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  • Study: 3D Video Games Help Improve Major Depressive Disorder Symptoms | High Times

    Study: 3D Video Games Help Improve Major Depressive Disorder Symptoms | High Times

    There are plenty of studies exploring how substances like cannabis and psilocybin can help treat depression, but far fewer research exploring how video games can positively treat that kind of condition. Recently in the journal Frontiers in Psychiatry, researchers from the University of Bonn in Germany found that people suffering from Major Depressive Disorder (MDD) saw a reduction in symptoms after a 3D video game (in this case, participants playing Super Mario Odyssey a game that release on Nintendo Switch in 2017). It’s the first randomized controlled study of its kind to examine the effects of a six-week video game intervention on those with depression.

    Researchers explained that people with MDD often experience “reduced affect, mood, and cognitive impairments such as memory problems,” but most treatments do not target the cognitive deficits, which is why they believed that video games could help. “Playing 3D video games has been found to improve cognitive functioning in healthy people, but it is not clear how they may affect depressed mood and motivation in people with MDD,” researchers wrote. “The aim of this study was to investigate whether a six-week video game intervention leads to improvements in depressed mood, training motivation, and visuo-spatial (working) memory functions in patients with MDD.”

    Forty-six clinically depressed people were split into three groups: 1.) the experimental “3D video gaming” group, an active control group who trained with a computer program called COGPACK (which is a cognitive remediation program), and 3.) a group that received typical treatment methods such as psychotherapy or pharmacotherapy. All participants were asked to perform a neuropsychological assessment, such as self-reporting questions.

    The reason Super Mario Odyssey was chosen was in part because of a previous study from 2015 identified benefits of 3D-based games (the study used “Super Mario World” as an example) “can promote hippocampal plasticity, which consequently led to an enhancement in hippocampus associated cognitive functions, such as visuo-spatial memory” in comparison to a 2D game (the example was Angry Birds).

    The results of the most recent study showed that there was a significant decrease in depressive symptoms. “Results indicate that after six weeks of training the 3D video gaming group showed a significant decrease in the proportion of participants with clinically significant levels of depressive symptoms by self-report and a higher mean training motivation when compared with the active control group,” researchers wrote in their conclusion. “Furthermore, results suggest significant improvements in tasks of visuo-spatial (working) memory performance during post-testing in both training groups, however, the 3D video gaming group demonstrates more selective improvements and does not perform significantly better than the other two groups.”

    As of September 2023, Super Mario Odyssey is one of the highest selling Nintendo Switch games of all time, placed in fifth place on a list of games in units. In first place is Mario Kart 8 (57.01 million units), second is Animal Crossing: New Horizons (43.38 million units), third is Super Smash Brothers Ultimate (32.44 million units), The Legend of Zelda: Breath of the Wild (31.15 million units), and finally Super Mario Odyssey (26.95 million units).

    We’ve also seen a steady increase in studies relating to treating various depression conditions with psychedelic substances. Medical cannabis studies continue to showcase the benefits on a variety of conditions. In November an Australian study reported the benefits of medical cannabis that improved patients’ quality of life, as well as reduced pain, anxiety, and depression.

    Psilocybin was found to be a promising treatment for people with depression in a September study conducted by the American Medical Association. Earlier in December, another study found that patients with bipolar II depression benefited from using psilocybin as a treatment. 

    Other studies have evaluated the effects of DMT for depression too, such as one that was conducted by a United Kingdom pharmaceutical company in January 2023. Researchers said that DMT offered “a significant antidepressant effect that was rapid and durable.”

    Ketamine is also being studied as a possibility for treating severe depression, as seen in a June 2023 research initiative. ECT has been the gold standard for treating severe depression for over 80 years,” researchers explained. “But it is also a controversial treatment because it can cause memory loss, requires anesthesia, and is associated with social stigma. This is the largest study comparing ketamine and ECT treatments for depression that has ever been done, and the only one that also measured impacts to memory.”

    There’s a lot of potential to be studied between these substances and depression, as well as many other conditions. And with the newest research putting the spotlight on 3D video games as a method of treating depression as well, it will be very interesting to see how these two separate methods of treatment continue to evolve, or even possibly overlap.

    Super Mario titles have always represented the more wholesome side of video games. Maybe all Mario games have the potential to treat depression because of this, or maybe some Super Mario games are more likely than others to offer cognitive benefits to players. While we eagerly await more studies on these topics, check out our review of Super Mario Bros. Wonder which offers a delightful journey into the strange and hilarious unknown.

    Nicole Potter

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  • Immune cells have a backup mechanism

    Immune cells have a backup mechanism

    Newswise — The enzyme TBK1 is an important component of the innate immune system that plays a critical role in the defense against viruses. Upon mutation-induced loss of TBK1 function, patients show an increased susceptibility to viral infections. Strikingly, if TBK1 is not expressed at all, this clinical effect is not seen. The mechanism behind this supposed discrepancy has now been elucidated by researchers led by Prof. Martin Schlee from the University Hospital Bonn and the Cluster of Excellence ImmunoSensation2 at the University of Bonn. The study was published in the journal Frontiers in Immunology.

    In the human body, viral particles are recognized by so called pattern recognition receptors (PRRs) situated within the cell or on the cell surface. Upon activation, a signaling cascade is initialized which ultimately results in the production and release of signaling molecules such as interferons and cytokines. These messenger molecules alert neighboring immune cells and point out the viral infection, inducing an immune reaction.

    Part of this signaling cascade is the TANK Binding Kinase 1 (TBK1). If viral particles are detected by PRRs, TBK1 is activated. TBK1 in turn activates two transcription factors which travel into the nucleus where they induce the transcription of interferon and cytokine genes.

    Susceptibility to viral infections

    Point-mutations in the TBK1 gene may induce a loss of function of TBK1. In humans, this manifests itself in clinical susceptibility to viral infections. Strikingly, this effect is not to be observed if TBK1 is not expressed and entirely lacking in the cell. “Surprisingly, a complete absence of TBK1 expression in humans is not associated with a reduced antiviral response,” says Prof. Martin Schlee of the Institute of Clinical Chemistry and Clinical Pharmacology at the University Hospital Bonn. Until now, it was unclear why a complete loss of TBK1 expression is better tolerated in terms of immunocompetence than a mutation of TBK1 affecting the kinase function.

    The Bonn researchers have now been able to provide an explanation for these previously unexplained observations. “A second enzyme that is very similar to TBK1 plays an important role in this: the IkB kinase epsilon, or IKKepsilon for short,” explains Dr. Julia Wegner, first author of the study. Just like TBK1, IKKepsilon acts downstream of PRRs and controls the expression of interferons. The two proteins are also very similar in structure, with more than 60 percent sequence homology. A novel finding is that TBK1 has a direct effect on IKKepsilon. “In myeloid cells, we could show that TBK1 regulates the expression of the related kinase IKKepsilon,” adds Dr. Wegner.

    No half measures

    TBK1 reduces the stability of IKKepsilon. This process is independent of the protein’s enzymatic function. “Accordingly, TBK1 that is nonfunctional due to point mutation is still able to destabilize IKKepsilon,” explains Prof. Gunther Hartmann, director of the Institute of Clinical Chemistry and Clinical Pharmacology and spokesperson of the ImmunoSensation2 Cluster of Excellence. “This leads to a continuous degradation of the kinase IKKepsilon in human immune cells.”

    Therefore, loss of TBK1 expression leads to an increased abundance of IKKepsilon. This mechanism ensures that an antiviral immune response can occur despite the absence of TBK1. Loss of function of TBK1 induced by point mutations, on the other hand, does not prevent destabilization and degradation of IKKepsilon, so that ultimately both factors are not available for viral defense. Increased susceptibility to viral infections is the result.

    Weapons of a virus

    In a healthy organism, increased amounts of IKKepsilon can thus compensate for the loss of TBK1. This becomes particularly important when viruses specifically seek to eliminate the body’s own defenses. Herpes simplex virus 1 (HSV-1), human immunodeficiency virus (HIV) but also severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are able to specifically induce TBK1 degradation. Also, several bacterial species are capable of causing the degradation of TBK1. “Our data clearly show that human immune cells have an important backup mechanism,” explains Dr. Wegner. “They are able to maintain an effective antiviral response even when pathogen-induced degradation of TBK1 occurs. Furthermore, the mechanism also takes effect in the case of genetic loss of TBK1.”

    Publication: Wegner Julia, Hunkler Charlotte, Ciupka Katrin, Hartmann Gunther, Schlee Martin (2023); Increased IKKepsilon protein stability ensures efficient type I interferon responses in conditions of TBK1 deficiency; Frontiers in Immunology , Vol. 14; DOI: 10.3389/fimmu.2023.1073608

    University of Bonn

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  • How nerve and vascular cells coordinate their growth

    How nerve and vascular cells coordinate their growth

    Newswise — Nerve cells need a lot of energy and oxygen. They receive both through the blood. This is why nerve tissue is usually crisscrossed by a large number of blood vessels. But what prevents neurons and vascular cells from getting in each other’s way as they grow? Researchers at the Universities of Heidelberg and Bonn, together with international partners, have identified a mechanism that takes care of this. The results have now appeared in the journal Neuron. 

    Nerve cells are extremely hungry. About one in five calories that we consume through food goes to our brain. This is because generating voltage pulses (the action potentials) and transmitting them between neurons is very energy-intensive. For this reason, nerve tissue is usually crisscrossed by numerous blood vessels. They ensure a supply of nutrients and oxygen.

    During embryonic development, a large number of vessels sprout in the brain and spinal cord, but also in the retina of the eye. Additionally, masses of neurons are formed there, which network with each other and with structures such as muscles and organs. Both processes have to be considerate of each other so as not to get in each other’s way. “We have identified a new mechanism that ensures this,” explains Prof. Dr. Carmen Ruiz de Almodóvar, member of the Cluster of Excellence ImmunoSensation2 and the Transdisciplinary Research Area Life & Health at the University of Bonn.

    The researcher moved to the Institute of Neurovascular Cell Biology at the University Hospital Bonn in early 2022. Since this spring, she has held one of the special established Schlegel Professorships, with which the university aims to attract outstanding researchers to Bonn. However, most of the research was still done at her old place of work, the European Center for Angioscience at the Medical Faculty Mannheim, which is part of the University of Heidelberg. The work was then completed at the University of Bonn. In her study, she and international partners took a close look at the formation of blood vessels in the spinal cord of mice.

    Growth pause in the spine

    “The appearance of blood vessels in the spinal cord begins in the animals about 8.5 days after fertilization,” she says. “Between days 10.5 and 12.5, however, blood vessels do not grow in all directions. This is despite the fact that large amounts of growth-promoting molecules are present in their environment during this time. Instead, during this time, numerous nerve cells – the motor neurons – migrate from their place of origin in the spinal cord to their final position. There, they then form extensions called axons that lead from the spine to the various targeting muscles.”

    This means that the motor neurons self-organize and grow at the time that blood vessels do not grow towards them. Only then after, do the vessels begin to sprout again. “The whole thing resembles a carefully choreographed dance,” explains José Ricardo Vieira. The doctoral student in Ruiz de Almodóvar’s research group did much of the work in the study. “In the course of this, each partner takes care not to get in the other’s way.”

    But how is this dance coordinated? Apparently, by the motor neurons shouting a “stop, now it’s my turn” message to the vascular cells. To do this, they use a protein that they release into their environment – semaphorin 3C (Sema3C). It diffuses to the vascular cells and docks there at a receptor called PlexinD1 – in a sense, this is the ear for which the molecular message is intended.

    Deafened vascular cells grow uncontrollably

    “When we stop the production of Sema3C in neurons in mice, blood vessels form prematurely in the region where these neurons are located,” explains Prof. Ruiz de Almodóvar. “This prevents the axons of the neurons from developing properly – they are prevented from doing so by the vessels.” The researchers achieved a similar effect when they experimentally stopped the formation of PlexinD1 in the vascular cells: Since these were now deaf to the Sema3C signal from the neurons, they did not stop growing but continued to sprout.

    The results document the importance of coordinated operation of the two processes during embryonic development. These findings could also contribute to a better understanding of certain diseases, such as retinal defects caused by strong and uncontrolled vessel growth. The use of the newly discovered mechanism may also potentially help in regenerating destroyed brain areas, for example after a spinal cord injury, in the long term.

    Participating institutions and funding:

    In addition to the University of Heidelberg and its Medical Faculty Mannheim, the University Hospital Bonn and the University of Bonn, the San Raffaele Scientific Institute in Milan, University College London, and the German Center for Neurodegenerative Diseases in Bonn were involved in the study. The work was financially supported by the German Research Foundation (DFG) and the European Research Council (ERC).

    Publication: José Ricardo Vieira et. al.: Endothelial PlexinD1 signaling instructs spinal cord vascularization and motor neuron development; Neuron; DOI: 10.1016/j.neuron.2022.12.005

    University of Bonn

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  • Gene plays important role in embryonic development

    Gene plays important role in embryonic development

    Newswise — An international study led by the medical Faculty of the University of Bonn has identified a gene that plays an important role in the development of the human embryo. If it is altered, malformations of various organ systems can result. The gene emerged very early in evolution. It also exists in zebrafish, for example, and performs a similar function there. The results have now been published in the Journal of Medical Genetics.

    The researchers tracked down the gene when they studied two individuals with congenital malformations. “It was a man and his niece,” explains Dr. Gabriel Dworschak. “Both had malformed kidneys, urinary tract and esophagus, and the man also had a malformed right arm and heart.”

    The physician at the University Children’s Hospital in Bonn conducts research on rare genetic diseases at the Institutes of Anatomy and Human Genetics. When the team looked at the genetic makeup of the family members, they came across an anomaly: A gene called SHROOM4 was altered in affected individuals compared to healthy individuals.

    SHROOM4 was already familiar from another context: It was known to play a key role in brain function. Mutations can result in intellectual impairment, epileptic seizures and behavioral abnormalities. “Our findings indicated though, that it may play a broader role in embryonic organ development,” Dworschak explains.

    The team from Bonn searched internationally for other cases in which abnormalities in the SHROOM4 gene had also been found – and succeeded: “Together with our cooperation partners, this led us to four more affected individuals from three families,” says Prof. Dr. Heiko Reutter, who has since moved from the University Hospital Bonn to the University of Erlangen-Nuremberg. “All of them had the SHROOM4 gene altered, but not always in the same way.”

    Zebrafish also needs SHROOM4

    However, this did not necessarily clarify whether SHROOM4 variants were actually responsible for the malformations. But there is an animal that has a very similar gene: the zebrafish. It serves as a model organism in many genetic studies today – and not only because it is easy to keep in a species-appropriate manner and to reproduce quickly: The skin of its larvae is almost transparent. This makes it easy to observe the animals’ embryonic development under the light microscope. “Here at the University Hospital, we have the advantage that the research group led by Prof. Dr. Benjamin Odermatt from the Institute of Neuroanatomy works a lot with zebrafish,” stresses Dr. Caroline Kolvenbach, who was also involved in the study of SHROOM4. “This expertise came in handy in our study.”

    The researchers almost completely inactivated SHROOM4 in the larvae. The animals then showed malformations similar to those seen in the patients. If, on the other hand, larvae with SHROOM4 switched off were injected with the intact human genetic material, they developed almost normally. “This shows first that they absolutely need a functional SHROOM4 for healthy development; and second, that the human gene can still take over the function of the fish gene,” Dworschak emphasizes.

    The team now wants to find out which part the gene plays in embryonic development. “We assume that it is needed for very basic processes in the cell,” says Dworschak. “It’s hard to explain otherwise why changes in the same gene cause such a variety of symptoms.”

    Small piece in the mosaic of an extremely complex picture

    How a mouse, a dog or a human being develops from a fertilized ovum is still not fully understood. This is because the ovum has the ability to form any type of tissue in the organism, whether it is bone, skin, muscle or the brain. Its daughter cells are genetically identical to it; so in principle they should be able to do the same. But at a very early stage, certain programs are activated in their cells that irrevocably determine their developmental fate.

    This process must be coordinated down to the finest detail. Because only then it is ensured that the eyes form in the appropriate spot on the face, while other cells very close by differentiate into the nasal cartilage. Surprisingly, however, there is no conductor wielding the baton. It is as if a Lego spaceship were assembling itself – only infinitely more complicated. “Our study is a small piece of the mosaic to this picture, which is still largely incomplete,” Dworschak says.

    Participating institutions and funding:

    In addition to the University of Bonn and the University Hospital Bonn, the study involved Children’s Mercy Hospital (USA), the Medical University of Silesia (Poland), the University of Zielona Góra (Poland), the University of Southern Denmark (Denmark), the University of Cologne, the University of Heidelberg, the University of Erlangen-Nuremberg, Medeor Hospital Lodz (Poland), and Goethe University Frankfurt. The work was supported by the German Research Foundation (DFG), the BONFOR program of the University Hospital Bonn, the Else Kröner-Fresenius Foundation, the Luise and Horst Köhler Foundation, and the National Institutes of Health (USA).

    Publication: Caroline M. Kolvenbach et al.: X-linked variations in SHROOM4 are implicated in congenital anomalies of the urinary tract, the anorectal, the cardiovascular, and the central nervous system; Journal of Medical Genetics; DOI: 10.1136/jmg-2022-108738

    University of Bonn

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