychiatric disorders and neurodegenerative disorders.
Maintaining the integrity of TLR9 inflammatory signalling thus emerges as a promising preventive strategy for neurocognitive deficits.
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DNA Damage and Inflammation Key to Memory Formation - Neuroscience News
Summary: A new study highlights the need to recognize and celebrate the diverse skills of individuals with neurodevelopmental conditions like ADHD, dyslexia, and autism. The research advocates for a shift in perspective, focusing on strengths such as creativity, resilience, and problem-solving, rather than deficits.
The study emphasizes that acknowledging these enhanced skills can lead to reduced stigma and better outcomes in education and employment for those with neurodevelopmental conditions. The teams findings encourage a systematic review to further explore and validate the unique abilities associated with neurodiversity.
Key Facts:
Source: Swansea University
New research says the wide variety of skills displayed by people with conditions such as ADHD, dyslexia and autism should be celebrated to help reduce stigma and change societys expectations.
Creativity, resilience and problem-solving are just some of the strengths exhibited and a study is now calling for a change in the way we think about people with neurodevelopmental conditions.
Dr Edwin Burns, senior lecturer from theSchool of Psychologyat Swansea University, worked with academics from Edge Hill University on the study andtheir findingshave just been published by online journalNeuropsychologia.
The researchers say people with these conditions are almost always discussed in terms of the problems that they face.
They are often characterised by a range of associated cognitive impairments in, for example, sensory processing, facial recognition, visual imagery, attention, and coordination.
However,Dr Burns said:We would say that if only the wider public were aware that these groups exhibit many strengths and skills some which are actuallyenhancedcompared to the general population then this should reduce stigma and improve their educational and employment outcomes.
For the study, the team identified a wide variety of skills exhibited in different groups such as Williams syndrome, dyslexia, autism, ADHD, developmental coordination disorder, aphantasia.
These skills include improved social skills, creativity, problem-solving, resilience, and visual search.
The research also puts forward reasons why these skills occur such as genetics, experience adapting to the environment, repurposing the brain, and medication.
Dr Burns added:In our research we present a table of potential strengths across conditions, and we hope that this may act as a stimulus for a major systematic review in the future. This should help reduce the stigma around neurodiversity, instead promoting greater social inclusion and significant societal benefits.
Author: Kathy Thomas Source: Swansea University Contact: Kathy Thomas Swansea University Image: The image is credited to Neuroscience News
Original Research: Open access. Cognitive strengths in neurodevelopmental disorders, conditions and differences: A critical review by Edwin Burns et al. Neuropsychologia
Abstract
Cognitive strengths in neurodevelopmental disorders, conditions and differences: A critical review
Neurodevelopmental disorders are traditionally characterised by a range of associated cognitive impairments in, for example, sensory processing, facial recognition, visual imagery, attention, and coordination. In this critical review, we propose a major reframing, highlighting the variety of unique cognitive strengths that people with neurodevelopmental differences can exhibit.
These include enhanced visual perception, strong spatial, auditory, and semantic memory, superior empathy and theory of mind, along with higher levels of divergent thinking.
Whilst we acknowledge the heterogeneity of cognitive profiles in neurodevelopmental conditions, we present a more encouraging and affirmative perspective of these groups, contrasting with the predominant, deficit-based position prevalent throughout both cognitive and neuropsychological research.
In addition, we provide a theoretical basis and rationale for these cognitive strengths, arguing for the critical role of hereditability, behavioural adaptation, neuronal-recycling, and we draw on psychopharmacological and social explanations.
We present a table of potential strengths across conditions and invite researchers to systematically investigate these in their future work. This should help reduce the stigma around neurodiversity, instead promoting greater social inclusion and significant societal benefits.
Continued here:
Embracing Neurodiversity: Beyond Stigma to Strength - Neuroscience News
Summary: Researchers conducted a pioneering study on prosopometamorphopsia (PMO), a rare condition where individuals perceive facial features as distorted. The study details the unique case of a 58-year-old male who experiences facial distortions exclusively in person, not when viewing images on screens or paper, allowing researchers to create accurate visualizations of his perceptions.
This novel approach offers insight into PMO, challenging previous diagnostic practices and aiming to enhance understanding and recognition of the condition, which has often been misdiagnosed as a psychiatric disorder due to a lack of awareness.
Key Facts:
Source: Dartmouth College
Imagine if every time you saw a face, it appeared distorted. Well, for those who have a very rare condition known asprosopometamorphopsia(PMO), which causes facial features to appear distorted, that is reality.
As the Dartmouth-basedwebsite about prosopometamorphopsiaexplains, Prosopo comes from the Greek word for face prosopon while metamorphopsia refers to perceptual distortions.
Specific symptoms vary from case to case and can affect the shape, size, color, and position of facial features. The duration of PMO also varies; it can last for days, weeks, or even years.
A new Dartmouth studypublished in the Clinical Pictures section ofThe Lancetreports on a unique case of a patient with PMO. The research is the first to provide accurate and photorealistic visualizations of the facial distortions experienced by an individual with PMO.
The patient, a 58-year-old male with PMO, sees faces without any distortions when they are viewed on a screen and on paper, but he sees distorted faces that appear demonic when viewed in-person.
Most PMO cases however, see distortions in all contexts, so his case is especially rare and presented a unique opportunity to accurately depict his distortions.
For the study, the researchers took a photograph of a persons face. Then, they showed the patient the photograph on a computer screen while he looked at the real face of the same person.
The researchers obtained real-time feedback from the patient on how the face on the screen and the real face in front of him differed, as they modified the photograph using computer software to match the distortions perceived by the patient.
In other studies of the condition, patients with PMO are unable to assess how accurately a visualization of their distortions represents what they see because the visualization itself also depicts a face, so the patients will perceive distortions on it too, says lead authorAntnio Mello, a PhD student in the Department of Psychological and Brain Sciences at Dartmouth. In contrast, this patient doesnt see distortions on a screen.
This means that the researchers were able to modify the face in the photograph, and the patient could accurately compare how similar his perception of the real face was to the manipulated photograph.
Through the process, we were able to visualize the patients real-time perception of the face distortions, says Mello.
In their research with other PMO cases, the co-authors state that some of their PMO participants have seen health professionals who wanted to help but diagnosed them with another health condition, not PMO.
Weve heard from multiple people with PMO that they have been diagnosed by psychiatrists as having schizophrenia and put on anti-psychotics, when their condition is a problem with the visual system, says senior authorBrad Duchaine, a professor of psychological and brain sciences and principal investigator of theSocial Perception Labat Dartmouth.
And its not uncommon for people who have PMO to not tell others about their problem with face perception because they fear others will think the distortions are a sign of a psychiatric disorder, says Duchaine. Its a problem that people often dont understand.
Through their paper, the researchers hope to increase public awareness of what PMO is. For more information about PMO, visit theprosopometamorphopsia website.
Author: Amy Olson Source: Dartmouth College Contact: Amy Olson Dartmouth College Image: The top image is credited to Neuroscience News. The image in the post is credited to A. Mello et al.
Original Research: The findings will be published in The Lancet
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Devil in the Details: The Visual World of Prosopometamorphopsia - Neuroscience News