Category Archives: Neuroscience

Eating with Your Eyes and Gut? How Your Brain Decides When to Eat – Neuroscience News

Summary: The science of eating behavior goes beyond hunger cues; it involves sensory stimuli, internal signals, and the gut-brain connection. External cues like food packaging and advertisements influence our eating decisions, but internal signals, such as hunger and fullness, play a profound role.

Research shows that animals, including rodents, use internal cues to shape their food-related choices. The vagus nerve, which connects the gut and brain, communicates nutrient information rapidly and can induce pleasurable states. Understanding interoceptive signals can lead to more mindful and intuitive eating during the holiday season and beyond.

Key Facts:

Source: The Conversation

The holiday season is upon us, and with it, opportunities to indulge in festive treats. The proverbial saying you eat with your eyes first seems particularly relevant at this time of year.

The science behind eating behavior, however, reveals that the process of deciding what, when and how much to eat is far more complex than just consuming calories when your body needs fuel. Hunger cues are only part of why people choose to eat. As a scientist interested in thepsychology and biology that drives eating behavior, Im fascinated with how the brains experiences with food shape eating decisions.

So how do people decide when to eat?

Food-related visual cuescan shape feeding behaviors in both people and animals. For example, wrapping food in McDonalds packaging is sufficient toenhance taste preferencesacross a range of foods from chicken nuggets to carrots in young children. Visual food-related cues, such as presenting a light when food is delivered, can also promoteovereating behaviorsin animals by overriding energy needs.

In fact, a whole host of sensory stimuli noises, smells and textures can be associated with thepleasurable consequences of eatingand influence food-related decisions. This is why hearing a catchy radio jingle for a food brand, seeing a television ad for a restaurant or walking by your favorite eatery can shape your decision to consume and sometimes overindulge.

However, your capacity to learn about food-related cues extends beyond just stimuli from the outside world and includes theinternal milieu of your body. In other words, you also tend to eat with your stomach in mind, and you do so by using the same learning and brain mechanisms involved in processing food-related stimuli from the outside world. These internal signals, also calledinteroceptive cues, include feelings of hunger and fullness emanating from your gastrointestinal tract.

Its no surprise that the signals from your gut help set the stage for when to eat, but the role these signals play is more profound than you might expect.

Feelings of hunger or fullness act as important interoceptive cues influencing your decision-making around food.

To examine how interoceptive states shape eating behaviors, researchers trained laboratory rats toassociate feelings of hunger or satietywith whether they receive food or not.

They did this by giving rats food only when they were hungry or full, such that the rats were forced to recognize those internal cues to calculate whether food would be available or not. If a rat is trained to expect food only when hungry, it would generally avoid the area where food is available when it feels full because it does not expect to be fed.

However, when rats were injected with a hormone thattriggers hungercalled ghrelin, they approached the food delivery location more frequently. This suggests that the rats used this artificial state of hunger as an interoceptive cue to predict food delivery and subsequently behaved like they expected food.

Interoceptive states are sufficient to shape feeding behaviors even in the absence of external sensory cues. One particularly striking example comes from mice that have been genetically engineered to be unable to taste food but nevertheless show preferences for specific foodssolely by caloric content. In other words, rodents can use internal cues to shape their food-related decision-making, including when and where to eat and which foods they prefer.

These findings also suggest that feelings of hunger and the detection of nutrients is not restricted to the stomach. They also involve areas of the brain important for regulation and homeostasis, such as thelateral hypothalamus, as well as centers of the brain involved in learning and memory, such as thehippocampus.

Thegut-brain axis, or the biochemical connection between your gut and your brain, shapes feeding behaviors in many ways. One of them involves thevagus nerve, a cranial nerve that helps control the digestive tract, among other things.

The vagus nerve rapidlycommunicates nutrient informationto the brain. Activating the vagus nerve can induce a pleasurable state, such that mice will voluntarily perform a behavior, such as poking their nose through an open port, to stimulate their vagus nerve. Importantly, mice also learn toprefer foods and placeswhere vagal nerve stimulation occurred.

The vagus nerve plays an essential role in not only communicating digestive signals but also an array of other interoceptive signals that can affect how you feel and behave. In people, vagal nerve stimulation canimprove learning and memoryand can be used totreat major depression.

Your bodys capacity to use both external and internal cues to regulate how you learn and make decisions about food highlights the impressive processes involved in how you regulate your energy needs.

Poor interoceptive awareness is associated with a range ofdysfunctional feeding behaviors, such as eating disorders. For instance,anorexia may resultwhen interoceptive signals, such as feelings of hunger, are unable to trigger the motivation to eat. Alternatively, the inability to use the feeling of fullness to dampen the rewarding and pleasurable consequences of eating palatable food couldresult in binge eating.

Your interoceptive signals play an important role in regulating your daily eating patterns. During the holidays, many stressors from the outside world surround eating, such as packed social calendars, pressures to conform and feelings of guilt when overindulging.

At this time, it is particularly important to cultivate a strong connection to your interoceptive signals. This can help promoteintuitive eatingand a more holistic approach to your dietary habits.

Rather than fixating on external factors and placing conditions on your eating behavior, enjoy the moment, deliberately savor each bite and provide time for your interoceptive signals to function in the role they are designed to play.

Your brain evolved to sense your current energy needs. Byintegrating these signalswith your experience of your food environment, you can both optimize your energetic needs and enjoy the season.

Author: Alex Johnson Source: The Conversation Contact: Alex Johnson The Conversation Image: The image is credited to Neuroscience News

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Eating with Your Eyes and Gut? How Your Brain Decides When to Eat - Neuroscience News

Uncovering Data Collection Practices in Student Research – Neuroscience News

Summary: A new study delves into the often opaque world of student data collection practices in research projects. Questionable and potentially fraudulent behaviors during data collection were investigated, revealing insights into student misconduct.

While 64% of students reported no problematic practices, some concerning behaviors, such as data deletion and participant manipulation, were found.

The study underscores the need for transparent communication between students and supervisors and promotes Open Science as a key element in improving research integrity.

Key Facts:

Source: Polish Association of Social Psychology

Recent efforts to improve on the openness and transparency in science have already begun paying off towards greater integrity in the way researchers do and report science. It is now common practice for scientists to pre-register their studies and share openly their materials and data, so that their research is easily available to scientific scrutiny and collaborations.

However, behaviors during data collection are still somewhat of a black box, especially when done by students. In fact, there are plenty of questionable and even fraudulent behaviors, such as telling participants the specific hypotheses of interest before starting the study or even instructing them to answer in a certain way, which are almost impossible to detect.

The major problem is that current practices and regulations are mostly ineffective in preventing or checking for problematic behaviors in the data collection process. Furthermore, detailed knowledge about the prevalence of such behaviors is relatively scarce. Past research has predominantly focused on questionable practices and misconduct in other stages of the research process like data analysis and reporting.

Importantly, questionable or even fraudulent behaviors might not only be problematic among researchers but also highly relevant in student projects. If public, the data collected from students may be reused by other students, supervisors and other researchers as part of their own work, including research articles published in journals.

Yet, there is no way for those reusers to fully be aware of what has been going during the data collection.

This is how a joint team of psychology students and researchers fromLMU Munichdecided to investigate students questionable practices and research misconduct during data collection.

We wondered: Can we trust student data? says Dr. Marlene Altenmller, corresponding author of the article.

We wanted to know whether and how students actually engage in questionable and even fraudulent practices when collecting data for their projects. And, we were interested in situational factors potentially amplifying or alleviating students engagement in such behaviors, she further explains.

The research team surveyed 473 psychology students and 199 supervisors at German-speaking universities. They asked them about 17 behaviors, ranging from questionable to fraudulent, to figure out whether and which of those the students had engaged in in previous projects. Examples include knowingly letting participants take part in the study while being aware they know the hypotheses; taking part in ones own survey; and deleting or creating data from scratch.

The researchers also sought to assess the students experiences during their projects. For example, they inquired what kind of expectations and future data use their supervisor had communicated to them.

The research team then also asked supervisors about their perceptions of students data collection behaviors and what they thought about how their students experienced their projects and their supervision.

The survey results reveal some reassuring, as well as some troubling insights into the black box of student data collection. While 64% of students did not report any problematic data collection practices, some behaviors were not uncommon: 4% admitted to having deleted data; 8% had participated in their own study; and 26% had let participants take part despite them knowing the hypothesis.

On average, supervisors had similar impressions of students questionable and fraudulent behaviors. Among the notable differences were that supervisors assumed a much lower prevalence for students to have taken part in their own survey and a lower prevalence for them to have deleted data.

Thus, the research team concluded, supervisors might be underestimating some highly problematic behaviors among students.

To reduce the prevalence of problematic data collection behaviors among students, and therefore prompt better quality of data, the researchers recommend addressing students perceptions of pressures, opportunities and rationalizations for engaging in these behaviours. Additionally, it would be helpful to make Open Science a central element of teaching.

Particularly, transparent and clear communication between students and supervisors might be one of the most important keys to high-quality, research-ready student data. Those students who knew their data would be used by others, also reported lower prevalence rates of problematic behaviors.

Supervisors should maybe consider how empirical student projects may not only be an opportunity for teaching, but also for research, concluded the authors with a positive outlook.

Author: Dimitar Boyadzhiev Source: Polish Association of Social Psychology Contact: Dimitar Boyadzhiev Polish Association of Social Psychology Image: The image is credited to Neuroscience News

Original Research: Closed access. Evading Open Science: The Black Box of Student Data Collection by Marlene Sophie Altenmller et al. Social Psychology Bulletin

Abstract

Evading Open Science: The Black Box of Student Data Collection

While Open Science has arguably initiated positive changes at some stages of the research process (e.g., increasing transparency through preregistration), problematic behaviors during data collection are still almost impossible to detect and pose a great risk to the validity and integrity of psychological researchespecially, when researchers use data collected by others (e.g., students).

Exploring students and supervisors perspectives, the present registered report enlightens this black box of student data collection, focusing on questionable research practices and research misconduct (QRP/M).

The majority of students did not report having engaged in any problematic behaviors during data collection, but some QRP/Mranging from somewhat questionable to highly fraudulentseem quite common (e.g., telling participants the hypothesis beforehand, participating in ones own survey).

We provide an overview of students reported and supervisors suspected data collection QRP/M, explore potential drivers for these behaviors based on the fraud triangle model (including pressures, opportunities, and rationalizations), and report how students and supervisors perceive the eligibility of student data for further uses (e.g., scientific publications).

Moreover, we explore the role of the student-supervisor relationship (e.g., communication and expectations) and Open Science practices in student projects.

In summary, our findings suggest the potential scientific value of data from student projects. Fostering transparent communication regarding expectations, experiences, and intentions between supervisors and students might further contribute to strengthening this prospect.

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Uncovering Data Collection Practices in Student Research - Neuroscience News

Unveiling the Intricate Blueprint of the Mammalian Brain – A Breakthrough in Neuroscience – Medriva

Unveiling the Intricate Blueprint of the Mammalian Brain

In an extraordinary scientific breakthrough, an international team of researchers has meticulously constructed a comprehensive cell atlas of the mammalian brain. This remarkable feat, a first in the annals of science, provides an intricate map of the mouse brain, replete with detailed information on cell connectivity. The atlas presents the diverse types of cells populating each region of the mouse brain, their spatial organization, and the entire set of gene readouts in a cell.

Moreover, this intricate blueprint reveals the chemical modifications to a cells DNA and chromosomes. These insights can be instrumental in understanding how chemical signals are initiated and transmitted in different parts of the brain. As such, this groundbreaking atlas can serve as a foundation in developing precision treatments for a variety of mental and neurological disorders.

Undeniably, the human brain is an incredibly complex organ. It is a labyrinth of billions of neurons intricately connected by trillions of synapses. The understanding of this complexity requires a detailed map a genetic atlas that precisely details the genetic organization of the human brain.

Now, researchers have presented an atlas of the human and nonhuman primate brain in unprecedented detail across 21 papers in Science, Science Advances, and ScienceTM. This atlas provides an intricate understanding of the genetic organization of the human brain, offering valuable insights into the unique genetic intricacies that differentiate humans from other primates.

The implications of such a comprehensive atlas extend beyond the realm of basic science. It can serve as a powerful tool in the hands of healthcare providers by enabling precision medicine for the treatment of mental and neurological disorders. By understanding the genetic underpinnings of these conditions, healthcare providers can tailor treatments to the individual, improving outcomes and reducing side effects.

Furthermore, the atlas could be instrumental in the development of therapeutics for neurodegenerative disorders like Alzheimers and Parkinsons disease. By providing a detailed understanding of the genetic organization of the brain, researchers can identify potential genetic targets for drug development.

The creation of this comprehensive atlas of the human and nonhuman primate brain is an unprecedented achievement in neuroscience. It represents a significant step forward in our understanding of the brains genetic organization and offers valuable insights that could potentially revolutionize the treatment of mental and neurological disorders.

As we continue to unravel the mysteries of the human brain, this atlas will undoubtedly serve as a valuable resource. It is a testament to the power of scientific collaboration and the potential of genetic research to improve human health.

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Unveiling the Intricate Blueprint of the Mammalian Brain - A Breakthrough in Neuroscience - Medriva

Uncovering the Hidden Risks of Young-Onset Dementia – Neuroscience News

Summary: A new study reveals 15 risk factors for young-onset dementia, challenging the notion that genetics are the sole cause. These factors, ranging from education and socioeconomic status to lifestyle and health issues, offer hope for prevention.

With around 370,000 new cases each year, this research sheds light on a condition often overlooked. International collaboration and big data played a crucial role in advancing our understanding of dementia.

Key Facts:

Source: University of Exeter

Researchers have identified a wide range of risk factors for young-onset dementia. The findings challenge the notion that genetics are the sole cause of the condition, laying the groundwork for new prevention strategies.

The largescale study identified 15 risk factors, which are similar to those for late-onset dementia. For the first time, they indicate that it may be possible to reduce the risk of young-onset dementia by targeting health and lifestyle factors.

Relatively little research has been done on young-onset dementia, though globally there are around 370,000 new cases of young-onset dementia each year.

Published inJAMA Neurology, the new research by the University of Exeter and Maastricht University followed more than 350,000 participants younger than 65 across the United Kingdom from the UK Biobank study. The team evaluated a broad array of risk factors ranging from genetic predispositions to lifestyle and environmental influences.

The study revealed that lower formal education, lower socioeconomic status, genetic variation, lifestyle factors such as alcohol use disorder and social isolation, and health issues including vitamin D deficiency, depression, stroke, hearing impairment and heart disease significantly elevate risk of young-onset dementia

Professor David Llewellyn of the University of Exeter emphasized the importance of the findings: This breakthrough study illustrates the crucial role of international collaboration and big data in advancing our understanding of dementia. Theres still much to learn in our ongoing mission to prevent, identify, and treat dementia in all its forms in a more targeted way.

This is the largest and most robust study of its kind ever conducted. Excitingly, for the first time it reveals that we may be able to take action to reduce risk of this debilitating condition, through targeting a range of different factors.

Dr Stevie Hendriks, Researcher at Maastricht University, said: Young-onset dementia has a very serious impact, because the people affected usually still have a job, children, and a busy life. The cause is often assumed to be genetic, but for many people we dont actually know exactly what the cause is. This is why we also wanted to investigate other risk factors in this study.

Sebastian Khler, Professor of Neuroepidemiology at Maastricht University, said: We already knew from research on people who develop dementia at older age that there are a series of modifiable risk factors.

In addition to physical factors, mental health also plays an important role, including avoiding chronic stress, loneliness and depression. The fact that this is also evident in young-onset dementia came as a surprise to me, and it may offer opportunities to reduce risk in this group too.

The studys support was supported by Alzheimers Research UK, The Alan Turing Institute/Engineering and Physical Sciences Research Council, Alzheimer Nederland, Gieskes Strijbis Fonds, the Medical Research Council, the National Institute for Health and Care Research (NIHR) Applied Research Collaboration South West Peninsula (PenARC), the National Health and Medical Research Council, the National Institute on Aging, and Alzheimer Netherlands.

Dr Janice Ranson, Senior Research Fellow at the University of Exeter, said: Our research breaks new ground in identifying that the risk of young-onset dementia can be reduced.We think this could herald a new era in interventions to reduce new cases of this condition.

Dr Leah Mursaleen, Head of Clinical Research at Alzheimers Research UK, which co-funded the study, said: Were witnessing a transformation in understanding of dementia risk and, potentially, how to reduce it on both an individual and societal level.

In recent years, theres been a growing consensus that dementia is linked to 12 specific modifiable risk factors such as smoking, blood pressure and hearing loss. Its now accepted that up to four in 10 dementia cases worldwide are linked to these factors.

This pioneering study shines important and much-needed light on factors influencing the risk of young-onset dementia. This starts to fill in an important gap in our knowledge. It will be important to build on these findings in broader studies.

Author: Louise Vennells Source: University of Exeter Contact: Louise Vennells University of Exeter Image: The image is credited to Neuroscience News

Original Research: Closed access. Risk factors for young-onset dementia in the UK Biobank: A prospective population-based study by David Llewellyn et al. JAMA Neurology

Abstract

Risk factors for young-onset dementia in the UK Biobank: A prospective population-based study

Importance

There is limited information on modifiable risk factors for young-onset dementia (YOD).

Objective

To examine factors that are associated with the incidence of YOD.

Design, Setting, and Participants

This prospective cohort study used data from the UK Biobank, with baseline assessment between 2006 and 2010 and follow-up until March 31, 2021, for England and Scotland, and February 28, 2018, for Wales. Participants younger than 65 years and without a dementia diagnosis at baseline assessment were included in this study. Participants who were 65 years and older and those with dementia at baseline were excluded. Data were analyzed from May 2022 to April 2023.

Exposures

A total of 39 potential risk factors were identified from systematic reviews of late-onset dementia and YOD risk factors and grouped into domains of sociodemographic factors (education, socioeconomic status, and sex), genetic factors (apolipoprotein E), lifestyle factors (physical activity, alcohol use, alcohol use disorder, smoking, diet, cognitive activity, social isolation, and marriage), environmental factors (nitrogen oxide, particulate matter, pesticide, and diesel), blood marker factors (vitamin D, C-reactive protein, estimated glomerular filtration rate function, and albumin), cardiometabolic factors (stroke, hypertension, diabetes, hypoglycemia, heart disease, atrial fibrillation, and aspirin use), psychiatric factors (depression, anxiety, benzodiazepine use, delirium, and sleep problems), and other factors (traumatic brain injury, rheumatoid arthritis, thyroid dysfunction, hearing impairment, and handgrip strength).

Main Outcome and Measures

Multivariable Cox proportional hazards regression was used to study the association between the risk factors and incidence of YOD. Factors were tested stepwise first within domains and then across domains.

Results

Of 356052 included participants, 197036 (55.3%) were women, and the mean (SD) age at baseline was 54.6 (7.0) years. During 2 891 409 person-years of follow-up, 485 incident YOD cases (251 of 485 men [51.8%]) were observed, yielding an incidence rate of 16.8 per 100000 person-years (95% CI, 15.4-18.3). In the final model, 15 factors were significantly associated with a higher YOD risk, namely lower formal education, lower socioeconomic status, carrying 2 apolipoprotein 4 allele, no alcohol use, alcohol use disorder, social isolation, vitamin D deficiency, high C-reactive protein levels, lower handgrip strength, hearing impairment, orthostatic hypotension, stroke, diabetes, heart disease, and depression.

Conclusions and Relevance

In this study, several factors, mostly modifiable, were associated with a higher risk of YOD. These modifiable risk factors should be incorporated in future dementia prevention initiatives and raise new therapeutic possibilities for YOD.

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Uncovering the Hidden Risks of Young-Onset Dementia - Neuroscience News

Enhancing Motor Learning with Visual-Motor Illusions – Neuroscience News

Summary: Researchers found that visual aids creating illusions of movement, like screens showing a hands motion, can enhance motor performance and early-stage motor learning. Functional near-infrared spectroscopy revealed distinct brain activity changes in motor learning regions compared to traditional third-person motion observation. These findings may have implications for innovative treatments for hemiplegic stroke patients.

Key Facts:

Source: Tokyo Metropolitan University

Researchers from Tokyo Metropolitan University showed that visual aids which create the illusion of movement, like a screen placed in front of ones hand showing the hand move, can improve motor performance and the early stages of motor learning.

Compared to observing third-person motions, functional near-infrared spectroscopy data also showed greater changes in brain activity in regions associated with motor learning. Findings like this might inform new treatment strategies for hemiplegic stroke patients.

Visual-motor illusion (VMI) is the curious illusion of watching your body move even while it is still. Imagine having a tablet screen placed in front of your hand. Your hand is hidden behind the tablet, and your hand is not moving. Now, imagine the screen playing a video of your hand moving; your eyes are telling you that your hand is moving, but it is not moving at all.

This unsettling situation is instantly resolved if you put the screen somewhere else; watching the screen now simply entails action observation (AO). Previous work has already shown that VMI and AO entail different responses in the brain, but the wider implications of VMI remained unclear.

Now, a team of scientists led by Assistant Professor Katsuya Sakai from Tokyo Metropolitan University have shown that VMI can improve motor performance and early-stage motor learning. Volunteers were set a specific task, rolling two metal ball around in one hand. After some initial testing, a visual aid was used which showed hands performing this exact action.

One group had the visual aid placed in front of their hand to invoke VMI, while another group simply watched the same video normally. Performance could be measured by the number of complete rolls that people managed.

Though both groups showed improvement, the VMI group showed more improvement than the AO group, both immediately after the video was shown to volunteers, and one hour afterwards. This not only shows improvement in performance but highlights that early-stage learning has also improved i.e. the changes can persist.

To understand what is happening in the brain, the team used functional near-infrared spectroscopy, a non-invasive technique that helps track activity in specific parts of the brain using external probes. They were able to find key differences between AO and VMI volunteers in parts of the brain associated with learning new movements.

Importantly, these changes were found to persist an hour after the visual stimuli, matching what they found from performance on the task. This was also in line with previous findings from the group showing how connectivity in parts of the brain responsible for motor execution was enhanced by VMI.

The team note that there is still a lot of work to be done. For example, these findings come from a study on healthy individuals, and there is yet to be any assessment of mid to long-term motor performance.

However, the insights gleaned from this study shed light on a unique strategy to improve motor performance and learning, which may one day be applied to the rehabilitation of hemiplegic stroke patients and guide the development of new treatments.

Funding: This work was supported by JSPS KAKENHI Grant Number 22K17569.

Author: GO TOTSUKAWA Source: Tokyo Metropolitan University Contact: GO TOTSUKAWA Tokyo Metropolitan University Image: The image is credited to Neuroscience News

Original Research: Open access. Differences in the early stages of motor learning between visualmotor illusion and action observation by Katsuya Sakai et al. Scientific Reports

Abstract

Differences in the early stages of motor learning between visualmotor illusion and action observation

The visual-motor illusion (VMI) induces a kinesthetic illusion by watching ones physically-moving video while the body is at rest. It remains unclear whether the early stages (immediately to one hour later) of motor learning are promoted by VMI. This study investigated whether VMI changes the early stages of motor learning in healthy individuals.

Thirty-six participants were randomly assigned to two groups: the VMI or action observation condition. Each condition was performed with the left hand for 20min.

The VMI condition induced a kinesthetic illusion by watching ones ball-rotation task video. The action observation condition involved watching the same video as the VMI condition but did not induce a kinesthetic illusion. The ball-rotation task and brain activity during the task were measured pre, post1 (immediately), and post2 (after 1h) in both conditions, and brain activity was measured using functional near-infrared spectroscopy.

The rate of the ball-rotation task improved significantly at post1 and post2 in the VMI condition than in the actionobservation condition. VMI condition lowers left dorsolateral prefrontal cortex and right premotor area activity from post1 to pre compared to the actionobservation condition. In conclusion, VMI effectively aids early stages ofmotor learning in healthy individuals.

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Enhancing Motor Learning with Visual-Motor Illusions - Neuroscience News

Tips from neuroscience to form healthy habits and break unhealthy ones – The Washington Post

Sharing your goal with friends to stay accountable or making a more public commitment, on social media for example, can be helpful tools for some people, Bermdez said.

Reframing the benefits of a goal can also be a powerful tool. If your goal is exercise-focused but the physical and psychological benefits arent motivation on their own, reframing time spent exercising as, Oh, this is a chance for me to catch up with my podcasts or with the music that I love, or its a chance for me to go outside, can be helpful, Bermdez said. Conversely, to break a habit, focus on the negatives of the tempting action, he said, because it will start to look increasingly less appealing.

Bermdez said its important to monitor if the strategy youve chosen is working and, if not, to be open to trying others. You may even need to reevaluate the goal itself.

Read the rest here:
Tips from neuroscience to form healthy habits and break unhealthy ones - The Washington Post

SYNGAP1 findings illuminate links between mutations, intellectual disability – The Transmitter: Neuroscience News and Perspectives

Brain communication relies on a complex set of connections, coordinated by important synaptic proteins. Mutations in one such protein, SYNGAP1, which is critical for brain plasticity, can lead to neurodevelopmental conditions.

SYNGAP1-related intellectual disability (SRID) makes up about 1 percent of intellectual disability cases. It is characterized by seizures, developmental delays and problems with motor coordination. About half of people with SRID have autism.

Recently, a flurry of new SYNGAP1 findings and the development of novel mouse models have expanded scientific understanding of the protein and gene. Together, this work may point to multiple therapeutic possibilities for SRID.

I think its an exciting time, says Gavin Rumbaugh, professor of neuroscience at UF Scripps Biomedical Research in Jupiter, Florida. There is a lot of increased interest in SYNGAP.

For example, past research has indicated that the protein acts as an enzyme to modulate the synaptic connections between neurons. But SYNGAP1 protein may also regulate synaptic plasticity and cognition by physically controlling the number of neurotransmitter receptors at excitatory synapses, according to a preprint posted on bioRxiv in August.

Other work suggests a new role for the gene and protein. In the past, they have primarily been recognized for their effects on synapse functioning. But now SYNGAP1 joins several autism-linked genes that code for synaptic proteins that also shape the developing brain.

A mutation that decreases SYNGAP1 protein levels may exert significant effects on the development of the cortical layers in a human organoid model by disrupting the differentiation of supporting cells that serve as a scaffold for neurons to migrate during development, Rumbaugh and his colleagues have found. Their study was published in Nature Neuroscience in November.

Its very important to use model systems to test the function of the proteins associated with disease at different developmental time points and in different cell types, says lead investigator Giorgia Quadrato, assistant professor of stem cell biology and regenerative medicine at the University of South California in Los Angeles.

A

In developing human neurons cultured in a dish, a lack of SYNGAP1 leads to increased cell size and dendrite length, and speeds up the onset of synaptic activity.

But it was unclear whether or how small mutations in the gene the situation typically seen in people with SRID affect the levels and function of the SYNGAP1 protein, synaptic plasticity and behavior in animals. To address this, lead investigator Richard Huganir and his team at Johns Hopkins University in Baltimore, Maryland, developed two new mouse models.

Each model is based on mutations in the SYNGAP1 gene as they appear in two people a young boy and girl. Its much better to have [models] with patient-based mutations for future therapeutics, says Huganir, professor of neuroscience.

Using CRISPR, the group introduced the two faulty versions of SYNGAP1 into different sets of healthy mice. Both mutations reduced SYNGAP1 protein levels by about 50 percent compared with those of wildtype mice. And the mice showed changes in the expression of genes involved in synaptic plasticity.

Brain slices revealed that the SYNGAP1 mice also had impaired long-term potentiation, the process by which synapses strengthen to facilitate learning and memory. In line with that finding, these mice less frequently went into the arms of a y-shaped maze they had not recently explored than did wildtype rodents.

That behavior indicates the mice might not recall the arm they were in last, which generally reflects deficits in working memory. The mice also displayed hyperactive and repetitive behaviors, typical characteristics in SRID. The results were published in PNAS in September.

I think its an exciting time. There is a lot of increased interest in SYNGAP.

A

The mice showed altered SYNGAP1 functioning that in turn affected synapse functioning, which, would suggest it could increase your risk for developing some sort of mental health disorder, Rumbaugh adds.

This work also reveals that a decrease in SYNGAP1 protein may be a crucial mechanism for the development of SRID. Researchers are already looking for ways to restore the SYNGAP1 protein to treat people with SRID and other neurodevelopmental conditions.

For example, one antisense oligonucleotide a short molecule of DNA or RNA increased the levels of SYNGAP1 in mice in a study published in Neuron in March. Yet another approach to intervention could involve new molecular technology that binds to mRNA and regulates gene expression. The resulting tool brings together the protein-producing machinery for a specific gene, according to a study published in Nature Communications in October.

With this technology, it is possible to elevate SYNGAP1 protein levels in neurons derived from induced pluripotent stem cells that lack one copy of the gene. The approach may open a new avenue for treating conditions such as SRID that are caused by the absence of a functional gene.

[SRID] kids have no direct treatments, says study investigator Bryan Dickinson, professor of chemistry at the University of Chicago in Illinois. There is a critical unmet medical need.

The new mouse strains also offer important therapeutic possibilities. These are actual patient mutations, and that is really cool, says Jill Silverman, professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute, who was not involved in any of the recent studies.

Its very innovative and important for precision medicine, Silverman says. The sky is the limit.

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SYNGAP1 findings illuminate links between mutations, intellectual disability - The Transmitter: Neuroscience News and Perspectives

How to keep neuroscience’s past racism from being its future – STAT – STAT

De-Shaine Murray is working at the cutting edge of neurotechnology. As a postdoctoral fellow at Yale, he is developing a device to monitor the brain following traumatic brain injury or stroke.

He is also trying to fight the long legacy of racism in neuroscience. During 2020, when it was difficult to conduct research, he said, I got the chance and the ability to read more widely and to just look into the legacy of neuroscience. He found a direct line from racist pseudoscience like phrenology to disparities in neuroscience today, like how the texture of Black peoples hair can sometimes exclude them from clinical trials because electrodes are not designed for them. In 2021, he co-founded Black in Neuro, an organization dedicated to improving Black representation in neuroscience.

On this episode of the First Opinion Podcast, I spoke to him about how the past and present racism in neuroscience could be reflected in the future, especially as neurotechnology like brain implants become more common.

Im not saying that whatever electrode that you made or created is racist. But when you have someone who creates a technology but doesnt think about the wide range of users that are potentially going to use it, then thats where the problem comes in, he told me.

We also discussed the way inequities in neuroscience research are visible in stroke wards, how brain implants might jump from helping disabled people to being used for human enhancement, and more.

Our conversation was inspired by his recent First Opinion essay, Neuroscience has to grapple with a long legacy of racism if it wants to move into the future. The book I mention at the end is Lock In by John Scalzi, a great sci-fi mystery exploring themes of race, socioeconomic status, neurotechnology, and more.

Be sure to sign up for the weekly First Opinion PodcastonApple Podcasts,Spotify,Google Play, or wherever you get your podcasts. And dont forget to sign up for theFirst Opinion newsletterto read each weeks best First Opinion essays.

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How to keep neuroscience's past racism from being its future - STAT - STAT

PhD in Neuroscience | Elson S. Floyd College of Medicine | Washington State University – Washington State University

WSU College of Medicine in Spokane is home to more than a dozen faculty members who are affiliated with the Neuroscience PhD program. These researchers recruit and mentor graduate students, providing outstanding opportunities for scientific training, scholarship, and collaboration. As the universitys health sciences hub, it is home to world-class health science facilities, faculty, and expertise, as well as partnerships with local and regional hospitals and research facilities.

Completing your studies through the Spokane campus provides a range of options for research areas of focus, with faculty who specialize in the following research areas:

Students complete three 8-week lab rotations during the first year to gain experience on different topics, learn a variety of techniques, and find the right mentor for continuing their research.

Spokane has the benefit of being located in the beautiful Pacific Northwest region, with ample options for outdoor sports and recreation; local shopping, dining, and events.

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PhD in Neuroscience | Elson S. Floyd College of Medicine | Washington State University - Washington State University