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Summary: A new study reveals that patients with schizophrenia or depression struggle with optimal information utilization in learning processes.
Using EEG and advanced computer modeling, researchers found that these patients place greater emphasis on less important information, leading to suboptimal decision-making. This diminished flexibility in processing new information was particularly pronounced in feedback management for future behavior.
The findings suggest cognitive limitations in schizophrenia and depression could be addressed through targeted treatments focusing on these specific learning deficits.
Key Facts:
Source: Otto von Guericke University Magdeburg
When learning, patients with schizophrenia or depression have difficulty making optimal use of information that is new to them. In the learning process, both groups of patients give greater weight to less important information and, as a result, make less than ideal decisions.
This was the finding of a several-months-long study conducted by a team led by neuroscientist Professor Dr. med. Markus Ullsperger from the Institute of Psychology at Otto von Guericke University Magdeburg in collaboration with colleagues from the University Clinic for Psychiatry & Psychotherapy and the German Center for Mental Health.
By using electroencephalography (EEG) and complex mathematical computer modeling, the team of researchers discovered that learning deficits in depressive and schizophrenicpatientsare caused by diminished/reduced flexibility in the use of new information.
The study has just beenpublishedinBrainand is titled Transdiagnostic inflexible learning dynamics explain deficits in depression and schizophrenia.
People with depression or schizophrenia often suffer from cognitive limitations, says the lead author of the study, Dr. Hans Kirschner. For example, they find it difficult to understand complex information, to learn, to plan or to generalize a situation.
In particular, deficits in using feedback from the past to manage future behavior, poses a fundamental problem for those affected.
Dr. Tilmann Klein, neuropsychologist and psychotherapist adds that these cognitive limitations are very onerous for the affected groups of patients and have a strong influence on the outcome of treatment.
If we understand these deficits and their causes better, in the long term we can design forms of treatment such as functional training to be more specific and targeted.
To find out whether the psychological and neuronal mechanisms that lead to cognitive limitations are the same in different mental disorders, the scientists examined patients with a diagnosis of a severe depressive disorder and of schizophrenia as well as acontrol groupcomprising 33 people.
The test subjects were repeatedly presented with images of animals on a screen that were associated with either a high or low probability of reward or punishment, that is positive ornegative feedback.
The test subjects had to decide whether they wanted to bet on the animal or not, and thus either win or lose 10 points. If they did not bet, they neither won nor lost anything, but would then see what would have happened, had they opted to bet.
Dr. Kirschner describes the test setup as follows: During the experiment, the objective for the participants was to find out whether it was worthwhile betting and therefore risking the loss that might entail, or if it was better not to bet and thus avoid losing.
The process is a little bit like a game of roulette, explains the neuroscientist. If you place your bet, you either win or lose. If you do not bet, you nevertheless get to see where the little ball ends up and you can work out what would have happened if you had placed a bet.
The difference in our study is that the participants were actually able to learn because over time they came to realize if an animal was more likely, on average, to be rewarded or punished and could then either always bet on the animal and thus maximize their winnings or minimize their losses.
According to Kirschner, optimal learning in this task would mean that thetest subjectstook more note of the feedbacki.e., the wins or losses of an animalat the beginning of thelearning process.
Once they have a feel for an animals likelihood of winning, they ignore misleading feedback, for example, a picture that usually is highly likely to lose also wins occasionally.
While healthy control participants did exactly this, the patient groups that were suffering from depression or schizophrenia were more strongly influenced by randomly occurring errors.
Imagine a basketball player throwing balls at a basket, Dr. Kirschner goes on to say. A poor player scores rarely and is not picked for the team. Even if they do not score every time, a good player scores often and is therefore picked for the team. However, in the study, both groups of patients would replace the good player after a poor shot.
In the EEG it could be seen that both patient groups have a diminished neuronal representation of reward expectation.
This means that the scoring rate of a good basketball player is not stored as well in the brain and is more quickly overwritten, when the player occasionally fails to score.
In summary, Dr. Kirschner explains that the study expanded the teams knowledge of cognitive limitations in patients with a diagnosis of schizophrenia or depression. In particular we were also able to demonstrate the benefits of computer models in which we attempt to describe complex learning mechanisms mathematically and implement them in the form of computer simulations.
This made it possible to simulate hard-to-predict learning behavior and compare it with the behavior of participants inspecific tasks.
With this approach in [the] future, we will be able to quantify and characterize learning deficits in a more nuanced way. And a better understanding of these deficits will, in turn, help direct us towards further developing existing treatments for depression and schizophrenia in a more targeted way.
We hope that in future our research will benefit patients affected by learning impairments and help them to cope better in their everyday lives.
Author: Katharina Vorwerk Source: Otto von Guericke University Magdeburg Contact: Katharina Vorwerk Otto von Guericke University Magdeburg Image: The image is credited to Neuroscience News
Original Research: Open access. Transdiagnostic inflexible learning dynamics explain deficits in depression and schizophrenia by Hans Kirschner et al. Brain
Abstract
Transdiagnostic inflexible learning dynamics explain deficits in depression and schizophrenia
Deficits in reward learning are core symptoms across many mental disorders. Recent work suggests that such learning impairments arise by a diminished ability to use reward history to guide behaviour, but the neuro-computational mechanisms through which these impairments emerge remain unclear. Moreover, limited work has taken a transdiagnostic approach to investigate whether the psychological and neural mechanisms that give rise to learning deficits are shared across forms of psychopathology.
To provide insight into this issue, we explored probabilistic reward learning in patients diagnosed with major depressive disorder (n= 33) or schizophrenia (n= 24) and 33 matched healthy controls by combining computational modelling and single-trial EEG regression. In our task, participants had to integrate the reward history of a stimulus to decide whether it is worthwhile to gamble on it. Adaptive learning in this task is achieved through dynamic learning rates that are maximal on the first encounters with a given stimulus and decay with increasing stimulus repetitions. Hence, over the course of learning, choice preferences would ideally stabilize and be less susceptible to misleading information.
We show evidence of reduced learning dynamics, whereby both patient groups demonstrated hypersensitive learning (i.e. less decaying learning rates), rendering their choices more susceptible to misleading feedback. Moreover, there was a schizophrenia-specific approach bias and a depression-specific heightened sensitivity to disconfirmational feedback (factual losses and counterfactual wins). The inflexible learning in both patient groups was accompanied by altered neural processing, including no tracking of expected values in either patient group.
Taken together, our results thus provide evidence that reduced trial-by-trial learning dynamics reflect a convergent deficit across depression and schizophrenia. Moreover, we identified disorder distinct learning deficits.
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Depression and Schizophrenia Impact Learning - Neuroscience News
Reservoir Neuroscience set to restore health to the aging brain Longevity.Technology
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Reservoir Neuroscience set to restore health to the aging brain - Longevity.Technology
Published in the journal Current Biology on January 12, the research focuses on prairie voles, understanding the intricate role of dopamine in maintaining long-term relationships similar to human bonds.
Prairie voles are among the rare 3% to 5% of mammals that form monogamous pair bonds, offering a unique opportunity to study the neurochemical basis of intimate relationships.
Like humans, prairie voles engage in long-term partnerships, share a home, raise offspring, and experience a sense of grief when separated from their partners.
The research, led by senior author Zoe Donaldson, associate professor of behavioural neuroscience at CU Boulder, utilises state-of-the-art neuroimaging technology to look into the real-time brain activity of voles during attempts to reunite with their partners.
The findings reveal that dopamine, a neurotransmitter associated with pleasure and reward, plays a pivotal role in sustaining the bonds of love.
Donaldson explains, As humans, our entire social world is basically defined by different degrees of selective desire to interact with different people, whether its your romantic partner or your close friends. This research suggests that certain people leave a unique chemical imprint on our brain that drives us to maintain these bonds over time.
certain people leave a unique chemical imprint on our brain
The researchers monitored the voles as they navigated obstacles to reach their partners, with a fibre-optic sensor tracking dopamine activity in the nucleus accumbens, a region responsible for motivating individuals to seek rewarding experiences.
The results showed that dopamine surges, lighting up the voles brains like a glow stick during interactions with their life partners.
Anne Pierce, the studys first author, explains, This suggests that not only is dopamine really important for motivating us to seek out our partner, but theres actually more dopamine coursing through our reward center when we are with our partner than when we are with a stranger.
In an experiment simulating separation, the voles were kept apart for four weeks, a significant duration in their lives. Upon reuniting, while the voles remembered each other, their signature dopamine surge had diminished significantly. The researchers interpret this as a neural reset, allowing the animals to form new bonds.
The implications for humans are deep, especially for those suffering from heartbreak or loss. The study hints at an inherent mechanism within the brain to protect individuals from prolonged, unrequited love.
The authors acknowledge the need for further research to determine how well these results translate to humans. They believe the findings could offer insights into mental health conditions affecting social relationships.
Zoe Donaldson expresses hope for the future, stating, The hope is that by understanding what healthy bonds look like within the brain, we can begin to identify new therapies to help the many people with mental illnesses that affect their social world.
This research provides a glimpse into the neuroscience of love and holds promise for potential therapeutic interventions to assist those struggling with forming or overcoming close relationships. As the field progresses, scientists aim to unlock the mysteries of the human brain, offering new perspectives on emotional bonds and avenues for mental health support.
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What makes love so strong? The neuroscience behind love and loss - Open Access Government
Summary: Researchers uncovered how cannabis triggers appetite in the brain. Using calcium imaging technology to observe brain cells in mice exposed to vaporized cannabis sativa, the team discovered that cannabis activates specific cells in the hypothalamus associated with the anticipation and consumption of food.
This finding could lead to novel treatments for appetite disorders in cancer patients, anorexia, and potentially obesity. The study highlights the cannabinoid-1 receptors role in controlling Agouti Related Protein neurons, essential for appetite, and demonstrates that disabling these neurons negates cannabiss appetite-stimulating effects.
Key Facts:
Source: Washington State University
While it is well known that cannabis can cause the munchies, researchers have now revealed a mechanism in the brain that promotes appetite in a set of animal studies at Washington State University.
The discovery, detailed in thejournalScientific Reports, could pave the way for refined therapeutics to treat appetite disorders faced by cancer patients as well as anorexia and potentially obesity.
After exposing mice to vaporized cannabis sativa, researchers used calcium imaging technology, which is similar to a brain MRI, to determine how their brain cells responded. They observed that cannabis activated a set of cells in the hypothalamus when the rodents anticipated and consumed palatable food that were not activated in unexposed mice.
When the mice are given cannabis, neurons come on that typically are not active, said Jon Davis, an assistant professor of neuroscience at WSU and corresponding author on the paper. There is something important happening in the hypothalamus after vapor cannabis.
Calcium imaging has been used to study the brains reactions to food by other researchers, but this is the first known study to use it to understand those features following cannabis exposure.
As part of this research, the researchers also determined that the cannabinoid-1 receptor, a known cannabis target, controlled the activity of a well-known set of feeding cells in the hypothalamus, called Agouti Related Protein neurons.
With this information, they used a chemogenetic technique, which acts like a molecular light switch, to home in on these neurons when animals were exposed to cannabis. When these neurons were turned off, cannabis no longer promoted appetite.
We now know one of the ways that the brain responds to recreational-type cannabis to promote appetite, said Davis.
This work builds onprevious research on cannabis and appetitefrom Davis lab, which was among the first to use whole vaporized cannabis plant matter in animal studies instead of injected THCin an effort to better mimic how cannabis is used by humans. In the previous work, the researchers identified genetic changes in the hypothalamus in response to cannabis, so in this study, Davis and his colleagues focused on that area.
Funding: The current research received support from the Alcohol and Drug Abuse Research Program, the National Institute on Alcohol Abuse and Alcoholism, and the U.S. Department of Agriculture as well as by funds provided by the state of Washington Initiative Measure No. 171.
Author: Sara Zaske Source: Washington State University Contact: Sara Zaske Washington State University Image: The image is credited to Neuroscience News
Original Research: Open access. Cannabis Sativa targets mediobasal hypothalamic neurons to stimulate appetite by Jon Davis et al. Scientific Reports
Abstract
Cannabis Sativa targets mediobasal hypothalamic neurons to stimulate appetite
The neurobiological mechanisms that regulate the appetite-stimulatory properties ofcannabis sativaare unresolved. This work examined the hypothesis that cannabinoid-1 receptor (CB1R) expressing neurons in the mediobasal hypothalamus (MBH) regulate increased appetite following cannabis vapor inhalation.
Here we utilized a paradigm where vaporized cannabis plant matter was administered passively to rodents. Initial studies in rats characterized meal patterns and operant responding for palatable food following exposure to air or vapor cannabis.
Studies conducted in mice used a combination of in vivo optical imaging, electrophysiology and chemogenetic manipulations to determine the importance of MBH neurons for cannabis-induced feeding behavior.
Our data indicate that cannabis vapor increased meal frequency and food seeking behavior without altering locomotor activity. Importantly, we observed augmented MBH activity within distinct neuronal populations when mice anticipated or consumed food.
Mechanistic experiments demonstrated that pharmacological activation of CB1R attenuated inhibitory synaptic tone onto hunger promoting Agouti Related Peptide (AgRP) neurons within the MBH.
Lastly, chemogenetic inhibition of AgRP neurons attenuated the appetite promoting effects of cannabis vapor. Based on these results, we conclude that MBH neurons contribute to the appetite stimulatory properties of inhaled cannabis.
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Munchies Mystery Solved: Cannabis Activates Brain's Appetite Neurons - Neuroscience News
Summary: A study uncovers distinct olfactory worlds between male and female silkmoths, contrasting with the similar sense of smell in human males and females. Female silkmoths, previously thought to be attuned to mulberry tree odors for egg-laying, surprisingly respond more to silkworm feces odors, crucial after mating.
This discovery, made using electrophysiological methods and behavioral tests, challenges previous assumptions about female moth sensilla. Additionally, the study explores the uncharted territory of male silkmoth pheromones and reveals unique co-expression of olfactory receptors in silkmoths, expanding understanding of insect olfaction.
Key Facts:
Source: Max Planck Institute
In humans, the sense of smell is similarly developed in men and women, although women have slightly more olfactory neurons and therefore a slightly more sensitive nose. On the whole, however, they perceive the same odors.
Male moths, on the other hand, live in a completely different olfactory world to their female counterparts. For example, the antennae of male silkmoths their nose are highly specialized to detect female sex pheromones, while females cannot even smell their own pheromones.
There are thousands of sensilla on the antennae, hair-like structures, which can be divided into morphologically and functionally distinct groups. The most common sensilla in males are long and contain two sensory neurons.
One is specialized to detect bombykol, the sex pheromone of females, while the other responds to bombykal, a component of the pheromone of other moth species. While bombykol is highly attractive to male silkmoths, bombykal is a deterrent.
Because female silkmoths cannot smell their own pheromone, it was long thought that their long sensilla also have a very specific function that is only found in females. After mating, the females only task is to find a suitable plant on which to lay her eggs.
It has therefore been suggested that the long sensilla of females are specialized to detect the attractive odor of mulberry trees. We wanted to test this assumption, says Sonja Bisch-Knaden, who leads a project group in the Department of Evolutionary Neuroethology at the Max Planck Institute for Chemical Ecology.
Long sensilla of female silkmoths recognize silkworm feces
Electrophysiological methods, such as measuring the activity of individual sensilla (single-sensillum recording), were crucial for the studys results. The scientists not only tested many different individual odors, but also natural odor mixtures, such as those found in the leaves of the mulberry tree, caterpillar droppings, the body odor of moths or the meconium, a liquid that moths secrete when they hatch.
All these odors, which play an ecological role in the silkmoths environment, had been collected. The research team was also able to match the expression of olfactory receptors to the corresponding sensillum type.
We were surprised to find that neurons in the long sensilla of female silkmoths were not specialized to detect the odor of the host plant, as expected, but that one of the two neurons in the long sensilla is very sensitive to odors such as isovaleric acid and benzaldehyde. The detection of the odor of the mulberry leaf itself is carried out by neurons in medium-length sensilla, summarizes Sonja Bisch-Knaden.
Isovaleric acid and benzaldehyde are odor components of silkworm feces. Using a simple Y-maze test with an entrance arm that splits into two side arms through which either an odor or clean air (control) is introduced, the research team was able to elicit behavior in the otherwise immobile females that expressed attraction or aversion. Major differences became apparent when comparing virgin and mated females.
The researchers showed that odors associated with caterpillar droppings did not trigger a specific reaction in virgin females, but had a deterrent effect on mated females. Presumably, the smell of feces helps females avoid mulberry trees, which are already full of silkworms when they lay their eggs.
In search of the male silkmoth pheromone
The pheromone of female silkmoths, bombykol, was chemically characterized as early as 1959 the first insect pheromone ever. So far, scientists have not been able to identify a male counterpart. The current study provides clues, but no answers to the question of a male pheromone.
The second neuron in the females long sensilla is highly specific for (+)-linalool, an odor already identified as a component of the male pheromone in other butterfly species. However, no linalool could be found in the body odor of male silkmoths, and (+)-linalool alone had neither an attractive nor a repellent effect on female silkmoths in behavioral experiments, says Sonja Bisch-Knaden.
Special features of the odor perception of silkmoths
While investigating the molecular basis of odor detection in female silkmoths, the researchers noticed a peculiarity in the spatial organization of olfactory receptors. There are two families of olfactory receptors, the evolutionary older ionotropic receptors (IRs), which detect mainly acids, and the odorant receptors (ORs), which detect a wide range of chemically diverse compounds.
Based on studies in the model flyDrosophila melanogaster, it was long thought that neurons expressing IRs or ORs usually occur in different types of sensilla, and that IRs never occur in long sensilla. In the silkmoth, however, an IR co-receptor for the detection of acids and the obligate OR co-receptor are both found in the same neurons located in long sensilla.
This co-expression of IRs and ORs increases the chemical receptivity of the sensory neurons. Odors detected by both receptor types are processed and transmitted together, which could be advantageous for the unambiguous detection of ecologically important odor mixtures.
It is amazing that research on insect olfaction continues to produce surprising results. Our study shows that it is important to study more than just one model, says Bill Hansson, head of the Department of Evolutionary Neuroethology.
The researchers also found this co-expression of the two receptor types in the long sensilla of male silkmoths, which is why they assume that the detection of acids could also play an important ecological role in males. Further investigations will now clarify this.
Author: Angela Overmeyer Source: Max Planck Institute Contact: Angela Overmeyer Max Planck Institute Image: The image is credited to Markus Knaden, Max Planck Institute for Chemical Ecology
Original Research: Open access. Females smell differently: characteristics and significance of the most common olfactory sensilla of female silkmoths by Sonja Bisch-Knaden et al. Proceedings of the Royal Society B Biological Sciences
Abstract
Females smell differently: characteristics and significance of the most common olfactory sensilla of female silkmoths
In the silkmothBombyx mori, the role of male sensilla trichodea in pheromone detection is well established. Here we study the corresponding female sensilla, which contain two olfactory sensory neurons (OSNs) and come in two lengths, each representing a single physiological type.
Only OSNs in medium trichoids respond to the scent of mulberry, the silkworms exclusive host plant, and are more sensitive in mated females, suggesting a role in oviposition.
In long trichoids, one OSN is tuned to (+)-linalool and the other to benzaldehyde and isovaleric acid, both odours emitted by silkworm faeces. While the significance of (+)-linalool detection remains unclear, isovaleric acid repels mated females and may therefore play a role in avoiding crowded oviposition sites.
When we examined the underlying molecular components of neurons in female trichoids, we found non-canonical co-expression ofIr8a, the co-receptor for acid responses, andORco, the co-receptor of odorant receptors, in long trichoids, and the unexpected expression of a specific odorant receptor in both trichoid sensillum types.
In addition to elucidating the function of female trichoids, our results suggest that some accepted organizational principles of the insect olfactory system may not apply to the predominant sensilla on the antenna of femaleB. mori.
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Male and Female Silkmoths Perceive Odors Differently - Neuroscience News
Summary: A new study reveals that women consuming higher amounts of plant-based protein experience fewer chronic diseases and maintain better health as they age.
Analyzing data from over 48,000 women in the Harvard-based Nurses Health Study, the research showed a significant link between plant protein intake and reduced risk of heart disease, cancer, diabetes, and cognitive decline. Protein source matters, with plant proteins being more beneficial for long-term health compared to animal proteins.
Key Facts:
Source: Tufts University
Women who consume higher amounts of protein, especially protein from plant-based sources, develop fewer chronic diseases and are more likely to be healthier overall as they age, according to astudyled by researchers at theJean Mayer USDA Human Nutrition Research Center on Aging(HNRCA) at Tufts University and published Jan. 17 inThe American Journal of Clinical Nutrition.
Analyzing self-reported data from more than 48,000 women, the researchers saw notably less heart disease, cancer, and diabetes, and cognitive and mental health decline, in those who included more protein in their diets from sources such as fruits, vegetables, bread, beans, legumes, and pasta, compared to those who ate less.
Consuming protein in midlife was linked to promoting good health in older adulthood, saidAndres Ardisson Korat, a scientist at the HNRCA and lead author of the study. We also found that the source of protein matters. Getting the majority of your protein from plant sources at midlife, plus a small amount of animal protein seems to be conducive to good health and good survival to older ages.
Findings were derived from the seminal Harvard-basedNurses Health Study, which followed female health care professionals from 1984 to 2016. The women were between the ages of 38 and 59 in 1984 and deemed to be in good physical and mental health at the start of the study.
Ardisson Korat and fellow researchers, including senior author Qi Sun of the Harvard T.H. Chan School of Public Health, examined thousands of surveys collected every four years from 1984 to 2016 on how frequently people ate certain foods to pinpoint dietary protein and its effects on healthy aging. They calculated protein intake by multiplying the number of times each food item was consumed by its protein content and then, using the Harvard University Food Composition Database, totaling the amount of protein across all food items.
The researchers then compared the diets of women who didnt develop 11 chronic diseases or lose a lot of physical function or mental health, with the diets of those who did.
Women who ate more plant-based protein, which in 1984 was defined as protein obtained from bread, vegetables, fruits, pizza, cereal, baked items, mashed potatoes, nuts, beans, peanut butter, and pasta, were 46 percent more likely to be healthy into their later years.
Those who consumed more animal protein such as beef, chicken, milk, fish/seafood, and cheese, however, were 6 percent less likely to stay healthy as they aged.
Those who consumed greater amounts of animal protein tended to have more chronic disease and didnt manage to obtain the improved physical function that we normally associate with eating protein, said Ardisson Korat.
Animal protein was modestly tied with fewer physical limitations in older age, but plant protein had a stronger, more consistent correlation across all observed models, and was more closely linked with sound mental health later in life.
For heart disease in particular, higher plant protein consumption came with lower levels of LDL cholesterol (bad cholesterol), blood pressure, and insulin sensitivity, while higher animal protein intake was tied to higher levels, along with increased insulin-like growth factor, which has been detected in multiple cancers.
Dairy protein alone (mainly milk, cheese, pizza, yogurt, and ice cream) was not significantly associated with better health status in older adulthood.
The team acknowledged that the benefits of plant protein might derive from components in plant-based food, rather than the proteincompared to animal foods, plants contain a higher proportion of dietary fiber, micronutrients, and beneficial compounds called polyphenols that are present in plants, rather than exclusively protein.
Ardisson Korat also said data from other groups is needed, as the Nurses Health Study surveyed primarily white females working in health care. The data from the study tended to be very homogeneous in terms of demographic and socioeconomic composition, so it will be valuable to follow up with a study in cohorts that are more diverse. Its a field that is still evolving, said Ardisson Korat.
But the teams findings so far support the recommendationthat women eat most of their protein in the form of fruits, vegetables, nuts, and seeds, although they should also consume some fish and animal protein for their iron and vitamin B12 content.
Dietary protein intake, especially plant protein, in midlife plays an important role in the promotion of healthy aging and in maintaining positive health status at older ages, Ardisson Korat said.
Funding: Research reported in this article was supported by the U.S. Department of AgriculturesAgricultural Research Service, and by the National Institutes of Health under award numbers UM1CA186107 (National Cancer Institute), P01CA87969 (National Cancer Institute), R01DK120870 (National Institute of Diabetes and Digestive and Kidney Diseases), U2CDK129670 (National Institute of Diabetes and Digestive and Kidney Diseases), R01DK127601 (National Institute of Diabetes and Digestive and Kidney Diseases), R01HL060712 (National Heart, Lung and Blood Institute), R01HL034594 (National Heart, Lung and Blood Institute), R01HL035464 (National Heart, Lung and Blood Institute), and R01HL088521 (National Heart, Lung and Blood Institute). Andres Ardisson Korat was supported by training grant KL2TR002545 from the National Institutes of Healths National Center for Advancing Translational Sciences. Complete information on authors, funders, limitations and conflicts of interest is available in the published paper.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the U.S. Department of Agriculture or the National Institutes of Health.
Author: Lisa LaPoint Source: Tufts University Contact: Lisa LaPoint Tufts University Image: The image is credited to Neuroscience News
Original Research: The findings will appear in American Journal of Clinical Nutrition
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Plant Protein-Based Diet Is Key to Healthier Aging for Women - Neuroscience News
Summary: Researchers made a breakthrough in understanding memory loss due to repeated head impacts, as often experienced by athletes. Their study reveals that memory issues following head injury in mice are linked to inadequate reactivation of neurons involved in memory formation.
This discovery is significant because it demonstrates that the memory loss is not a permanent, degenerative condition but potentially reversible. By using lasers to activate specific memory neurons, the researchers successfully reversed amnesia in mice, opening new avenues for treating cognitive impairments in humans caused by repeated head impacts.
Key Facts:
Source: Georgetown University
A mouse study designed to shed light on memory loss in people who experience repeated head impacts, such as athletes, suggests the condition could potentially be reversed. The research in mice finds that amnesia and poor memory following head injury is due to inadequate reactivation of neurons involved in forming memories.
The study, conducted by researchers at Georgetown University Medical Center in collaboration with Trinity College Dublin, Ireland, is reported January 16, 2024, in theJournal of Neuroscience.
Importantly for diagnostic and treatment purposes, the researchers found that the memory loss attributed to head injury was not a permanent pathological event driven by a neurodegenerative disease. Indeed, the researchers could reverse the amnesia to allow the mice to recall the lost memory, potentially allowing cognitive impairment caused by head impact to be clinically reversed.
The Georgetown investigators had previously found that the brain adapts to repeated head impacts by changing the way the synapses in the brain operate. This can cause trouble in forming new memories and remembering existing memories. In their new study, investigators were able to trigger mice to remember memories that had been forgotten due to head impacts.
Our research gives us hope that we can design treatments to return the head-impact brain to its normal condition and recover cognitive function in humans that have poor memory caused by repeated head impacts, says the studys senior investigator, Mark Burns, PhD, a professor and Vice-Chair in Georgetowns Department of Neuroscience and director of the Laboratory for Brain Injury and Dementia.
In the new study, the scientists gave two groups of mice a new memory by training them in a test they had never seen before. One group was exposed to a high frequency of mild head impacts for one week (similar to contact sport exposure in people) and one group were controls that didnt receive the impacts. The impacted mice were unable to recall the new memory a week later.
Most research in this area has been in human brains with chronic traumatic encephalopathy (CTE), which is a degenerative brain disease found in people with a history of repetitive head impact, said Burns. By contrast, our goal was to understand how the brain changes in response to the low-level head impacts that many young football players regularly experience.
Researchers have found that, on average, college football players receive 21 head impacts per week with defensive ends receiving 41 head impacts per week. The number of head impacts to mice in this study were designed to mimic a week of exposure for a college football player, and each single head impact by itself was extraordinarily mild.
Using genetically modified mice allowed the researchers to see the neurons involved in learning new memories, and they found that these memory neurons (the memory engram) were equally present in both the control mice and the experimental mice.
To understand the physiology underlying these memory changes, the studys first author, Daniel P. Chapman, Ph.D., said, We are good at associating memories with places, and thats because being in a place, or seeing a photo of a place, causes a reactivation of our memory engrams. This is why we examined the engram neurons to look for the specific signature of an activated neuron.
When the mice see the room where they first learned the memory, the control mice are able to activate their memory engram, but the head impact mice were not. This is what was causing the amnesia.
The researchers were able to reverse the amnesia to allow the mice to remember the lost memory using lasers to activate the engram cells.
We used an invasive technique to reverse memory loss in our mice, and unfortunately this is not translatable to humans, Burns adds.
We are currently studying a number of non-invasive techniques to try to communicate to the brain that it is no longer in danger, and to open a window of plasticity that can reset the brain to its former state.
In addition to Burns and Chapman the authors include Stefano Vicini at Georgetown University and Sarah D. Power and Toms J. Ryan at Trinity College Dublin, Ireland.
Funding: This work was supported by the Mouse Behavior Core in the Georgetown University Neuroscience Department and by the National Institutes of Health (NIH) / National Institute of Neurological Disorders and Stroke (NINDS) grants R01NS107370 & R01NS121316. NINDS also supported F30 NS122281 and the Neural Injury and Plasticity Training Grant housed in the Center for Neural Injury and Recovery at Georgetown University (T32NS041218). Seed funding is from the CTE Research Fund at Georgetown.
The authors report having no personal financial interests related to the study.
Author: Karen Teber Source: Georgetown University Contact: Karen Teber Georgetown University Image: The image is credited to Neuroscience News
Original Research: Closed access. Amnesia after repeated head impact is caused by impaired synaptic plasticity in the memory engram by Mark Burns et al. Journal of Neuroscience
Abstract
Amnesia after repeated head impact is caused by impaired synaptic plasticity in the memory engram
Sub-concussive head impacts are associated with the development of acute and chronic cognitive deficits. We recently reported that high-frequency head impact (HFHI) causes chronic cognitive deficits in mice through synaptic changes. To better understand the mechanisms underlying HFHI-induced memory decline, we used TRAP2/Ai32 transgenic mice to enable visualization and manipulation of memory engrams.
We labeled the fear memory engram in male and female mice exposed to an aversive experience and subjected them to sham or HFHI. Upon subsequent exposure to natural memory recall cues, sham, but not HFHI mice, successfully retrieved fearful memories.
In sham mice the hippocampal engram neurons exhibited synaptic plasticity, evident in amplified AMPA:NMDA ratio, enhanced AMPA-weighted tau, and increased dendritic spine volume compared to non-engram neurons. In contrast, although HFHI mice retained a comparable number of hippocampal engram neurons, these neurons did not undergo synaptic plasticity.
This lack of plasticity coincided with impaired activation of the engram network, leading to retrograde amnesia in HFHI mice. We validated that the memory deficits induced by HFHI stem from synaptic plasticity impairments by artificially activating the engram using optogenetics, and found that stimulated memory recall was identical in both sham and HFHI mice.
Our work shows that chronic cognitive impairment after HFHI is a result of deficiencies in synaptic plasticity instead of a loss in neuronal infrastructure, and we can reinstate a forgotten memory in the amnestic brain by stimulating the memory engram. Targeting synaptic plasticity may have therapeutic potential for treating memory impairments caused by repeated head impacts.
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Memory Loss from TBI Reversed - Neuroscience News
NEUROSCIENCE
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UMHS Campus in St. Kitts, West Indies
The University of Medicine and Health Sciences-St. Kitts (UMHS) invites applications for a faculty position in Neuroscience.Neuroscience/Neuroanatomy is focused on team-teaching and, as such, faculty have adequate time to engage in research and/or writing. The UMHS academic year has three semesters; therefore, teaching responsibilities occur throughout the year.
Responsibilities include:
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Course Description: MNEU 0810 Neuroscience/Neuroanatomy 7 credits. Neuroscience begins with an overview of the entire nervous system. As the course progresses, the focus is on comprehending the basic structure and function of each level of the nervous system, integrating both the anatomy and physiology of the nervous system. The principles that underlie the anatomical structure of each system of the brain are correlated with its physiology; correlations between the functional deficits, and the pathological anatomy in several neurological diseases which require working knowledge of anatomy and physiology are stressed. Special attention is given to integrating current understandings of human neurological and psychiatric diseases, and each topic is supplemented by relevant lab exercises which include detailed brain dissection and exposure to angiograms, CT scans, MRI, etc.
About UMHS.Students complete the Basic Science Program at the UMHS at our state-of-the-art campus in St Kitts. The fifth semester occurs at the UMHS campus in Portland, Maine. Students complete their third year of core clinical rotations and fourth year of elective rotations in one of our many affiliated, accredited teaching hospitals throughout the United States. To graduate, students must successfully complete the UMHS medical program and pass the USMLE Step1 and Step 2. Our graduates have obtained residencies through the United States and Canada. Please visit our website for further details about our academic program and student successes
Course Benefits:The position is full time and the salary is commensurate with teaching experience and degree. The faculty member is provided with an excellent health care plan which covers both the US and St. Kitts health care. Since there are three fifteen week semesters, the faculty member has seven weeks vacation a year which comes as the last two weeks of May and August and three weeks in December. Faculty are also provided an annual one week leave with expenses to attend a pre approved professional convention. Please note that we recruit highly credentialed faculty worldwide to promote diversity, equity and inclusion. UMHS offers a tax-free annual salary within certain limits, a state of the art institution on an idyllic island, the opportunity to become involved in the growth and success of the institution, and most importantly the opportunity to educate and nurture a new generation of physicians.
Send letter of interest, CV, and references to: Dr. Jerry Thornton, Executive Vice President at drjerrythornton@gmail.com andhr@umhs-sk.net
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NEUROSCIENCE PROFESSOR (ASSISTANT, ASSOCIATE OR FULL PROFESSOR) job with University of Medicine ... - The Chronicle of Higher Education
Summary: Researchers found a connection between the increased use of acetaminophen during pregnancy, particularly in the second trimester, and attention and behavior problems in young children. The research, part of the Illinois Kids Development Study, involved tracking prenatal chemical exposures and assessing the behaviors and traits of children at ages 2, 3, and 4.
While acetaminophen is deemed the safest painkiller during pregnancy, the study reveals a trend where higher usage, especially in the second trimester, corresponds to more attention-related problems and ADHD-type behaviors in children. However, the studys authors emphasize the need for more research and caution against interpreting the findings as an indication of ADHD or other disorders.
Key Facts:
Source: University of Illinois
A new study links increased use of acetaminophen during pregnancy particularly in the second trimester to modest but noticeable increases in problems with attention and behavior in 2-, 3- and 4-year-olds.
The study adds to a growing body of evidence linking the frequent use of acetaminophen in pregnancy to developmental problems in offspring.
The findings are detailed in the journalNeurotoxicology and Teratology.
The research is part of theIllinois Kids Development Studyat the University of Illinois Urbana-Champaign, which explores how environmental exposures influence child development. The study tracked hundreds of children, collecting data on their prenatal chemical exposures and asking caregivers to assess their behaviors and traits at ages 2, 3 and 4.
While acetaminophen is considered the safest painkiller and fever reducer available during pregnancy, previous studies have found evidence of a range of possible negative outcomes for children exposed to the drug in gestation, said Megan Woodbury, who led the research as a graduate student at the U. of I. withcomparative biosciencesprofessor emeritaSusan Schantz, the principal investigator of the IKIDS program at Illinois. Woodbury is now a postdoctoral researcher at Northeastern University in Boston. Schantz is a faculty member of theBeckman Institute for Advanced Science and Technologyat the U. of I.
Arecent studyled by Woodbury and Schantz linked higher acetaminophen exposure in pregnancy to language delays in children.
Some previous studies have found no relationship between acetaminophen use in pregnancy and attention and behavior in childhood, while other, usually larger studies found relationships between more frequent use of the medication during pregnancy and attention-related and behavioral problems in offspring.
Most of the latter studies were conducted in older children and questioned pregnant participants about their use of acetaminophen at most once per trimester.
The new study asked pregnant parents about their acetaminophen use six times over the course of the pregnancy roughly once every four-to-six weeks offering a more precise picture of the magnitude and timing of the drug exposures.
The researchers also asked caregivers to answer dozens of standardized questions about their childs behavior and ability to pay attention at ages 2, 3 and 4. More than 300 children were assessed at age 2, with 262 assessed again at 3, and 196 at age 4.
Our most important finding was that with increasing acetaminophen use by pregnant participants, especially during the second trimester, their children showed more attention-related problems and ADHD-type behaviors, which we call externalizing behaviors, at every age we measured, Woodbury said.
The kinds of behaviors the caregivers reported included things like the child talking out of turn, not paying attention, not being quiet when they were supposed to be quiet, not sitting down when they were supposed to be sitting down, and being a little aggressive with other children, Schantz said.
The findings are not an indication that the children have attention-deficit/hyperactivity disorder or that they will be diagnosed with ADHD at a later date, Schantz said. But the children seem to be having more trouble with attention than peers of the same age who were less exposed or not exposed to acetaminophen in the womb.
Woodbury, who herself is pregnant, says she does not want to scare others away from using acetaminophen in pregnancy when needed. Extreme headaches or other painful episodes and fevers can be debilitating and even dangerous, calling for use of the drug. She said she has turned to acetaminophen once per trimester so far. But she also chooses not to use it for minor aches, pains or slight fevers.
More research is needed to test whether more frequent use of acetaminophen during the second trimester of pregnancy may be particularly problematic for the developing brain, the researchers said.
The study also is limited as participants were mostly white, non-Hispanic and of higher economic status. Schantz and her team are working to broaden the cohort of participants in IKIDS to include pregnant people from a greater diversity of social, economic and racial backgrounds.
Funding: This research was supported by the Childrens Environmental Health and Disease Prevention Research Center funded by the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency and the National Institutes of Health Environmental Influences on Child Health Outcomes program.
Author: Diana Yates Source: University of Illinois Contact: Diana Yates University of Illinois Image The image is credited to Neuroscience News
Original Research: Open access. The relationship of prenatal acetaminophen exposure and attention-related behavior in early childhood by Susan Schantz et al. Neurotoxicology and Teratology
Abstract
The relationship of prenatal acetaminophen exposure and attention-related behavior in early childhood
Acetaminophenis currently the only analgesic considered safe for use throughout pregnancy, but recent studies indicate thatprenatal exposureto acetaminophen may be related to poorer neurodevelopmental outcomes. Multiple studies have suggested that it may be associated with attention problems, but few have examined this association by trimester of exposure.
The Illinois Kids Development Study is a prospective birth cohort located in east-central Illinois. Exposure data were collected between December 2013 and March 2020, and 535 newborns were enrolled during that period. Mothers reported the number of times they took acetaminophen at six time points across pregnancy.
When children were 2, 3, and 4years of age, caregivers completed the ChildBehaviorChecklist for ages 1.55years (CBCL). Associations of acetaminophen use during pregnancy with scores on the Attention Problems andADHDProblems syndrome scales, the Internalizing and Externalizing Behavior composite scales, and the Total Problems score were evaluated.
Higher acetaminophen exposure during the second trimester of fetal development was associated with higher Attention Problems, ADHD Problems, Externalizing Behavior, and Total Problems scores at ages 2 and 3. Higher second trimester exposure was only associated with higher Externalizing Behavior and Total Problems scores at 4years.
Higher cumulative exposure across pregnancy was associated with higher Attention Problems and ADHD Problems scores at ages 2 and 3. Findings suggest that prenatal acetaminophen exposure, especially during the second trimester, may be related to problems with attention in early childhood.
Original post:
Acetaminophen Use in Pregnancy Linked to ADHD in Kids - Neuroscience News