Category Archives: Neuroscience

Neuroscience

The Neuroscience of Choice – Newsmax

Misplacing your keys, forgetting someone's name at a party, or coming home from the market without the most important item these are just some of the many common memory slips we all experience from time to time.

The international bestseller that provides pioneering brain-enhancement strategies, memory exercises, a healthy brain diet, and stress reduction tps for enhancing cognitive function and halting memory loss.

Dr. Gary Small,author of The Mind Health Report newsletter, is a professor of psychiatry and aging and director of the UCLA Longevity Center at the Semel Institute for Neuroscience and Human Behavior. Dr. Small, one the nations top brain health experts, frequently appears on The Today Show, Good Morning America, and The Dr. Oz Show. He is co-author with his wife Gigi Vorgan of many popular books, including The New York Times best-seller, The Memory Bible, and The Alzheimers Prevention Program.

Let's face it without a decent mind, you have no quality of life. With Dr. Gary Small's Mind Health Report, you'll gain greater health, happiness, and fulfillment in your relationships, personal life, work life or retirement, and more. Dr. Small fills every issue with the latest advancements in brain research from the far-reaching frontiers of neuroscience and psychiatry. You'll not only read about breakthrough techniques for rejuvenating your brain health, but also see actual case studies from Dr. Small, one of the nation's leading brain and aging experts and director of the UCLA Longevity Center.

Each month, you'll embark on a new journey into the world of your brain. You'll discover the latest on topics such as Alzheimer's disease and memory loss, anxiety and depression, diet advice for a healthy brain, natural supplements and drugs that aid mental functioning and lessen pain and fatigue, and much more.

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The Neuroscience of Choice - Newsmax

Neuroscience

Drug helps mice with autism-linked mutation recognize others – Spectrum

Ion flow: A protein (red) that ferries potassium out of nerve cells abounds in a small part of the brains memory hub linked to social behavior.

Courtesy of Macayla Donegan

A drug that has been tested in clinical trials as a treatment for depression restores social memory in a mouse model of 22q11.2 deletion syndrome, according to a new study. The findings hint that the drug might also be useful to treat social cognitive difficulties in people with conditions such as autism, experts say.

People who are missing one copy of a chromosomal region known as 22q11.2 have heart abnormalities, distinctive facial features and an increased risk of schizophrenia and other psychiatric conditions. About 16 percent have autism. People with the syndrome also have a smaller-than-average hippocampus, a structure that functions as the brains memory hub.

The findings extend what researchers know about the role of the hippocampus in social behavior by suggesting that a small region of the hippocampus known as CA2 springs to life when an animal encounters an individual it hasnt met before.

A strength of the study is that it describes the basic biology of a brain circuit, shows how that circuit is disrupted in a mouse model and identifies a therapeutic target to reverse those disruptions, says Anthony LaMantia, professor of developmental disorders and genetics at Virginia Polytechnic Institute and State University in Blacksburg, who was not involved in the work. This is one of the best papers sort of going from soup to nuts that has come out.

Previous studies showed that CA2 is crucial for social memory, the ability to recognize and remember others. But we really didnt have a good handle on what type of information CA2 was providing to the rest of the brain, says study leader Steven Siegelbaum, professor of neuroscience and pharmacology at Columbia University.

Siegelbaums team recorded the electrical activity of CA2 neurons in six wildtype mice, as well as that of neurons in the neighboring CA1 region in three of the animals.

Most of the cells in CA2 show little activity as a mouse explores its cage or objects placed in it, the team found. But the cells become more active when another mouse is present. And some of the cells are even more active when that mouse is a stranger. The findings appeared in October in Nature Neuroscience.

In order to remember an individual, you first have to recognize whether you know them or you dont, and we think that CA2 is initially providing this novelty signal, Siegelbaum says.

The team fed information about the activity of CA1 and CA2 neurons into a machine-learning algorithm. Based on CA2 activity, the algorithm could decode when a mouse was interacting with another mouse, and whether that mouse was a stranger. Based on activity in CA1 a region known for making mental maps the algorithm could identify a mouses location in the cage.

The algorithm is a clever approach, says Enrico Cherubini, professor of neuroscience at the International School for Advanced Studies in Trieste, Italy, who was not involved in the work. Mice move during social interactions, so it can be difficult to distinguish place-related neural activity from that related to social behavior.

Because mice navigate by sight and recognize each other largely by smell, whereas people depend on sight for both functions, it does raise the issue of whether or not you can really make the comparisons, LaMantia says.

The hippocampus is known to be able to integrate multiple sources of sensory information, Siegelbaum says.

The researchers also recorded the activity of CA2 neurons in five 22q11.2 mice. These mice are known to have deficits in social memory, although they are just as interested in socializing as wildtype mice are. The model mice also show a loss of a certain type of neuron in CA2, as do postmortem brains of people with schizophrenia.

The CA2 neurons in the 22q11.2 mice are less active than those in controls, regardless of what the mice are doing, the researchers found. The cells dont become as active when the mice interact with other mice, and they dont show the marked increase in activity when theres a new mouse around.

Instead, the cells activity tends to reflect where the mouse is in the cage similar to the typical behavior of CA1 neurons. The gain of function was surprising, Siegelbaum says.

The researchers had evidence that the abnormally sluggish firing of CA2 neurons in the 22q11.2 mice could be due to overactivity of TREK-1, a protein that aids the flow of potassium ions out of the cell. (Too much potassium ion outflow inhibits a neuron from firing.)

So they injected the mice with spadin, a drug that blocks TREK-1 activity. The treatment normalized the activity of the CA2 neurons. It also enabled the mice to remember other mice that they had met before.

The researchers also used a genetic technique to turn down the activity of TREK-1 in the CA2 region. This method, too, corrects social memory problems in the 22q11.2 mice.

Siegelbaum plans similar studies to investigate CA2 function in other mouse models with genetic alterations linked to autism, such as those affecting SHANK3 and CNTNAP2.

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Drug helps mice with autism-linked mutation recognize others - Spectrum

Neuroscience

A brain and behavior expert explains how to give better gifts – Business Insider – Business Insider

Q: Do you have advice on how to find a good gift for a family member who already has everything and they don't need anything?

Giving gifts is easy if you pay attention throughout the year. It is very likely that the person you're giving gifts to, at some point, mentioned something they wanted/needed during the year. If you had listened and made a note you will have had the answer already.

So, as a first tip for the future, start a mini diary where you make a note every time someone says they want/need/miss something. Come Christmas you'll find that you have a lot of ideas in your diary. This not only makes things easier, it also highly impresses the recipient to know that you've been paying attention.

This is true, by the way, even if by now they actually already gotten the Bluetooth speaker they mentioned in July, or the silk bedding that came up in the conversation in March.

So now, let's assume you don't have this diary and have no inside information. What now?

For someone who has everything, there are a couple of answers. One quite popular these days is to gift a shared experience (i.e., a dinner you cook, a kayaking trip you go to together, or a spa day you arrange for the two of you).

Moran Cerf. Moran Cerf

Even if they had that experience before, they haven't had it with you. So the experience context is new, and assuming they like you is seen as a gift.

If you want to go for something material, and you believe the person really does have everything, or can afford to have everything they want, one thing you can do is aim for something in your budget that is the "top of a category they wouldn't buy themselves." John Ruhlin, author of "Giftology," has the example of buying an expensive "box" for a friend.

Read more: The lucrative lives of professional Christmas decorators, who charge as much as $80,000 to deck a house's halls and say business is booming this year

He suggests that if you were going to spend $50 on a gift, and the person really loves watches, for example, then buying them a $50 watch may not do the job compared to the ones a watch collector may own. But getting them a box for a watch that costs $50 may actually prove quite fancy.

So instead of getting a cheaper thing in category A, you get an expensive item in category B, a cheaper category. You get the top item in a different domain rather than a lower item in a domain you cannot afford. Instead of a fancy new game console, you can buy the best game for it; or instead of an expensive power tool, you get a really good level.

Thinking about the brain in that context, the way our brain resolves internal challenges is often not by identifying the optimal solution, but rather by reframing the problem. This is a key tool in emotion regulation and in therapy that allows our brain to overcome problems without always solving them.

Q: This year for Christmas, we're not to be there in person for the gift-giving, so I'm wondering: Is there any advice on how to make the people mostly kids, but not only who receive the gift associate it with me? (Sorry about the vanity, but I hate that my nieces don't know the gift came from me, after all the effort.)

One way to make a gift associated with you rather than, say, Santa is to put yourself in the gift. Here are a few ways.

If the gift has a visual component (i.e., a picture frame, or an external hard drive) you can add something of yours to it. If it's a picture frame you can put a picture of you and your nieces in it when you gift it. They may replace the picture, but the initial link is generated in their episodic memory. If it is a hard drive, you may leave a file that you want them to have: maybe a movie that you want them to watch, or a folder with some app they like.

Research in neuroscience shows that only a single association between an item and a person is needed to create a memory, IF it is the first association created for an experience meaning, if your nieces get a picture of you and them in the frame you will be registered with this frame even after the replaced your initial content.

Read more: Sleep-tracking ring Oura is beloved by some of the biggest names in tech. We asked 7 investors and execs how it's helped them revamp their routines to sleep better and live healthier.

And one last thought on the nieces' gift.

There are quite a few studies in brain development and memory, and the unfortunate bottom line is that it's likely that kids until the age of 2 will not really form explicit memories. They will form impressions (and events leave marks on them, and define trajectories of their personality development), but most likely won't remember much of the gift or your involvement in it at this stage.

So think of the gift as a way to shape their future self, and to start building a path together. And if you optimize for explicit memory, save some of the planned expenses for the next year or two, when they are more likely to code your role in the summoning of the Barbie Dollhouse.

Moran Cerf is a professor of neuroscience and business who explores how we can harness our understanding of the brain to improve our behavior, our business, and society. He's a former hacker, a science consultant to Hollywood films and TV shows, and the founder of a number of companies.

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A brain and behavior expert explains how to give better gifts - Business Insider - Business Insider

Neuroscience

You Do Not Want to Mess With This Virus Research Strongly Suggests COVID-19 Virus Enters the Brain – SciTechDaily

The S1 protein likely causes the brain to release inflammatory products causing a storm in the brain, researchers said. Credit: Alice Gray

A study published in Nature Neuroscience shows how spike protein crosses the blood-brain barrier.

More and more evidence is coming out that people with COVID-19 are suffering from cognitive effects, such as brain fog and fatigue.

And researchers are discovering why. The SARS-CoV-2 virus, like many viruses before it, is bad news for the brain. In a study published on December 16, 2020, in Nature Neuroscience, researchers found that the spike protein, often depicted as the red arms of the virus, can cross the blood-brain barrier in mice.

This strongly suggests that SARS-CoV-2, the cause of COVID-19, can enter the brain.

The spike protein, often called the S1 protein, dictates which cells the virus can enter. Usually, the virus does the same thing as its binding protein, said lead author William A. Banks, a professor of medicine at the University of Washington School of Medicine and a Puget Sound Veterans Affairs Healthcare System physician and researcher. Banks said binding proteins like S1 usually by themselves cause damage as they detach from the virus and cause inflammation.

The S1 protein likely causes the brain to release cytokines and inflammatory products, he said.

In science circles, the intense inflammation caused by the COVID-19 infection is called a cytokine storm. The immune system, upon seeing the virus and its proteins, overreacts in its attempt to kill the invading virus. The infected person is left with brain fog, fatigue and other cognitive issues.

Banks and his team saw this reaction with the HIV virus and wanted to see if the same was happening with SARS CoV-2.

Banks said the S1 protein in SARS-CoV2 and the gp 120 protein in HIV-1 function similarly. They are glycoproteins proteins that have a lot of sugars on them, hallmarks of proteins that bind to other receptors. Both these proteins function as the arms and hand for their viruses by grabbing onto other receptors. Both cross the blood-brain barrier and S1, like gp120, is likely toxic to brain tissues.

It was like dj vu, said Banks, who has done extensive work on HIV-1, gp120, and the blood-brain barrier.

The Banks lab studies the blood-brain barrier in Alzheimers, obesity, diabetes, and HIV. But they put their work on hold and all 15 people in the lab started their experiments on the S1 protein in April. They enlisted long-time collaborator Jacob Raber, a professor in the departments of Behavioral Neuroscience, Neurology, and Radiation Medicine, and his teams at Oregon Health & ScienceUniversity.

The study could explain many of the complications from COVID-19.

We know that when you have the COVID infection you have trouble breathing and thats because theres infection in your lung, but an additional explanation is that the virus enters the respiratory centers of the brain and causes problems there as well, said Banks.

Raber said in their experiments transport of S1 was faster in the olfactory bulb and kidney of males than females. This observation might relate to the increased susceptibility of men to more severe COVID-19 outcomes.

As for people taking the virus lightly, Banks has a message:

You do not want to mess with this virus, he said. Many of the effects that the COVID virus has could be accentuated or perpetuated or even caused by virus getting in the brain and those effects could last for a very long time.

Reference: The S1 protein of SARS-CoV-2 crosses the bloodbrain barrier in mice by Elizabeth M. Rhea, Aric F. Logsdon, Kim M. Hansen, Lindsey M. Williams, May J. Reed, Kristen K. Baumann, Sarah J. Holden, Jacob Raber, William A. Banks and Michelle A. Erickson, 16 December 2020, Nature Neuroscience.DOI: 10.1038/s41593-020-00771-8

This study was partially supported by a National Institute on Aging-funded COVID-19 supplement to a shared RF1 grant of Banks and Raber.

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You Do Not Want to Mess With This Virus Research Strongly Suggests COVID-19 Virus Enters the Brain - SciTechDaily

Neuroscience

Study reveals individuals with high ADHD-traits are more vulnerable to insomnia – EdexLive

Image for representational purpose only

Individuals with high ADHD-traits that do not meet the criteria for a diagnosis are less able to perform tasks involving attentional regulation or emotional control after a sleepless night than individuals with low ADHD-traits, suggest the findings a new study. The study from Karolinska Institutet published in Biological Psychofiatry: Cognitive Neuroscience and Neuroimaging reports.

While it can cause multiple cognitive impairments, there is considerable individual variation in sensitivity to the effects of insomnia. The reason for this variability has been an unresolved research question for long. In the present study, KI researchers investigated how sleep deprivation affects our executive functions, which is to say the central cognitive processes that govern our thoughts and actions. They also wanted to ascertain if people with ADHD tendencies are more sensitive to insomnia, with more severe functional impairments as a result.

ADHD (attention deficit hyperactivity disorder) is characterised by inattention, impulsiveness and hyperactivity; however, the symptoms vary from person to person and often also include emotional instability. "You could say that many people have some subclinical ADHD-like symptoms but a diagnosis is only made once the symptoms become so prominent that they interfere with our everyday lives," says Predrag Petrovic, consultant and associate professor in psychiatry at the Department of Clinical Neuroscience at Karolinska Institutet, Sweden, who led the study along with Tina Sundelin and John Axelsson, both researchers at Karolinska Institutet and the Stress Research Institute at Stockholm University.

The study included 180 healthy participants between the ages of 17 and 45 without an ADHD diagnosis. Tendencies towards inattentiveness and emotional instability were assessed on the Brown Attention Deficit Disorder (B-ADD) scale. The participants were randomly assigned to two groups, one that was allowed to sleep normally and one that was deprived of sleep for one night. They were then instructed to perform a test that measures executive functions and emotional control the following day (a Stroop test with neutral and emotional faces).

The researchers found that the sleep-deprived group showed worse performance in the experimental tasks (including more cognitive response variability). Moreover, people with high ADHD-traits were more vulnerable to sleep deprivation and showed greater impairment than those with low ADHD-traits. The effects were also related to the most prominent type of subclinical ADHD-like symptom, in that after being deprived of sleep, the participants who displayed more everyday problems with emotional instability had larger problems with the cognitive task involving emotional regulation, and those who had more everyday inattention symptoms had larger problems with the non-emotional cognitive task.

"One of the reasons why these results are important is that we know that young people are getting much less sleep than they did just ten years ago," explains Dr Petrovic. "If young people with high ADHD-traits regularly get too little sleep they will perform worse cognitively and, what's more, their symptoms might even end up at a clinically significant level."

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Study reveals individuals with high ADHD-traits are more vulnerable to insomnia - EdexLive

Neuroscience

Novartis buys neuroscience company Cadent for up to $770 million – CNBC

Signage is displayed on the exterior of the Novartis AG Institutes for BioMedical Research building in Cambridge, Massachusetts, U.S., on Friday, Aug. 5, 2016.

Scott Eisen | Bloomberg | Getty Images

Novartis said on Thursday it would acquire U.S.-based neuroscience company Cadent for up to $770 million, gaining full rights to Cadent's portfolio.

"Cadent will receive a $210 million upfront payment and will be eligible for up to $560 million in milestone payments, for a total potential consideration of $770 million," Cadent said in a statement.

Novartis said the acquisition added two new clinical stage programs to its neuroscience portfolio, one for schizophrenia and the other for movement disorders.

It also includes a buyout of milestones and royalties for MIJ821, a clinical stage molecule that Novartis licensed exclusively from Cadent in 2015 and that it is actively developing for treatment resistant depression, Novartis said.

Cadent and Novartis said they expected the transaction to close in the first quarter of 2021. Closing of the transaction is subject to customary closing conditions.

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Novartis buys neuroscience company Cadent for up to $770 million - CNBC

Neuroscience

Theranexus : THERANEXUS, LYON NEUROSCIENCE RESEARCH CENTER AND CERMEP ANNOUNCE THE CREATION AND FUNDING OF NEW JOINT PUBLIC/PRIVATE LABORATORY…

The laboratory obtained funding of350,000 from the French National Research Agency (ANR).

Lyon, 18 December 2020 Theranexus, a biopharmaceutical company innovating in the treatment of neurological diseases has announced the creation and funding of a new joint public/private laboratory in partnership with the BIORAN team from the Lyon Neuroscience Research Center (CRNL) and CERMEP (Hospices Civils de Lyon, Claude Bernard Lyon 1 University, INSERM, CNRS), the regional biomedical imaging core dedicated to clinical and basic research.

This laboratory, NeuroImaging for Drug Discovery(NI2D), aims to improve understanding of the cellular and molecular mechanisms of drug candidates developed by Theranexus in particular at the neuronal and astrocyte level using novel preclinical neuroimaging tools.

The approach taken by Theranexus calls for the development of novel neuroimaging tools and we are delighted to continue our successful collaboration with this company in connection with our joint NI2D laboratory explains Prof. Luc Zimmer, Director of CERMEP and the BIORAN team at the Lyon Neuroscience Research Center.

We are very happy to be given the opportunity to create this joint laboratory with the research teams at the cutting edge of innovation in neuroimaging from BIORAN and CERMEP and we would like to thank ANR for its funding. This laboratory will be dedicated to improving understanding of the neuronal and glial cell mechanisms of Theranexus drug candidates concludes Franck Mouthon, Chairman, CEO and co-founder of Theranexus.

This project is supported by funding of350,000 from the French National Research Agency, which comes in addition to the200,000 already obtained from the Auvergne-Rhne-Alpes Region1. The two partners are actively contributing through the provision of staff and equipment.

About Lyon Neuroscience Research Center (CRNL; supervisory authorities: Claude Bernard Lyon 1 University, INSERM, CNRS)

CRNL combines the expertise of 18 teams whose common aim is to develop multidisciplinary research in a bid to understand the complexity of brain function as well as certain dysfunctions in relation to neurologic or psychiatric conditions.

Within CRNL, the BIORAN team (Radiopharmaceutical and neurochemical biomarkers) brings together expertise in neurochemistry, neuropharmacology and neuroimaging with the aim of inventing novel probes and imaging protocols for investigating the biochemistry of the brain in diagnostic and therapeutic settings.

1https://www.theranexus.com/images/pdf/Theranexus_CP_Point_Actualite_Scientifique_VDEF.pdf

2020 ActusNews

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Theranexus : THERANEXUS, LYON NEUROSCIENCE RESEARCH CENTER AND CERMEP ANNOUNCE THE CREATION AND FUNDING OF NEW JOINT PUBLIC/PRIVATE LABORATORY...

Neuroscience

Whether it’s 2020 or Baby Shark: Study offers clues on how to stop thinking about it – CU Boulder Today

Let it go. Think about something else. Clear your head.

In our attempts to de-clutter our busy minds and make room for new, often more productive thoughts, people tap an array of different approaches. Which works best, and how does each strategy distinctly impact the brain?

Researchers at the University of Colorado Boulder and the University of Texas at Austin have taken a first stab at answering this question, combining novel brain imaging with machine learning techniques to offer an unprecedented window into what happens in the brain when we try to stop thinking about something.

The findings, published this month in the journal Nature Communicationslend new insight into the basic building blocks of cognition and could inform new therapies for issues like post-traumatic stress disorder and obsessive compulsive disorder. They also provide clues on how to form better study habits or innovate at work.

We found that if you really want a new idea to come into your mind, you need to deliberately force yourself to stop thinking about the old one, said co-author Marie Banich, a professor of psychology and neuroscience at CU Boulder.

For the study, Banich teamed up with Jarrod Lewis-Peacock, a cognitive neuroscience at UT Austin, to examine brain activity in 60 volunteers as they tried to flush a thought from their working memory.

As Lewis-Peacock describes it, working memory is the scratch pad of the mind where we store thoughts temporarily to help us carry out tasks. But we can only keep three or four thoughts in working memory at a time. Like a sink full of dirty dishes, it must be cleaned out to make new ideas possible.

Once were done using that information to answer an email or address some problem, we need to let it go so it doesnt clog up our mental resources to do the next thing, he said.

When we ruminate over something perhaps the fight we had with a friend or an offending text that can color new thoughts in a negative light. Such rumination is at the root of many mental health disorders, said Banich.

In obsessive compulsive disorder it could be the thought of as, If I dont wash my hands again I will get sick. In anxiety, it might be, This plane is going to crash.

A study subject has her brain scanned in an fMRI machine at CU Boulder.

To determine if people can truly purge a thought, and how, the team asked each volunteer to lay down inside a functional magnetic resonance imaging machine (fMRI) at the Intermountain Neuroimaging Center on the Boulder campus.

They were shown pictures of faces, fruits and scenes and asked to maintain the thought of them for 4 seconds. Meanwhile, researchers created individualized brain signatures showing precisely what each persons brain looked like when they thought of each picture.

Afterward, participants were told to: replace the thought (replace apple with mountain); clear all thoughts (akin to mindfulness meditation); or suppress the thought (focus on it and then deliberately try to stop thinking about it). In each case, the brain signature associated with the image visibly faded.

We were thrilled, said Banich. This is the first study to move beyond just asking someone, Did you stop thinking about that? Rather, you can actually look at a persons brain activity, see the pattern of the thought and then watch it fade as they remove it.

The researchers also found that replace, clear and suppress had very different impacts.

While replace and clear prompted the brain signature of the image to fade faster, it didnt fade completely, leaving a shadow in the background as new thoughts were introduced.

Suppress, on the other hand, took longer to prompt forgetting but was more complete in making room for a new thought.

Behavioral studies outside the scanner yielded similar results.

The bottom line is: If you want to get something out of your mind quickly use clear or replace, said Banich. But if you want to get something out of your mind so you can put in new information, suppress works best.

More research is necessary, but the findings suggest that students may want to pack up their algebra notes, take a break and deliberately try not to think about quadratic equations before moving on to study for physics.

Hit a wall on that report at work? Let it go for a while.

People often think, If I think about this harder I am going to solve this problem. But work by clinicians suggests it can actually give you tunnel vision and keep you in a loop that is hard to get out of, said Banich.

In a counseling setting, the findings suggest that to fully purge a problematic memory that keeps bubbling up, one might need to deliberately focus on it and then push it away.

Someday, the brain imaging technique could potentially be used during sessions as a sort of cognitive mirror to help people learn how to put destructive thoughts out of their minds.

Banich and Lewis-Peacock intend to study that next.

If we can get a sense of what their brain should look like if they are successfully suppressing a thought, then we can navigate them to a more effective strategy for doing that, said Lewis-Peacock. Its an exciting next step.

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Whether it's 2020 or Baby Shark: Study offers clues on how to stop thinking about it - CU Boulder Today

Neuroscience

Individuals with high ADHD-traits are more vulnerable to insomnia – Newswise

Newswise Individuals with high ADHD-traits that do not meet the criteria for a diagnosis are less able to perform tasks involving attentional regulation or emotional control after a sleepless night than individuals with low ADHD-traits, a new study from Karolinska Institutet published inBiological Psychiatry: Cognitive Neuroscience and Neuroimagingreports.

While it can cause multiple cognitive impairments, there is considerable individual variation in sensitivity to the effects of insomnia. The reason for this variability has been an unresolved research question for long. In the present study, KI researchers investigated how sleep deprivation affects our executive functions, which is to say the central cognitive processes that govern our thoughts and actions. They also wanted to ascertain if people with ADHD tendencies are more sensitive to insomnia, with more severe functional impairments as a result.

ADHD (attention deficit hyperactivity disorder) is characterized by inattention, impulsiveness and hyperactivity; however, the symptoms vary from person to person and often also include emotional instability.

"You could say that many people have some subclinical ADHD-like symptoms but a diagnosis is only made once the symptoms become so prominent that they interfere with our everyday lives," says Predrag Petrovic, consultant and associate professor in psychiatry at the Department of Clinical Neuroscience at Karolinska Institutet, Sweden, who led the study along with Tina Sundelin and John Axelsson, both researchers at Karolinska Institutet and the Stress Research Institute at Stockholm University.

The study included 180 healthy participants between the ages of 17 and 45 without an ADHD diagnosis. Tendencies towards inattentiveness and emotional instability were assessed on the Brown Attention Deficit Disorder (B-ADD) scale.

The participants were randomly assigned to two groups, one that was allowed to sleep normally and one that was deprived of sleep for one night. They were then instructed to perform a test that measures executive functions and emotional control the following day (a Stroop test with neutral and emotional faces).

The researchers found that the sleep-deprived group showed worse performance in the experimental tasks (including more cognitive response variability). Moreover, people with high ADHD-traits were more vulnerable to sleep deprivation and showed greater impairment than those with low ADHD-traits.

The effects were also related to the most prominent type of subclinical ADHD-like symptom, in that after being deprived of sleep, the participants who displayed more everyday problems with emotional instability had larger problems with the cognitive task involving emotional regulation, and those who had more everyday inattention symptoms had larger problems with the non-emotional cognitive task.

"One of the reasons why these results are important is that we know that young people are getting much less sleep than they did just ten years ago," explains Dr Petrovic. "If young people with high ADHD-traits regularly get too little sleep they will perform worse cognitively and, what's more, their symptoms might even end up at a clinically significant level."

###

The study was supported by grants from the Swedish Research Council, Forte (the Swedish Research Council for Health, Working Life and Welfare), Riksbankens Jubileumsfond, Karolinska Institutet, Region Stockholm, the Swedish Society of Medicine, the Sderstrm-Knigska Foundation and the Osher Centre for Integrative Medicine. The study is part of a doctoral project by Orestis Floros, who is also a psychiatrist specialising in ADHD.

Publication: "Vulnerability in executive functions to sleep deprivation is predicted by subclinical ADHD symptoms". Orestis Floros, John Axelsson, Rita Almeida, Lars Tigerstrm, Mats Lekander, Tina Sundelin, Predrag Petrovic.Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 17 December 2020, doi: 10.1016/j.bpsc.2020.09.019.

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Individuals with high ADHD-traits are more vulnerable to insomnia - Newswise

Neuroscience

Spike Protein Study Gives More Evidence That COVID-19 Enters the Brain – Technology Networks

More and more evidence is coming out that people with COVID-19 are suffering from cognitive effects, such as brain fog and fatigue.

And researchers are discovering why. The SARS-CoV-2 virus, like many viruses before it, is bad news for the brain. In a study published Dec.16 in Nature Neuroscience, researchers found that the spike protein, often depicted as the red arms of the virus, can cross the blood-brain barrier in mice.

This strongly suggests that SARS-CoV-2, the cause of COVID-19, can enter the brain.

The spike protein, often called the S1 protein, dictates which cells the virus can enter. Usually, the virus does the same thing as its binding protein, said lead author William A. Banks, a professor of medicine at the University of Washington School of Medicine and a Puget Sound Veterans Affairs Healthcare System physician and researcher. Banks said binding proteins like S1 usually by themselves cause damage as they detach from the virus and cause inflammation.

"The S1 protein likely causes the brain to release cytokines and inflammatory products," he said.

In science circles, the intense inflammation caused by the COVID-19 infection is called a cytokine storm. The immune system, upon seeing the virus and its proteins, overreacts in its attempt to kill the invading virus. The infected person is left with brain fog, fatigue and other cognitive issues.

Banks and his team saw this reaction with the HIV virus and wanted to see if the same was happening with SARS CoV-2.

Banks said the S1 protein in SARS-CoV2 and the gp 120 protein in HIV-1 function similarly. They are glycoproteins - proteins that have a lot of sugars on them, hallmarks of proteins that bind to other receptors. Both these proteins function as the arms and hand for their viruses by grabbing onto other receptors. Both cross the blood-brain barrier and S1, like gp120, is likely toxic to brain tissues.

"It was like dj vu," said Banks, who has done extensive work on HIV-1, gp120, and the blood-brain barrier.

The Banks' lab studies the blood-brain barrier in Alzheimer's, obesity, diabetes, and HIV. But they put their work on hold and all 15 people in the lab started their experiments on the S1 protein in April. They enlisted long-time collaborator Jacob Raber, a professor in the departments of Behavioral Neuroscience, Neurology, and Radiation Medicine, and his teams at Oregon Health & Science University.

The study could explain many of the complications from COVID-19.

"We know that when you have the COVID infection you have trouble breathing and that's because there's infection in your lung, but an additional explanation is that the virus enters the respiratory centers of the brain and causes problems there as well," said Banks.

Raber said in their experiments transport of S1 was faster in the olfactory bulb and kidney of males than females. This observation might relate to the increased susceptibility of men to more severe COVID-19 outcomes.

As for people taking the virus lightly, Banks has a message:

"You do not want to mess with this virus," he said. "Many of the effects that the COVID virus has could be accentuated or perpetuated or even caused by virus getting in the brain and those effects could last for a very long time."

Reference: Rhea EM, Logsdon AF, Hansen KM, et al. The S1 protein of SARS-CoV-2 crosses the bloodbrain barrier in mice. Nat Neurosci. 2020. doi:10.1038/s41593-020-00771-8

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