Publisher Health

Immigrants imprisoned in immigration facilities across the country face health conditions and often have chronic illnesses that would expose them to greater risk with COVID-19, a new University of California, Davis, study suggests.
“The research is clear: immigration detention is not only unnecessary for facilitating a just immigration system, but also causes extensive harm to detained people, perhaps especially to those facing chronic health conditions,” said the study’s lead author, Caitlin Patler, professor of sociology. “This is particularly alarming in the context of the COVID-19 pandemic. The government must act quickly to permanently reduce reliance on this overly punitive and systematically unjust practice.”
The study was published earlier this month in the Journal of Immigrant and Minority Health.
“Even beyond the context of the COVID-19 pandemic, immigration detention harms people’s health by disrupting the continuity of their medical care,” added the study’s co-author, Altaf Saadi, a neurologist at Massachusetts General Hospital and Harvard Medical School. “The vast majority of people have a stable place to stay and would be able to receive better health care if not detained.”
The report cites the May 2020 death of Carlos Ernesto Escobar Mejia, the first person in ICE custody to die from COVID-19. “Health and legal professional have raised alarm that many detainees may be similarly imperiled by COVID-19 infection [in detention],” authors wrote.
Researchers looked at health data of more than 500 people detained in 2013-14 by U.S. Immigration and Customs Enforcement, or ICE, at hundreds of facilities across California. This data is the only publicly available health information for ICE detainees. Researchers said the detainees’ health conditions are likely similar to a current population.
Of the individuals detained in 2013-14, at least 42 percent had at least one chronic condition, combined with other health issues, and additionally face disruption in care upon entering the facility.
The vast majority, or 95.6 percent, reported having access to stable housing in the country.
“Even one chronic condition can increase risk for severe consequences from COVID-19,” the authors said. One study of COVID-19 patients, they said, revealed that more than 80 percent had more than one underlying medical condition. These risks are heightened if health conditions are not adequately managed and there is disruption of pre-existing health care because they are incarcerated, researchers said.
.” ..Decision-makers must consider every available option to mandate release from the congregate setting of detention centers in which social distancing is almost impossible even under ideal conditions,” researchers concluded in their study. “Release can be easily facilitated through existing Alternatives to Detention (ATD) programs in which individuals can be released to their families and communities as they continue with their immigration legal proceedings.”
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Materials provided by University of California – Davis. Original written by Karen Nikos-Rose. Note: Content may be edited for style and length.

A cytokine “hurricane” centered in the lungs drives respiratory symptoms in patients with severe COVID-19, a new study by immunologists at Columbia University Vagelos College of Physicians and Surgeons suggests.
Two cytokines, CCL2 and CCL3, appear critical in luring immune cells, called monocytes, from the bloodstream into the lungs, where the cells launch an overaggressive attempt to clear the virus.
Targeting these specific cytokines with inhibitors may calm the immune reaction and prevent lung tissue damage. Currently, one drug that blocks immune responses to CCL2 is being studied in clinical trials of patients with severe COVID-19.
Survivors of severe COVID-19, the study also found, had a greater abundance of antiviral T cells in their lungs than patients who died, suggesting these T cells may be critical in helping patients control the virus and preventing a runaway immune response.
The study, published online March 12 in the journal Immunity, is one of the first to examine the immune response as it unfolds in real time inside the lungs and the bloodstream in patients who are hospitalized with severe COVID-19.
Treatments for Severe COVID-19 Needed
In patients with severe COVID-19, the lungs are damaged, and patients need supplemental oxygen. The risk of mortality is over 40%.

Researchers at Massachusetts General Hospital (MGH) have uncovered new clues that add to the growing understanding of how female mammals, including humans, “silence” one X chromosome. Their new study, published in Molecular Cell, demonstrates how certain proteins alter the “architecture” of the X chromosome, which contributes to its inactivation. Better understanding of X chromosome inactivation could help scientists figure out how to reverse the process, potentially leading to cures for devastating genetic disorders.
Female mammals have two copies of the X chromosome in all of their cells. Each X chromosome contains many genes, but only one of the pair can be active; if both X chromosomes expressed genes, the cell couldn’t survive. To prevent both X chromosomes from being active, female mammals have a mechanism that inactivates one of them during development. X chromosome inactivation is orchestrated by a noncoding form of RNA called Xist, which silences genes by spreading across the chromosome, recruiting other proteins (such as Polycomb repressive complexes) to complete the task.
Jeannie Lee, MD, PhD, an investigator in the Department of Molecular Biology at MGH and the paper’s senior author, has led pioneering research on X chromosome inactivation. She believes that understanding the phenomenon could lead to cures for congenital diseases known as X-linked disorders, which are caused by mutations in genes on the active X chromosome. “Our goal is to reactivate the inactive X chromosome, which carries a good copy of the gene,” says Lee. Doing so could have profound benefits for people with conditions such as Rett syndrome, a disorder brought on by a mutation in a gene called MECP2 that almost always occurs in girls and causes severe problems with language, learning, coordination and other brain functions. In theory, reactivating the X chromosome could cure Rett syndrome and other X-linked disorders.
In this study, Lee and Andrea Kriz, a PhD student and first author of the paper, were interested in understanding the role of clusters of proteins called cohesins in X inactivation. Cohesins are known to play a critical role in gene expression. Imagine a chromosome as a long piece of string with genes and their regulatory sequences being far apart, says Lee. For the gene to be turned “on” and do its job, such as producing a specific protein, it has to come in contact with its distant regulator. Chromosomes allow this to happen by forming a small loop that brings together the gene and regulator. Ring-shaped cohesins help these loops form and stabilize. When the gene’s work is done and it’s time to turn off, a scissor-like protein called WAPL snips it, causing the gene to disconnect from its regulator. An active chromosome has many of these loops, which are continually forming and dissociating (or separating).
These small loops, which are essential for gene expression, are relatively suppressed on an inactivated X chromosome. One reason, as Lee and her colleagues have already shown, is that Xist “evicts” most cohesins from the inactive X chromosome and that this cohesin depletion may be necessary to reorganize the shape and structure of the chromosome for silencing.
In the current study, Lee and Kriz used embryonic stem cells from female mice to find out what happens when cohesin or WAPL levels are manipulated during X chromosome inactivation by using protein-degradation technology. “We found that if cohesin levels build up too high, the X chromosome cannot inactivate properly,” says Lee. Normally, retaining cohesins (which are normally supposed to be evicted) prevented the X chromosome from folding into an inactive shape and gene silencing was affected. “You need a fine balance between eviction and retention of cohesins during X chromosome inactivation,” says Lee.
Next, the authors asked what happens when cohesin is manipulated in an active X chromosome. The short answer: It takes on some peculiar qualities of an inactivated X chromosome. First, when there is insufficient cohesin, the active X develops structures called “superloops” that are usually only seen on the inactive X. Second, when there is too much cohesin, the active X develops “megadomains,” which Lee calls two “big blobs,” and are also ordinarily unique to the inactive X. “The fact that we can confer some features of the inactive X chromosome onto the active X chromosome just by toggling cohesin levels is intriguing,” says Lee. She and her colleagues are trying to understand how and why that happens.
These findings suggests that shape and structure of the X chromosome play a vital role in allowing Xist to spread from one side to the other and achieve inactivation. “The more we learn about what’s important for silencing the X chromosome,” says Lee, “the more likely we’ll be to find ways to reactivate it and to treat conditions like Rett syndrome.”
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A home-based parenting programme to prevent childhood behaviour problems, which very unusually focuses on children when they are still toddlers and, in some cases, just 12 months old, has proven highly successful during its first public health trial.
The six-session programme involves providing carefully-prepared feedback to parents about how they can build on positive moments when playing and engaging with their child using video clips of everyday interactions, which are filmed by a health professional while visiting their home.
It was trialled with 300 families of children who had shown early signs of behaviour problems. Half of the families received the programme alongside routine healthcare support, while the other half received routine support alone. When assessed five months later, the children whose families had access to the video-feedback approach displayed significantly reduced behavioural problems compared with those whose families had not.
All of the children were aged just one or two: far younger than the age at which interventions for behaviour problems are normally available. The results suggest that providing tailored support for parents at this earlier stage, if their children show early signs of challenging behaviour — such as very frequent or intense tantrums, or aggressive behaviour — would significantly reduce the chances of those problems worsening.
Children with enduring behaviour problems often experience many other difficulties as they grow up: with physical and mental health, education, and relationships. Behaviour problems currently affect 5% to 10% of all children.
The trial — one of the first ever ‘real-world’ tests of an intervention for challenging behaviours in children who are so young — was carried out by health professionals at six NHS Trusts in England and funded by the National Institute for Health Research. It was part of a wider project called ‘Healthy Start, Happy Start’, which is testing the video-based approach, led by academics at the University of Cambridge and Imperial College London.

Researchers at the University of Gothenburg, Sweden, have now presented results that may change our basic view of how type 2 diabetes occurs. Their study indicates that free fatty acids (FFAs) in the blood trigger insulin release even at a normal blood-sugar level, without an overt uncompensated insulin resistance in fat cells. What is more, the researchers demonstrate the connection with obesity: the amount of FFAs largely depends on how many extra kilos of adipose tissue a person carries, but also on how the body adapt to the increased adiposity.
Worldwide, extensive research is underway to clarify exactly what happens in the body as type 2 diabetes progresses, and why obesity is such a huge risk factor for the disease. For almost 50 years, diabetes researchers have been discussing their version of the chicken-or-egg question: Which comes first — insulin resistance or elevated insulin levels? The dominant hypothesis has long been that the pancreas steps up its insulin production because the cells have already become insulin-resistant, and blood sugar then rises. However, the results now published in the journal EBioMedicine support the opposing idea: that it is the insulin that increases first.
Detailed investigations
The study indicates that high FFA levels in the blood after the overnight fast raise insulin production in the morning. FFAs have long been part of the main research equation for type 2 diabetes, but it is now proposed that they also have another role: in progression of the disease.
For the study, researchers compared metabolism in adipose (fat-storing) tissue among 27 carefully selected research subjects (nine of normal weight, nine with obesity and normal blood sugar, and nine with both obesity and progressed type 2 diabetes). For several days, they underwent extensive examinations in which they had samples taken under varying conditions. The researchers analyzed metabolism and gene expression in the participants’ subcutaneous fat, and the levels of blood sugar, insulin, and FFAs in their blood.
FFAs seem to trigger insulin production
The people with obesity but not diabetes proved to have the same, normal blood-sugar levels as the healthy individuals of normal weight.

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“Interestingly, the nondiabetics with obesity had elevated levels of both free fatty acids and insulin in their blood, and those levels were similar to or higher than the levels we were able to measure in blood from the participants with both obesity and type 2 diabetes,” says Emanuel Fryk, resident doctor specializing in general medicine and doctoral student at Sahlgrenska Academy, University of Gothenburg, who is one of the study’s first authors.
In collaboration with researchers at Uppsala University, he observed the same pattern in a population study based on blood samples taken from 500 people after an overnight fast.
“The fact that we saw a link between free fatty acids and insulin there too suggests that the fatty acids are connected with the insulin release, and contribute to increased insulin production on an empty stomach, when blood sugar hasn’t risen,” says Fryk, who nevertheless points out that the finding needs to be confirmed with more research.
Ongoing research
Free fatty acids are found naturally in the bloodstream and, like glycerol, are a product of the body’s fat metabolism. In the subjects, the amount of glycerol released proved to be broadly the same per kilo of body fat, regardless of whether they were of normal weight, had obesity alone, or also had type 2 diabetes.

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“Our hypothesis is that the free fatty acids increase in the blood because the adipose tissue can’t store the excess energy anymore. We believe, in that case, it could be an early sign of incipient type 2 diabetes. If our findings are confirmed when other research methods are used, there may be a chance that some specific fatty acids could be developed into biomarkers. But that’s a long way off,” Fryk says.
Lifestyle crucial
Diabetes is one of the most common diseases, with an estimated 500,000 people affected in Sweden. There are also a large number of undetected cases, since many with type 2 diabetes are not yet aware they are ill. Diabetics are at an increased risk for a number of serious conditions, such as cardiovascular disease (which may result in heart attacks and strokes).
“There are many factors that contribute to the progression of type 2 diabetes, but it’s our lifestyle that has, in absolute terms, the largest impact for most people. Our study provides another argument that the most important thing you can do to slow diabetes progression is to change your life style early in the progression of the disease, before blood glucose is elevated, Fryk says.

Researchers at the University of Illinois Chicago have discovered that heparanase, HPSE, a poorly understood protein, is a key regulator of cells’ innate defense mechanisms.
Innate defense responses are programmed cellular mechanisms that are triggered by various danger signals, which have been conserved in many species throughout evolution. These systems can be set into action by pathogens, such as viruses, bacteria and parasites, as well as by environmental toxins and dysfunctional cells that can accumulate in the body over time. A more thorough understanding of the commonalities and connections between these processes has the potential to generate multi-target therapy against a variety of human diseases.
In a multi-institution team led by Alex Agelidis, a UIC MD/Ph.D. dual degree medical student, and Dr. Deepak Shukla, the UIC Marion Schenk Professor of Ophthalmology and UIC professor of microbiology and immunology at the College of Medicine, researchers used a systems approach to track shifts in important cellular building blocks in cells and mice genetically engineered to lack HPSE.
In this collaborative multidisciplinary study, Agelidis and coauthors show for the first time that HPSE acts as a cellular crossroads between antiviral immunity, proliferative signals and cell death.
“HPSE has been long known to drive late-stage inflammatory diseases yet it was once thought that this was primarily due to enzymatic activity of the protein breaking down heparan sulfate, a sugar molecule present in chains on the surface of virtually all cells,” Agelidis said.
While a major focus of the study was on identifying mechanisms of pathogenesis of herpes simplex virus (HSV-1), their work has broad implications for the treatment of diseases involving dysregulation of HPSE, including cancer, atherosclerosis and autoimmune disorders.

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Materials provided by University of Illinois at Chicago. Note: Content may be edited for style and length.

When SARS-CoV-2, the virus that causes COVID-19, infects a human cell, it quickly begins to replicate by seizing the cell’s existing metabolic machinery. The infected cells churn out thousands of viral genomes and proteins while halting the production of their own resources. Researchers from Brigham and Women’s Hospital, Massachusetts General Hospital (MGH), and the Broad Institute, studying cultured cells shortly after infecting them with the virus, now have more insight into the metabolic pathways co-opted by the virus. The findings, published in Nature Communications, highlight the potential therapeutic benefit of drugs such as methotrexate, which inhibit folate and one-carbon metabolic pathways appropriated by the virus.
“One of the things we’re lacking in this pandemic is a pill that can be taken orally, as a prophylactic agent, before someone is hospitalized or even before they’re infected,” said corresponding author Benjamin Gewurz, MD, PhD, of the Division of Infectious Diseases. “Monoclonal antibodies have a lot of promise but need to be given intravenously. Blocking the metabolism pathways that viruses rely on to replicate could be a new strategy for treating patients at an early timepoint.”
To identify which metabolic pathways to target, the researchers obtained samples of the virus and cultivated them in a highly protected facility called a BSL-3 laboratory, located at the Broad Institute. They then paired up with the laboratory of co-senior author Vamsi Mootha, MD, of MGH, to apply mass spectrometry approaches to identify the resources being consumed and produced by healthy cells and infected cells. They studied the infected cells at an “eclipse point,” eight hours after infection, when the virus has begun manufacturing its RNA and proteins but has not yet exerted a serious effect on host cell growth and survival.
In analyzing the amino acids and thousands of chemical metabolites produced by the cells, the researchers observed that infected cells had depleted stores of glucose and folate. They demonstrated that the SARS-CoV-2 virus diverts building blocks from glucose production to the assembly of purine bases, which are necessary for creating large amounts of viral RNA. Additionally, they found that the 1-carbon pathway used to metabolize folate was hyperactive, thus supplying the virus with more carbon groups for making bases for DNA and RNA.
Drugs that inhibit folate metabolism, like methotrexate, are often used to treat autoimmune conditions like arthritis and could be therapeutic candidates for COVID-19. Methotrexate is currently being assessed as a treatment for the inflammation that accompanies more advanced COVID-19 infections, but the researchers suggest that it could also be beneficial early on. Their study also found that it could offer a synergistic effect when administered with the anti-viral drug remdesivir. Methotrexate’s immune-suppressing properties could make its proper administration as a prophylactic challenging, however. Researchers would need to determine how to maximize the drug’s antiviral effects without significantly compromising a patient’s natural immune response.
Still, Gewurz points out that oral antivirals are an important addition to an arsenal of therapies for COVID-19, serving both as an immediate treatment for infection as well as a defense against new variants and other coronaviruses.
“We’re hoping that, ultimately, we can find a way of preventing viruses from using cells’ metabolism pathways to replicate themselves because that could limit the ability of viruses to evolve resistance,” Gewurz said. “We’re starting to see new viral variants, and we’re hoping that we can stay ahead of that — treating patients before the virus has the chance to make copies of itself that could become resistant to antibodies.”
This work was supported by the National Institutes of Health (R01 AI137337, R01 CA228700, R35 GM122455), EMBO (ALTF 486-2018), a Burroughs Wellcome Career Award in Medical Sciences, the Howard Hughes Medical Institute and MassCPR. Gewurz and Mootha are listed as inventors on a patent application filed by the Broad Institute based on results from this manuscript.
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A new concept of on-demand drug delivery system has emerged in which the drugs are automatically released from in vivo medical devices simply by shining light on the skin.
A research team led by Professor Sei Kwang Hahn of the Department of Materials Science and Engineering and Professor Kilwon Cho of the Department of Chemical Engineering at POSTECH have together developed an on-demand drug delivery system (DDS) using an organic photovoltaic cell coated with upconversion nanoparticles. This newly developed DDS allows nanoparticles to convert skin-penetrating near-infrared (NIR) light into visible light so that drug release can be controlled in medical devices installed in the body. These research findings were published in Nano Energy on March 1, 2021.
For patients who need periodic drug injections as in the case of diabetes, DDSs that automatically administer drugs in lieu of repetitive shots are being researched and developed. However, its size and shape have been restricted due to limitations in power supply for operating such a device.
The research team found the answer in solar power. Upconversion nanoparticles were used for the photovoltaic device to induce photovoltaic power generation with NIR light that can penetrate the skin. An organic photovoltaic cell coated with a core-shell structured upconversion nanoparticles was designed to operate a drug delivery system made of a mechanical and electronic system by generating an electric current upon irradiation of NIR light. When electricity is applied in this manner, the thin gold film sealing the drug reservoir melts and the drug is released.
“The combination of a flexible photovoltaic cell and a drug delivery system enables on-demand drug release using light,” explained Professor Sei Kwang Hahn. “The drug delivery system is activated using near-infrared light that is harmless to the human body and is highly skin-penetrating.”
He added, “Since this enables nimble control of drug release of medical devices inserted into the body by using near-infrared light, it is highly anticipated to contribute to the development of phototherapy technology using implantable medical devices.”

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Materials provided by Pohang University of Science & Technology (POSTECH). Note: Content may be edited for style and length.

An RCSI study conducted in Beaumont Hospital in Dublin has found that surgery, rather than antibiotics-only, should remain as the mainstay of treatment for acute uncomplicated appendicitis.
Published in the Annals of Surgery and led by researchers from the RCSI University of Medicine and Health Sciences, the study entitled the COMMA trial (Conservative versus Open Management of Acute uncomplicated Appendicitis) examined the efficacy and quality of life associated with antibiotic-only treatment of acute uncomplicated appendicitis versus surgical intervention. The results revealed that antibiotic-only treatment resulted in high recurrence rates and an inferior quality of life for patients.
Acute uncomplicated appendicitis is a commonly encountered acute surgical condition. Traditional management of the condition has involved surgery to remove the appendix (appendectomy). Antibiotic-only treatment has emerged as a potential alternative option that could offer benefits to patients and hospitals, such as a faster recovery, less scaring, less pain, a better quality of life for patients and reduced demand on operating theatres. There has been a reluctance to adopt antibiotic-only treatment due to previous research that has shown wide variability in failure rates and a lack of evidence regarding the impact on quality of life for patients.
In this research, 186 patients with radiological evidence of acute, uncomplicated appendicitis were randomised to two groups. One group received antibiotic-only treatment and patients in the other group were treated with surgery. Patients in the surgery group underwent a laparoscopic appendectomy. In those treated with antibiotics-only, intravenous (IV) antibiotics were administered until there was an improvement in a patient’s signs and symptoms and this was followed by five days of oral antibiotics.
In the weeks and months following treatment, patients were followed up with questionnaires including a quality of life questionnaire at 1 week, 1 month, 3 months and 12 months. At these points, the patient’s pain score, need for additional sick leave, surgical site infections and the development of recurrent appendicitis were recorded.
The results from the antibiotic-only group demonstrated that 23 patients (25%) experienced a recurrence of acute appendicitis within one year. In the quality of life questionnaires, it was found that patients in the surgery group experienced a significantly better quality of life score compared with the antibiotic-only group.
Professor Arnold Hill, Head of School of Medicine and Professor of Surgery, RCSI, said: ‘Antibiotic-only treatment of acute uncomplicated appendicitis has been proposed as an alternative less-invasive treatment option for patients. The COMMA Trial set out to establish if antibiotic-only treatment could replace surgery in some cases, which could offer many benefits for patients and hospitals alike. The results indicate that the treatment protocols should not change. Surgery will deliver the best outcomes for patients in terms of quality of life and recurrence and therefore should remain as the mainstay of treatment for acute uncomplicated appendicitis.’
 
The study was carried out by researchers from RCSI and Beaumont Hospital Dublin. The research was supported by RCSI.

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Researchers uncovered for the first time what happens in animals’ brains when they learn from subconscious, visual stimuli. In time, this knowledge can lead to new treatments for a number of conditions. The study, a collaboration between KU Leuven, Massachusetts General Hospital, and Harvard was published in Neuron.
An experienced birdwatcher recognises many more details in a bird’s plumage than the ordinary person. Thanks to extensive training, he or she can identify specific features in the plumage. This learning process is not only dependent on conscious processes. Previous research has shown that when people are rewarded during the presentation of visual stimuli that are not consciously perceivable, they can still perceive these stimuli afterwards.
Although this is a known phenomenon, researchers were unsure as to how exactly this unconscious perceptual learning comes about. To find out, Professor Wim Vanduffel and colleagues studied the brains of two rhesus monkeys before and after they were exposed to subconscious visual stimuli.
Dopamine
The researchers activated part of the reward system at the base of the brain stem, the ventral tegmental area. This includes cells that produce dopamine, a molecule that is also released when you receive a reward. “Dopamine is a crucial messenger molecule of our motor and reward systems, and is extremely important for learning and enjoyment,” says Vanduffel. Activating the ventral tegmental area released dopamine, among other things. “By stimulating the brain area directly, we can causally link the activity in that area to perception or complex cognitive behaviour,” explains Vanduffel.
While the brain area was activated, the monkeys were shown virtually invisible images of human faces and bodies. Because the images were very blurry and the monkeys had to perform a very different and difficult task at the same time, they could not consciously perceive these images. The same process was followed during the control tests, but the brain was not stimulated.

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When the monkeys received subconscious visual stimuli while the ventral tegmental area was stimulated, they knew details about those images afterwards. For example, they knew whether the bodies shown were turned to the left or to the right. This was not the case when there had been no brain stimulation.
“Thanks to this experiment, we can demonstrate for the first time a direct causal relationship between this brain region and, as a result, also the likely link between dopamine and the subconscious learning of complex visual stimuli.”
The parts in the darker colour regulate, among others, the production of dopamine. Disturbances in this region can lead to Parkinson’s disease and other conditions. | © Shutterstock
The researchers also made a brain scan of the animals before and after the test. “We can see the blood flow in the brain, which gives an indication of which neurons are active. The more blood flow, the more activity,” explains Vanduffel. The scans showed that the task caused activity in the visual cortex of the brain and in areas important for memory. “With this data, we can zoom in to find out what is happening exactly at a neuronal level in these brain areas, in future experiments.”
“Since Freud’s insights in the 20th century, the scientific community has been wondering how subconscious sensations can affect us. Thanks to the present awareness that there is a strong resemblance between humans and monkeys, and new and advanced technologies, we can finally map such processes physiologically.”
Parkinson’s disease

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Disturbances in the dopaminergic system can lead to numerous psychiatric and motor disorders, such as depression, addiction and Parkinson’s disease. A better understanding of how this system works, in various forms of learning, is therefore crucial to developing targeted therapies for these conditions.
“Parkinson’s is a motor disorder and is caused by dopamine-producing neurons dying off. However, current dopamine treatments may produce side effects because they also trigger the entire reward system, which not only reduces motor symptoms but can also lead to addictive behaviour.” Fundamental research into the functioning of these brain areas will eventually lead to more targeted treatments with fewer side effects.
Plasticity
This insight is also useful in situations such as trauma, ageing or oncological problems where an increase in brain plasticity, i.e. the ability to change, could be very useful. “By stimulating areas of the brain that produce dopamine, we could, for example, enable people to regain their speech more quickly or improve their motor skills after an accident or illness. This could even be done through medication, although we are still a long way from that,” explains Vanduffel.
Insights about our brain and the conditions under which we and other primates visually shape our world are therefore crucial, because, as Vanduffel concludes: “you have to know how a car’s engine works before you can fix a problem with it.”

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Materials provided by KU Leuven. Original written by Elisa Nelissen. Note: Content may be edited for style and length.