Category Archives: Neuroscience

Neuroscience

Sleeplessness Makes You Feel Up To Ten Years Older – Neuroscience News

Summary: Researchers unveiled a link between sleep quality and subjective age, demonstrating that insufficient sleep can make individuals feel significantly older. Through two studies involving over 600 participants, they found that each night of inadequate sleep contributed to feeling 0.23 years older, with sleep restriction causing participants to feel on average 4.4 years older.

This research highlights the profound impact of sleep on subjective age, suggesting that feeling alert can make one feel four years younger, whereas feeling extremely sleepy can age ones perceived age by six years. The findings underscore the importance of quality sleep for maintaining a youthful sense of self and promoting health and activity.

Key Facts:

Source: Stockholm University

Do you ever find yourself longing for the energy and vitality of your younger years? Feeling young is not just a matter of perception it is actually related to objective health outcomes.

Previous studies have shown that feeling younger than ones actual age is associated with longer, healthier lives. There is even support for subjective age to predict actual brain age, with those feeling younger having younger brains.

Given that sleep is essential for brain function and overall well-being, we decided to test whether sleep holds any secrets to preserving a youthful sense of age, says Leonie Balter, researcher at the Department of Psychology, Stockholm University.

In the first study, 429 individuals aged 18 to 70 were asked how old they felt, how many days in the past month they had not gotten enough sleep, and how sleepy they were. It turned out that for each night with insufficient sleep in the past month, participants felt on average 0.23 years older.

In a second study, the researchers tested whether it was indeed the lack of sleep causing participants to feel older. Therefore, they conducted an experimental sleep restriction study involving 186 participants aged 18 to 46. Participants restricted their sleep for two nights only four hours in bed each night and another time slept sufficiently for two nights, with nine hours in bed each night.

After sleep restriction, participants felt on average 4.4 years older compared to when having enjoyed sufficient sleep. The effects of sleep on subjective age appeared to be related to how sleepy they felt. Feeling extremely alert was related to feeling 4 years younger than ones actual age, while extreme sleepiness was related to feeling 6 years older than ones actual age.

This means that going from feeling alert to sleepy added a striking 10 years to how old one felt, says Leonie Balter, and states that the implications for our daily lives are clear:

Safeguarding our sleep is crucial for maintaining a youthful feeling. This, in turn, may promote a more active lifestyle and encourage behaviours that promote health, as both feeling young and alert are important for our motivation to be active.

Author: Gunilla Nordin Source: Stockholm University Contact: Gunilla Nordin Stockholm University Image: The image is credited to Neuroscience News

Original Research: Open access. Sleep and subjective age: Protect your sleep if you want to feel young by Leonie Balter et al. Proceedings of the Royal Society B Biological Sciences

Abstract

Sleep and subjective age: Protect your sleep if you want to feel young

The current studies examined the impact of insufficient sleep and sleepiness on the subjective experience of age.

Study 1, a cross-sectional study of 429 participants (282 females (66%), 144 males, 3 other gender; age range 1870), showed that for each additional day of insufficient sleep in the last 30 days, subjective age increased by 0.23 years.

Study 2, an experimental crossover sleep restriction study (n= 186; 102 females (55%), 84 males; age range 1846), showed that two nights of sleep restriction (4 h in bed per night) made people feel 4.44 years older compared to sleep saturation (9 h in bed per night).

Additionally, moving from feeling extremely alert (Karolinska Sleepiness Scale (KSS) score of 1) to feeling extremely sleepy (KSS score of 9) was associated with feeling 10 years older in both studies.

These findings provide compelling support for insufficient sleep and sleepiness to exert a substantial influence on how old we feel, and that safeguarding sleep is probably a key factor in feeling young.

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Sleeplessness Makes You Feel Up To Ten Years Older - Neuroscience News

Neuroscience

Aging Brain Cells Have Prolonged Death Process – Neuroscience News

Summary: Mature oligodendrocytes, crucial for brain function and myelin production, have an unusually prolonged death process after damage, surviving up to 45 days post-trauma, a stark contrast to the rapid demise of their younger counterparts within 24 hours.

This study illuminates a previously unknown pathway of cell longevity, suggesting a potential shift in strategies for treating aging-related damage and neurodegenerative diseases like multiple sclerosis. By utilizing innovative techniques, including a living-tissue model and a cellular death ray, the team has highlighted the need for tailored approaches in preserving myelin and supporting brain health, challenging the one-size-fits-all treatment paradigm.

Key Facts:

Source: Dartmouth College

For oligodendrocytesthe central nervous system cells critical for brain functionage may not bring wisdom, but it does come with the power to cling to life for much, much longer than scientists knew.

Thatsaccording to a new studyfeatured on the March 27 cover of theJournal of Neuroscience.

Mature oligodendrocytes took a shocking 45 days to die following a fatal trauma that killed younger cells within the expected 24 hours, Dartmouth researchers report. The findings suggest theres a new pathway for efforts to reverse or prevent the damage that aging and diseases such as multiple sclerosis cause to these important cells.

In the brain, oligodendrocytes wrap around the long, skinny connections between nerve cells known as axons, where they produce a lipid membrane called a myelin sheath that coats the axon. Axons transmit the electrical signals that nerve cells use to communicate; myelin sheathslike the plastic coating on a copper wirehelp these signals travel more efficiently.

Old age and neurodegenerative diseases like MS damage oligodendrocytes. When the cells die, their myelin production perishes with them, causing myelin sheaths to break down with nothing to replenish them. This can lead to the loss of motor function, feeling, and memory as neurons lose the ability to communicate.

Scientists have assumed that damaged oligodendrocyteslike all injured cellsinitiate a cellular self-destruct called apoptosis in which the cells kill themselves. But Dartmouth researchers discovered that mature oligodendrocytes can experience an extended life before their death that has never been seen before.

The findings pose the critical question of what in these cells changes as they mature that allows them to persist.

We found that mature cells undertake a pathway that is still controlled, but not the classical programmed cell-death pathway, saidRobert Hill, an assistant professor ofbiological sciencesand corresponding author of the paper.

We think this is showing us what happens in brains as we age and revealing a lot about how these cells die in older people, Hill said.

That unique mechanism is important for us to investigate further. We need to understand why these cells are following this pathway so we can potentially encourage or prevent it, depending on the disease context.

First author Timothy Chapman, who led the project as a PhD candidate in Hills research group, said that efforts to develop treatments for preserving myelin have focused on cultivating young oligodendrocytes and protecting mature ones. But this study suggests the cells may change significantly as they age and that a one-size-fits-all treatment might not work.

In response to the same thing, young cells go one way and old cells go another, said Chapman, who is now a postdoctoral researcher at Stanford University. If you wanted to protect the old cells, you may have to do something completely different than if you wanted to help the young cells mature. Youll likely need a dual approach.

The paper builds on a living-tissue modelthe teamreportedin the journal Nature Neurosciencein March 2023 that allows them to initiate the death of a single oligodendrocyte to observe how the cells around it react.

They reported that when an oligodendrocyte in a young brain died, the cells around it immediately replenished the lost myelin. In a brain equivalent to that of a 60-year-old, however, the surrounding cells did nothing and the myelin was lost.

That model gets us as close as we can get to the cell-death process that happens in the brain, Hill said.

Were able to model the effects of aging really well. Our ability to select a single oligodendrocyte, watch it die, and watch it regenerate or fail to regenerate allows us to understand what drives this process at the cellular level and how it can be controlled.

For the latest study, the researchers used their model to fatally damage oligodendrocyte DNA using what amounts to a cellular death raya photon-based device called 2Phatal that Hill developed. They also used the standard method for removing myelin that uses the copper-based toxin cuprizone as a comparison.

As previous studies have reported, the immature cells died quickly. But the older cells lived on, which the Dartmouth team at first interpreted as a resistance to DNA damage.

The study came into focus when the researchers examined the mature cells 45 days later using a long-term, high-resolution imaging technique developed inthe Hill lab.

Thats when we saw that it wasnt that the cells were resistant to damagethey were experiencing this extended cell death instead, Hill said.

No ones ever checked for cell death that long after DNA damage. Its the only example we can find in the literature where a cell experiences such a traumatic event and sticks around longer than a week, he said.

Because humans have oligodendrocytes for life, the cells are known to accumulate DNA damage and be more resilient than other cells, Chapman said.

Thats why we think this effect is applicable to aging. One reason these cells may persist for such a long time is because theyre used to experiencing this kind of damage naturally in aging, he said.

The study opens the first door of a vast labyrinth of more questions, Hill and Chapman say, such as whether the extended death is a good thing. It may be the equivalent of dysfunctional myelin, which is worse just sitting on an axon than if there was no myelin at all, Hill said. It isolates the cell from the surrounding tissue and essentially starves it of nutrients.

Its almost like there is garbage sitting on the axon for 45 days. Do we want to save that garbage or speed up its removal? We didnt even know that was a question until we saw this, Hill said.

If we understand the cell-death mechanism, maybe we can speed it up and get rid of that dysfunctional myelin, he said. Were always trying to save the cells and save the tissue, but you have to know if theyre worth saving.

The version of record of Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination was published March 27, 2024, in the Journal of Neuroscience.

Funding: This work was supported by the National Institutes of Health (R01NS122800), the Esther A. and Joseph Klingenstein Fund, the Simons Foundation, and the Department of Biological Sciences at Dartmouth.

Author: Morgan Kelly Source: Dartmouth College Contact: Morgan Kelly Dartmouth College Image: The image is credited to Neuroscience News

Original Research: Closed access. Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination by Robert Hill et al. Journal of Neuroscience

Abstract

Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination

Myelinating oligodendrocytes die in human disease and early in aging. Despite this, the mechanisms that underly oligodendrocyte death are not resolved and it is also not clear whether these mechanisms change as oligodendrocyte lineage cells are undergoing differentiation and maturation.

Here, we used a combination of intravital imaging, single-cell ablation, and cuprizone-mediated demyelination, in both female and male mice, to discover that oligodendrocyte maturation dictates the dynamics and mechanisms of cell death.

After single-cell phototoxic damage, oligodendrocyte precursor cells underwent programmed cell death within hours, differentiating oligodendrocytes died over several days, while mature oligodendrocytes took weeks to die. Importantly cells at each maturation stage all eventually died but did so with drastically different temporal dynamics and morphological features.

Consistent with this, cuprizone treatment initiated a caspase-3dependent form of rapid cell death in differentiating oligodendrocytes, while mature oligodendrocytes never activated this executioner caspase.

Instead, mature oligodendrocytes exhibited delayed cell death which was marked by DNA damage and disruption in poly-ADP-ribose subcellular localization. Thus, oligodendrocyte maturation plays a key role in determining the mechanism of death a cell undergoes in response to the same insult.

This means that oligodendrocyte maturation is important to consider when designing strategies for preventing cell death and preserving myelin while also enhancing the survival of new oligodendrocytes in demyelinating conditions.

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Aging Brain Cells Have Prolonged Death Process - Neuroscience News

Neuroscience

Anxiety Drives Wishful Thinking to Risky Levels – Neuroscience News

Summary: Individuals tend to become overly optimistic in situations marked by insecurity and anxiety, potentially to their detriment. The research, involving more than 1,700 participants, demonstrated that people are less accurate in recognizing patterns linked to negative outcomes, like electrical shocks or monetary loss, indicating a clear bias towards wishful thinking. Interventions to reduce this bias included simplifying tasks to reduce uncertainty and offering rewards for accuracy, which showed mixed results. The findings suggest that while wishful thinking can help cope with stress, it may also hinder necessary actions in critical situations like health or environmental crises.

Key Facts:

Source: University of Amsterdam

Everyone indulges in wishful thinking now and again. But when is that most likely to happen and when could it actually be harmful?

A new study, led by the University of Amsterdam (UvA), demonstrates unequivocally that the greater the insecurity and anxiety of a situation, the more likely people are to become overly optimistic even to the point where it can prevent us from taking essential action.

The studys results have now been published in the journalAmerican Economic Review.

People arent purely truth-seekers many beliefs are influenced by emotions and driven by what is pleasant or comforting. Like belief in an afterlife or optimism about health outcomes, says Jol van der Weele, professor of Economic Psychology at the UvA. Working alongside professor of Neuroeconomics Jan Engelmann and an international team, Van der Weele set out to answer whether people become overly optimistic when facing potential hardships.

So far studies havent provided clear evidence for wishful thinking, with many not backing up the idea, explains Engelmann. But these mainly focused on positive outcomes, like winning a lottery. We examined how both positive and negative outcomes influence biased beliefs.

Choosing the most pleasant outcome

Understanding self-deception and its causes is difficult in real-world situations. The study involved a set of experiments with over 1,700 participants, conducted in a lab and online.

Participants were briefly shown various patterns, such as sets of differently oriented stripes or coloured dots, and were asked what kind of pattern they saw. Some of these patterns were linked to a negative outcome to induce anxiety, either a mild and non-dangerous electrical shock (in the lab) or a loss of money (online).

We wanted to see if people make more mistakes in recognising patterns associated with a negative outcome, thinking it was actually a harmless pattern. That would indicate wishful thinking, explains Van der Weele.

The study consistently found that participants were less likely to correctly identify patterns associated with a shock or loss.

The participants tended to see a pattern that aligned with what was more desirable, Engelmann says.

Previous research looked at wishful thinking related to positive outcomes and found mixed results, with many studies not finding an effect. Our study demonstrates very clearly thatthe negative emotionof anxiety about an outcome leads to wishful thinking.

Making people more realistic

The researchers also tested interventions designed to make people more realistic. The first involved making the patterns easier to recognise.

Reducing uncertainty did indeed turn out to reduce wishful thinking, says Van der Weele.

The second intervention was to offer higher potential earnings for correct pattern recognition. This intervention had little effect, except when participants could gather more evidence about the exact pattern they were shown.

When people had more time to collect evidence and were better rewarded for a correct answer, they became more realistic, explains Engelmann.

Finally, in the experiments where negative outcomes were replaced by positive outcomes, participants showed no wishful thinking. According to the authors this shows that reducing negative emotions can lessen overoptimism.

Wishful thinking in the real world

The authors recognise that wishful thinking can be useful because it helps us deal with bad feelings and manage uncertainty.

Engelmann: Wishful thinking is important for humans in coping with anxiety about possible future events.

For Van der Weele and Engelmann, the concern is situations in which too much optimism stops people from getting the information they need or from acting in a way that would benefit them.

People can get too hopeful when things are uncertain. We observe this happening with climate change, when financial markets fluctuate, and even in personal health situations when people avoid medical help because they think everything will be fine. We need to know more about when wishful thinking helps and when it hurts.

Author: Laura Erdtsieck Source: University of Amsterdam Contact: Laura Erdtsieck University of Amsterdam Image: The image is credited to Neuroscience News

Original Research: Open access. Anticipatory Anxiety and Wishful Thinking by Jol van der Weele et al. American Economic Review

Abstract

Anticipatory Anxiety and Wishful Thinking

Across five experiments (N = 1,714), we test whether people engage in wishful thinking to alleviate anxiety about adverse future outcomes.

Participants perform pattern recognition tasks in which some patterns may result in an electric shock or a monetary loss.

Diagnostic of wishful thinking, participants are less likely to correctly identify patterns that are associated with a shock or loss.

Wishful thinking is more pronounced under more ambiguous signals and only reduced by higher accuracy incentives when participants cognitive effort reduces ambiguity.

Wishful thinking disappears in the domain of monetary gains, indicating that negative emotions are important drivers of the phenomenon.

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Anxiety Drives Wishful Thinking to Risky Levels - Neuroscience News

Neuroscience

Prolonged Progestogen Use Linked to Brain Tumor Risk – Neuroscience News

Summary: A new study highlights a significant link between prolonged use of certain progestogen hormone drugs and an increased risk of developing intracranial meningioma, a type of brain tumor. Researchers analyzed data from 18,061 women who underwent surgery for intracranial meningioma, comparing their progestogen use to 90,305 controls.

The study found that prolonged use of specific progestogens, including medrogestone, medroxyprogesterone acetate, and promegestone, is associated with an elevated risk of requiring surgery for meningioma. This research underscores the urgent need for further studies to understand this risk fully, especially given the widespread use of these hormones in treating conditions like endometriosis and as part of contraceptive methods.

Key Facts:

Source: BMJ

Prolonged use of certain progestogen hormone drugs is associated with an increased risk of developing a type of brain tumour known as an intracranial meningioma, finds a study from France published byThe BMJtoday.

The researchers say this study is the first to assess the risk associated with progestogens used by millions of women worldwide, and further studies are urgently needed to gain a better understanding of this risk.

Progestogens are similar to the natural hormone progesterone, which are widely used for gynaecological conditions such as endometriosis and polycystic ovary syndrome, and in menopausal hormone therapy and contraceptives.

Meningiomas are mostly non-cancerous tumours in the layers of tissue (meninges) that cover the brain and spinal cord. Factors such as older age, female sex, and exposure to three high-dose progestogens (nomegestrol, chlormadinone, and cyproterone acetate) are already known to increase the risk of meningioma.

But there are many other progestogens for which the risk of meningioma associated with their use has not been estimated individually.

To address this knowledge gap, researchers set out to evaluate the real life risk of intracranial meningioma requiring surgery in women associated with use of several progestogens with different routes of administration.

They used data from the French national health data system (SNDS) for 18,061 women (average age 58) who underwent intracranial meningioma surgery from 2009-18.

Each case was matched to five control women without intracranial meningioma (total 90,305) by year of birth and area of residence.

The progestogens examined were progesterone, hydroxyprogesterone, dydrogesterone, medrogestone, medroxyprogesterone acetate, promegestone, dienogest, and levonorgestrel intrauterine systems.

For each progestogen, use was defined as at least one prescription in the year before hospital admission or within 3-5 years for levonorgestrel intrauterine systems.

Use of at least one of the three high-dose progestogens known to increase the risk of meningioma in the 3 years before hospital admission was also recorded to minimise bias.

After taking account of other potentially influential factors, prolonged use (a year or more) of medrogestone was associated with a 4.1-fold increased risk of intracranial meningioma requiring surgery.

Prolonged use of medroxyprogesterone acetate injection was associated with a 5.6-fold increased risk, and prolonged use of promegestone was linked to a 2.7-fold increased risk.

There appeared to be no such risk for less than one year of use of these progestogens.

As expected, there was also an excess risk of meningioma for women exposed to chlormadinone acetate, nomegestrol acetate, and cyproterone acetate, all of which are known to increase the risk of meningioma.

However, results showed no excess risk of meningioma for progesterone, dydrogesterone, or the widely used hormonal intrauterine systems, regardless of the dose of levonorgestrel they contained.

No conclusions could be drawn about dienogest or hydroxyprogesterone as the number of exposed individuals was too small.

This is an observational study so cant establish cause and effect, and the authors acknowledge that the SNDS database lacked information on all the clinical details and medical indications for which progestogens are prescribed. Nor were they able to account for genetic predisposition and exposure to high dose radiation.

However, they say, given that medroxyprogesterone acetate is estimated to be used for birth control by 74 million women worldwide, the number of attributable meningiomas may be potentially high.

Further studies using other sources of data are urgently needed to gain a better understanding of this risk, they conclude.

Author: BMJ Media Relations Source: BMJ Contact: BMJ Media Relations BMJ Image: The image is credited to Neuroscience News

Original Research: The findings will appear in The BMJ

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Prolonged Progestogen Use Linked to Brain Tumor Risk - Neuroscience News

Neuroscience

Big research, little time: Medical neuroscience student wins 3 Minute Thesis finals – Dal News

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

Neuroscience

The Genetic Secrets of Neuron Formation – Neuroscience 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.

Key Facts:

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

Neuroscience

The new NeuroAI – Nature.com

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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Neuroscience

Exploring Aphantasia: The Mind Without a Mental Picture – Neuroscience News

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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Neuroscience

Altered Brain pH Linked to Cognitive Disorders – 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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