Researchers answer decades-old question about protein found in Alzheimer’s brain plaques

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Alzheimer’s-affected brains are riddled with amyloid plaques, protein aggregates consisting mainly of amyloid-β. However, amyloid-β is a fragment produced from a precursor protein whose normal function has remained enigmatic for decades. A team of scientists at VIB and KU Leuven led by professors Joris de Wit and Bart De Strooper has now discovered that this amyloid precursor protein modulates neuronal signal transmission by binding to a specific receptor. Modulating this receptor could potentially help treat Alzheimer’s or other brain diseases. The results are published in Science.

More than 30 years have passed since the was first identified. In the late 1980s, several research teams around the globe traced the fragment found in amyloid plaques back to a gene located on chromosome 21. The gene encodes a longer protein that is cleaved into several fragments, one of which ends up in .

Decades of research have focused on the cleavage process that leads to the formation of the amyloid-β fragment and its subsequent aggregation, in the hope of identifying new therapeutic avenues for Alzheimer’s. Meanwhile, an important question remained unanswered: What does the rest of the amyloid precursor protein actually do?

In search of a binding partner

To answer this question, Dr. Heather Rice, a postdoctoral researcher in the labs of Joris de Wit and Bart De Strooper at the VIB-KU Leuven Center for Brain & Disease Research, set out to identify the nerve cell receptor that interacts with the amyloid precursor protein.

“We knew that the amyloid precursor protein exerts its role through the part of the protein that is released outside of the cell. To understand its function, we needed to look for binding partners located on the cell surface,” explains Rice.

The researchers identified a receptor present at the synapse, the structure where two different neurons connect to pass on signals. “We found that the secreted part of the amyloid precursor protein interacts with a receptor called GABABR1a, and that this in turn suppressed neuronal communication at the synapse,” says Rice.

Modulating signal transmission

“Although mutations in the amyloid precursor protein in familial cases of Alzheimer’s disease all affect the production of amyloid-β, we don’t really know whether other aspects of the protein’s function contribute to Alzheimer’s as well,” says Bart De Strooper. He believes that the new findings add a fresh perspective to previous studies on the amyloid precursor protein and Alzheimer’s disease. “The newly identified role of the amyloid protein may underlie the neuronal network abnormalities we see in mouse models of Alzheimer’s disease and preceding clinical onset in human patients. It is exciting to consider that a therapy targeting this receptor might attenuate these abnormalities in people with Alzheimer’s.”

De Wit adds that the clinical implications may reach much further than just Alzheimer’s: “Interestingly, GABABR signaling has been implicated in a diverse range of neurological and psychiatric disorders, including epilepsy, depression, addiction and schizophrenia. Now that we know how the secreted part of the modulates neuronal signaling through the GABAB receptor, we could think of new ways to develop drugs that can restore this type of neuronal signaling in other clinical contexts.”

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Researchers map previously unknown disease in children

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Two children from Europe and one from Canada, aged four, six and 10, suffer from a previously unknown disease that causes epileptic seizures, loss of magnesium and reduced intelligence. There is currently no way to treat or alleviate their symptoms.

But researchers in an international consortium have now discovered the cause of their illness. Professor Bente Vilsen and her research group at the Department of Biomedicine at Aarhus University, Denmark, are part of the consortium, which also includes researchers from universities in Germany, England, Austria, the Netherlands and Canada. The research results have been published in the American Journal of Human Genetics.

Using a , the researchers have discovered that the disease is caused by a newly occurring mutation in one of the sodium-potassium pump’s four forms, known as Alpha-1. Even though the children have exactly the same three symptoms, they do not have the same , as the amino acids in the pump protein which are genetically altered are different, explains Bente Vilsen.

“It turns out that the form of sodium-potassium pump that mutates is found in both the kidneys and the brain. The mutation leads to the kidneys, which normally absorb magnesium, instead secreting the substance in the urine; however, it is not the loss of magnesium that triggers the epileptic seizures. The convulsions occur because the sodium-potassium pump is also extremely important for the brain’s functions, meaning that giving extra magnesium supplements won’t prevent the seizures,” says Bente Vilsen.

She adds that the third frightening sign of the disease, , should probably be attributed to a lack of oxygen to the brain during the seizures.

Jens Christian Skou received the Nobel Prize in Chemistry in 1997 for discovering these molecular pumps, which are mutated in all three children. This knowledge is important, because understanding the role of the sodium-potassium pump is the first step toward developing effective treatment methods. The research group is now working toward this goal, even though the disease is rare.

“But three cases have turned up in two different places in Europe and in Canada, and they’re not likely to be the only ones,” says Bente Vilsen. She explains that the new knowledge about the disease will probably mean that medical doctors will in future be more aware that loss of magnesium in combination with epilepsy may be caused by genetic defects in the sodium-potassium pump.

“I believe that we will find many more children with the disease, and that this is a good example of why international research cooperation is absolutely necessary—there are simply too few cases of the disease for a single country to carry out the research alone,” says Bente Vilsen.

She points out that in future, it will be possible to replace sick genes with healthy ones, and that it is therefore important to know precisely which gene is affected by a mutation. She also points out that the understanding of the disease mechanisms causing rare diseases often lead to better treatment of patients with related but far more commonly occurring diseases.

Jens Chr. Skou’s sodium-potassium pump is best known as the membrane pump that is needed for the normal functioning of nerve cells, kidney cells and most of the body’s other cells.

The pump works like a battery, separating sodium and potassium on either side of the membrane. This creates an electrical current across the cell membrane that drives many other processes such as, e.g., electric conduction along the nerve cells and the absorption of magnesium and a range of nutrients from the urine into the kidney cells, so that they are not normally lost in the urine.

Jens Christian Skou, who died in early summer at the age of 99, originally had the idea that mutations in the sodium-potassium pump would be incompatible with life. But it has since been found that serious, non-fatal diseases can originate from genetic defects in the sodium-potassium pump—exactly the case with the disease afflicting the three children.

This is due to two factors. First, there are several variants of the sodium-potassium pump in different body tissues which are able to supplement each other if one of the forms does not work. And, secondly, humans have genetic material from both parents, so even in the kidneys, which in contrast to the brain contain only one variant of the (Alpha-1), not all of the sodium-potassium pumps will be defective, but only those derived from one of the two parents.

Therefore, in both the brain and kidneys, there will be a reduced number of functioning sodium-potassium pumps, but not a total absence of pumps—because if this was the case, the children would have died before birth, as predicted by Jens Christian Skou.

The patients were discovered by medical doctors working in clinical practice. Bente Vilsen’s group contributed their expertise in examining sick sodium-potassium pumps by inserting the diseased gene in cultured cells that originally come from monkey kidneys, making it possible to measure their pump function in the laboratory. As it turned out, the three mutations each in their own way caused the pump to be unable to transport sodium and potassium.

There is a long way to go before the benefit the patients, as the discovery is still basic research. However, Bente Vilsen explains that Postdoc Rikke Holm from her research group recently discovered how it was possible to use an additional mutation—a so-called ‘rescue’ mutation—to nullify the effects of the disease mutations on the pump’s binding of sodium.

“This provides an insight into the molecular mechanism that we in the research group are working to use to improve the pump’s transport activities, meaning that we can possibly one day develop a drug with a similar rescue effect. In any event, that’s our hope. The fact is that it’s basic research that generates the knowledge that forms the basis for the development of the vast majority of drugs and forms of treatment,” says Vilsen.

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New app gives throat cancer patients their voice back

Vlastimil Gular’s life took an unwelcome turn a year ago: minor surgery on his vocal cords revealed throat cancer, which led to the loss of his larynx and with it, his voice

Vlastimil Gular’s life took an unwelcome turn a year ago: minor surgery on his vocal cords revealed throat cancer, which led to the loss of his larynx and with it, his voice.

But the 51-year-old father of four is still chatting away using his own voice rather than the tinny timbre of a robot, thanks to an innovative app developed by two Czech universities.

“I find this very useful,” Gular told AFP, using the app to type in what he wanted to say, in his own voice, via a mobile phone.

“I’m not very good at using the voice prosthesis,” he added, pointing at the hole the size of a large coin in his throat.

This small silicon device implanted in the throat allows people to speak by pressing the hole with their fingers to regulate airflow through the prosthesis and so create sound.

But Gular prefers the new hi-tech voice app.

It was developed for patients set to lose their voice due to a laryngectomy, or removal of the larynx, a typical procedure for advanced stages of throat cancer.

The joint project of the University of West Bohemia in Pilsen, Prague’s Charles University and two private companies—CertiCon and SpeechTech—kicked off nearly two years ago.

The technology uses recordings of a patient’s voice to create synthetic speech that can be played on their mobile phones, tablets or laptops via the app.

Jindrich Matousek, an expert on text-to-speech synthesis, heads the project at the University of West Bohemia in Pilsen

Ideally, patients need to record more than 10,000 sentences to provide scientists with enough material to produce their synthetic voice.

“We edit together individual sounds of speech so we need a lot of sentences,” said Jindrich Matousek, an expert on text-to-speech synthesis, speech modelling and acoustics who heads the project at the Pilsen university.

‘A matter of weeks’

But there are drawbacks: patients facing laryngectomies usually have little time or energy to do the recordings in the wake of a diagnosis that requires swift treatment.

“It’s usually a matter of weeks,” said Barbora Repova, a doctor at the Motol University Hospital, working on the project for Charles University.

“The patients also have to tackle issues like their economic situation, their lives are turned upside down, and the last thing they want to do is to make the recording,” she told AFP.

To address these difficulties, scientists came up with a more streamlined method for the app, which is supported by the Technology Agency of the Czech Republic.

Working with fewer sentences—ideally 3,500 but as few as 300—this method uses advanced statistical models such as artificial neural networks.

Working on the project to develop an app to help give throat cancer patients their voice back is doctor Barbora Repova, who represents Charles University

“You use speech models with certain parameters to generate synthesised speech,” said Matousek.

“Having more data is still better, but you can achieve decent quality with less data of a given voice.”

The sentences are carefully selected and individual sounds have to be recorded several times as they are pronounced differently next to different sounds or at the beginning and end of a word or sentence, he added.

So far, the Pilsen university has recorded 10 to 15 patients, according to Matousek.

Besides Czech, the Pilsen scientists have also created synthesised speech samples in English, Russian and Slovak.

‘Baby dinosaurs’

Gular—an upholsterer who lost his job due to his handicap—managed to record 477 sentences over the three weeks between his diagnosis and the operation.

But he was stressed and less than satisfied with the quality of his voice.

Entrepreneur Jana Huttova records sentences to be able to use the app if she loses her voice to minor throat surgery

“Throat cancer patients often suffer from some form of dysphonia (hoarseness) before the surgery, so in combination with a limited speech sample it makes the voice sound unnatural,” said Repova.

In a studio at the Pilsen university meanwhile, entrepreneur Jana Huttova is recording outlandish phrases.

The 34-year-old mother of three faces the risk of losing her voice to minor throat surgery—an operation on her parathyroid gland.

“The Chechens have always preferred a dagger-like Kalashnikov,” she says, reading from the text before her.

“I have small kids and I want them to hear my own voice, not a robot,” Huttova said.

Then she moved on to her next sentence: “We were attacked by a tyrannosaur’s baby dinosaurs.”

Connected to the brain

Matousek believes that in the future, patients will be able to use the app to record their voice at home using a specialised website to guide them through the process.

Jana Huttova, 34, a mother of three, says she is recording phrases for the app because she would want her children to hear her voice, not a robot

And he hopes that one day it will go even further.

“The ultimate vision is a miniature device connected to the brain, to the nerves linked to speech—then patients could control the device with their thoughts,” he said.

This kind of advanced solution is a very long way off, said Repova.

“But look at cochlear implants—40 years ago when they started, we had no idea how it would develop, how widely they would end up being used,” she said, referring to the inner-ear implants used to tackle severe deafness.

“A happy end would be a device implanted in the throat that could talk with the patient’s own voice,” she told AFP.

“It’s realistic: it may not come in a year or even in 10 years, but it’s realistic and we’re on the way.”

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Fatal drug ODs soaring among middle-aged women: CDC

(HealthDay)—The rate at which middle-aged American women die from overdoses involving opioids and other drugs nearly quadrupled between 1999 and 2017, new government data shows.

In 1999, about seven out of every 100,000 deaths among U.S. aged 30 to 64 was caused by a , but by 2017 that rate had risen to about 24 women per 100,000—a 260 percent increase, the U.S. Centers for Disease Control and Prevention said.

At the same time, rates of fatal ODs from opioids, specifically, rose nearly sixfold for middle-aged women.

The steepest increase was actually seen among —those aged 55 to 64—noted a team led by Karin Mack, of the CDC’s National Center for Injury Prevention and Control.

In fact, the average age of death from overdose crept up by about three years over the course of the study period. In 1999, the average age of a fatal OD in middle-aged women was 43.5 years, but by 2017 it had risen to 46.3 years, Mack’s team reported.

The bottom line, the researchers said, is that “efforts are needed to reduce the number of deaths in this evolving epidemic among middle-aged women.”

One physician on the frontlines of the overdose crisis said multiple factors are contributing to these tragedies.

“We know that prescription opioids are still the main driver of the current opioid epidemic, but it’s important to understand the sharp rise of fentanyl-laced heroin responsible for increased numbers of deaths,” said Dr. Robert Glatter. He’s an emergency physician at Lenox Hill Hospital in New York City.

Fentanyl is an opioid that’s thought to be 50 times more potent than heroin and 100 times more potent than morphine.

“Cheap, illicitly manufactured fentanyl from China and Southeast Asia is making its way onto the streets in the U.S.,” Glatter explained.

He said that while men tend to have higher rates of drug abuse than women, women can be especially vulnerable.

“Women’s substance use tends to progress more rapidly from first-time use until addiction develops,” Glatter said. “Withdrawal can also be more intense for women, and they may also respond differently than men to specific medical treatments.”

The new CDC study relied on 1999-2017 data from the National Vital Statistics System.

The data revealed that for women aged 30 to 64, deaths linked to “synthetic opioids”—a class that includes fentanyl—rose about 17-fold during the study period. Steep increases were also seen for deaths involving heroin (a 10-fold rise), as well as those involving Valium, Xanax or other benzodiazepine drugs (a ninefold rise). Often, overdoses involved multiple drugs.

Why are women in middle age being hit especially hard by the opioid abuse crisis? Addiction specialist Dr. Harshal Kirane had some theories.

“Middle-aged women are often prevented from accessing care due to family responsibilities, child care considerations and financial disparities,” said Kirane, who directs addiction services at Staten Island University Hospital in New York City.

“Moreover, certain —such as anxiety and depression—tend to occur at higher rates in women, which create profound obstacles to engagement in care,” he said.

Glatter agreed.

“People with untreated or undertreated depression or anxiety are at higher risk for substance abuse, with middle-aged women in this demographic at higher risk for opiate as well as benzodiazepine abuse,” Glatter said. “Women who are victims of domestic violence are also at higher risk of substance abuse.”

All of this means that more outreach must be done to help women who are vulnerable to addiction.

Kirane suggested that “we must expand the entire infrastructure for addiction care in our country, and address the comprehensive needs for women struggling with opioid-related issues.”

Crucial to these efforts are boosting women’s access to education about overdose, allowing them easy access to the overdose antidote naloxone, and widening the availability of medication-assisted treatments aimed at weaning people off addictive drugs, Kirane said.

The new report was published Jan. 11 in the CDC’s Morbidity and Mortality Weekly Report.

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Phat on potential, lipidomics is gaining weight

Another example of LIPID MAPS database content. Credit: Edward Dennis, UC San Diego

The post-holiday New Year might not seem like an ideal time to celebrate fat. But when it comes to lipids, there is no better time. For the past 15 years, scientists have been working to specify and classify these fatty acids in order to develop techniques, tools and terms to better study them. Now a new generation of chemists and biochemists is pounding out research to further understand the complex nature of lipids. The pending results, according to a new article in Science Signaling, could reshape the diagnosis and treatment of various acute and chronic conditions—from diabetes and atherosclerosis to cancer and auto-immunity.

Dubbed “lipidomics,” the study of lipids is weighty in terms of its potential for —an emerging approach for treating and preventing disease by considering an individual’s genes, environment and lifestyle, according to the U.S. National Library of Medicine. With new methods for precision medicine expected to develop over the next five to 10 years, lipids are considered “phat” (i.e., excellent) candidates for integration with these emerging methodologies. This is why next-generation researchers look at lipids with a more holistic, systems biology perspective.

Biologically versatile and essential, lipids help keep cells intact, store energy and communicate signals within the body. They also function as termini for complex cellular and organ functions and denote normal and disease states. Additionally, they are easily accessible through blood and urine, and they are quantifiable. Yet advances are needed for new analytical, statistical and informatics tools to progressively study them. Since new lipids continue to be discovered, new technology is needed to reveal exactly how many lipids our cells contain, to locate new lipids and to determine in which cellular membranes lipid changes occur.

A leader on the journey of lipids research is UC San Diego Distinguished Professor and Chair of the Department of Chemistry and Biochemistry Edward Dennis. Along with UC San Diego colleagues Christian Glass, Michael van Nieuwenhze, Shankar Subramaniam and Joseph Witztum, as well as researchers from other universities, Dennis collaboratively established the gold standard classification system called LIPID MAPS in 2003, with $73 million from the National Institutes of Health (NIH). The database of about 40,000 lipid structures is referenced by the world’s lipid researchers and cited in scientific journals.

Example of information found on the LIPID MAPS database. Credit: Edward Dennis, UC San Diego

“While the LIPID MAPS Consortium included a dozen U.S. investigators sponsored by the U.S. NIH, we invited scientists from Asia and Europe to join us in developing the LIPID MAPS Classification, Nomenclature and Structural Drawing Standards that contributed to international acceptance of LIPID MAPS,” explained Dennis. “This led to the rapid development of the lipidomics field.”

Beyond its emphasis on classification and structural representation, as well as its practice of openness and collaboration, LIPID MAPS has become a significant resource that helped to usher in the bioinformatics era. Now new researchers envision a big data picture of lipids study. With recent funding from the Wellcome Trust led by Valerie O’Donnell and Michael Wakelam from Cardiff University and Babraham Institute in the UK, further development of the LIPID MAPS database and website will continue.

Michael Wakelam, Director of the Babraham Institute, which now hosts the LIPID MAPS database, said: “The new Wellcome Trust funding for LIPID MAPS is vital in allowing us to build upon the excellence of the initial system supported by NIH. We look forward to expanding the research opportunities that LIPID MAPS enables, particularly in the area of pathway analysis while continuing to develop and maintain existing provisions and accessibility.”

“Lipidomics is a significant part of the metabolomics, which is a measure of all metabolites in any species. Metabolomics can differentiate between a state of wellness and illness in humans,” said Subramaniam, distinguished professor of bioengineering, who is also affiliated with cellular and molecular medicine and computer science and engineering at UC San Diego, and who serves as the Principal Investigator on the National Metabolomics Repository Grant from the NIH.

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Seeing shapeshifting receptors at work could yield new drugs

Just as squeezing the top of a balloon changes its overall shape, the interaction of hormones and drugs in the bloodstream changes the shape of cell surface receptors. A pair of new papers map those shapes in detail, giving researchers hope of developing more specific, more effective medications. Credit: Lefkowitz Lab, Duke University

Blood pressure drugs, like many medications in use today, often have ‘off-target’ effects because we don’t yet understand exactly how they work.

New research out of Duke, UCLA, Stanford and Harvard is showing precisely how the crucial cell surface receptors interact differently with various drugs, giving the researchers hope that they may be able to tailor more specific medications for heart patients.

High blood pressure affects one in three American adults, increasing the risk of heart disease and stroke for about 75 million Americans.

The blood vessel constriction which raises blood pressure is triggered by the interaction of a hormone, II, with the angiotensin receptor on the surface of cells in the heart, blood vessels, kidney, adrenal cortex, lungs and brain. Blood pressure drugs called (ARBs) treat high blood pressure by preventing angiotensin II from binding to its receptor.

But in doing so, these drugs also block angiotensin II’s beneficial effects, including increases in the heart’s strength and performance.

Ideally, physicians would like to block the angiotensin receptor’s effects on blood pressure without losing its positive effects on heart function, said cardiologist Robert Lefkowitz, M.D., the James B. Duke professor of Medicine and senior author of one of two companion papers coming out in Cell on Jan. 10.

Duke researchers collaborated with scientists across the country to determine the various shapes the angiotensin receptor assumes when it is turned on by different types of drugs, a key step towards being able to design better heart medicines.

“For a long time, people assumed that these receptors had one ‘off state’ and one ‘on state,’ like a light switch,” said lead author Laura Wingler, Ph.D., a postdoctoral researcher in the Lefkowitz laboratory. “But they aren’t light switches; these receptors are more like dials with multiple settings, or states. What’s been unclear for the past 10 years is what these receptor states look like and why each state triggers different events inside the cell.”

Just as squeezing only the top of a balloon alters its entire shape, the binding of hormones and drugs to the outside of a receptor causes changes in parts of the receptor which face into the cell. Different hormones and drugs push different “buttons” on a receptor, changing its shape in different ways.

Seeing those specific shapes of the angiotensin receptor for the first time “helps us approach the design of drugs more rationally,” Wingler said. “Now we know what to be aiming for and the mechanisms we need to target.”

The Duke-led study, which included colleagues at UCLA and Stanford, used a sophisticated technique called double electron-electron resonance spectroscopy to map the shape of the receptor when it interacts with different classes of hormones and drugs.

“It’s like seeing a silhouette of the receptor—an outline of its shape from one viewpoint,” Wingler said.

The researchers discovered that the receptor assumes four main shapes: one associated with ARBs that turn the receptor completely off, one associated with angiotensin II and drugs that turn the receptor fully on (both increasing blood pressure and improving heart function), and two associated with the drugs that improve heart function without increasing blood pressure.

In a second paper, the Duke group worked with the laboratory of Andrew C. Kruse, a professor at Harvard Medical School, to use X-ray crystallography to see the fine details of the receptor when it is frozen in the “fully on” state.

Wingler compares this approach to seeing an intricate, three-dimensional statue of the receptor. Importantly, it let them see how one interacts with the receptor and what “buttons” it presses to change the shape of the receptor.

The angiotensin receptor is a member of a family of proteins called G protein-coupled receptors (GPCRs), which sit in the membrane that surrounds cells and interact with hormones and drugs in the bloodstream. The GPCR family includes receptors for adrenaline, histamine, opioids, and the many molecules responsible for taste and smell, and they are the target of about one-third of all FDA-approved drugs.

Lefkowitz and Stanford University Professor Brian Kobilka, a senior co-author on one of the Cell papers, shared the 2012 Nobel Prize in Chemistry for discovering the GPCR family and defining how these receptors work.

The researchers hope these latest findings may lead to tailor-made drugs for other GPCRs that could separate desired therapeutic effects from unwanted side effects.

For example, these same principles have already been used to develop new drugs for the opioid receptor that have advanced to clinical trials. These next-generation opioid receptor drugs relieve pain but are less prone to cause the side effects associated with morphine and fentanyl, such as constipation and potentially lethal slowed breathing.

“Our papers go way beyond anything which has been done in this field before,” Lefkowitz said. “This research is likely to lead to discovery and development of novel types of drugs which can manipulate these ‘ shapes in ways that have not previously been possible.”

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Millennials’ odds for depression rise with social media use

(HealthDay)—Millennials struggling with depression aren’t being helped by their use of Facebook, Instagram or Snapchat, a new study reports.

College students who meet the criteria for tend to use social media more often and are more heavily addicted to social media, researchers found.

They’re also more likely to use social media in ways that exacerbate or highlight their depression, the study said.

For example, depressed are more likely to compare themselves on social media to people who appear better off than them, said first author Anthony Robinson. He’s a research assistant in the psychology department at Texas State University.

Folks who post to Facebook or Instagram take pains to portray themselves in a flattering light, Robinson said.

“If people are making comparisons based on this inflated image that’s being presented, it can cause feelings of inferiority,” Robinson said.

Depressed young adults were also more likely to be bothered if tagged in an unflattering picture, less likely to post pictures of themselves with other people, and more likely to self-censor what they posted to avoid the judgment of others, results showed.

For the study, Robinson and his colleagues asked 504 undergraduates at Texas State to complete an . The survey assessed their social media use and asked a variety of psychological questions.

Those with symptoms of depression reported behaviors like excessive sleeping, feelings of hopelessness and guilt, or a loss of pleasure in activities they used to enjoy, Robinson said.

About 16 percent of the students met the criteria for major depressive disorder, which Robinson said was an “extremely high” proportion.

Major depressive disorder affects nearly 7 percent of Americans 18 and older in any given year, according to the U.S. National Institute of Mental Health. Young adults 18 to 25 are the age group most likely to have had a major depressive episode in 2016, around 11 percent.

The no-holds-barred, say-anything-without-consequences nature of social media could contribute to people feeling bad about themselves, Robinson said.

“If you’re spending more time on these platforms and you’re being trolled or cyberbullied, it’s going to have a negative effect on your psychological well-being,” Robinson said.

But because this was an observational study, the researchers can’t say in what direction the association between depression and social media works, noted Joseph McGuire, an assistant professor of psychiatry and behavioral sciences at Johns Hopkins Children’s Center in Baltimore. He was not involved with the study.

“Is it that people who tend to be on social media more then start to feel depressed, or is it that the people who are more depressed are more withdrawn and this is their only ?” McGuire asked.

“If I spend two hours a day, am I more likely to be a little bit down or depressed compared with someone who is only on 20 minutes a day? Or do I never go out because I’m depressed, but I still want that social contact, so I log on to social ?” he continued.

Another new study backs up these findings. Researchers found that people are more aware of their own physical ailments if they tend to use Facebook a lot and frequently compare themselves to people apparently better off than themselves, according to findings in the January issue of the journal Heliyon.

College students who are feeling depressed should assess their own use, and either cut back or try to change their online behaviors if they are using the technology in ways linked to depression, Robinson said.

It wouldn’t hurt at all if they also sought counseling, McGuire said.

“There’s a lot of counseling centers available at academic centers. There’s that support there, and it’s intended to help kids who are struggling,” McGuire said. “Reaching out to a professional, even if you don’t think you have a problem, then you can at least start to have that dialogue.”

The new study was published Jan. 9 in the Journal of Applied Biobehavioral Research.

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Perceptions of chronic fatigue syndrome in the emergency department

Findings from a novel online questionnaire of people with chronic fatigue syndrome (CFS) who rated their perceptions of care in a hospital’s emergency department suggest the majority of these patients do not receive proper care, say researchers from Georgetown University Medical Center.

The study, published in the journal Open Access Emergency Medicine, is the first known investigation of the presentation of CFS in the emergency department (ED). The findings highlight a profound lack of understanding of CFS by , says the study’s senior investigator, allergist and immunologist James N. Baraniuk, MD, a professor of medicine at Georgetown who treats people with CFS.

He says two-thirds of respondents report they either would not go to an ED because they believed they wouldn’t be taken seriously, or had previous unsatisfactory experiences. Only a third of patients in the survey said they received appropriate treatment in the ED.

“The high proportion of patients who were basically told ‘It is all in your head’ by ED staff indicates that there is much misunderstanding and misgivings about the diagnosis of CFS. These patients should feel they are respected and that they can receive thorough care when they feel sick enough to go to an ED,” he says.

Baraniuk says more training is needed for ED staff and physicians to better understand the disorder.

The 282 participants in the survey all had physician-diagnosed CFS. Participants were predominantly women (87 percent), educated (70 percent had at least a college degree), and had a primary care physician (93 percent).

From the survey, researchers determined that:

  • Only 59 percent of CFS patients had gone to an ED. In this group, 42 percent were dismissed as having psychosomatic complaints.
  • 33 percent had symptoms consistent with a condition known as orthostatic intolerance, which occurs when a person feels faint when standing or sitting upright because not enough blood is reaching the brain and heart. The symptoms only improve when a person lies down.
  • CFS patients who went to the ED collectively rated caregivers’ knowledge about CFS at 3.6 on a 10-point scale.
  • 41 percent of CFS respondents did not go to the ED when ill because they felt nothing could be done or they would not be taken seriously.

“An already-available CFS Symptom Severity Questionnaire can be used in the ED to assist with the diagnosis of CFS, and to differentiate exacerbations of CFS symptoms from medical emergencies such as heart attacks or infections,” Baraniuk says.

The number one reason for going to the ED was orthostatic intolerance.

“This is of importance because it provides a starting point for diagnosis and treatment by ED physicians,” Baraniuk says. “This condition is something that can be readily addressed by ED caregivers. There is a real need for physician education that will improve their efficiency in identifying and treating CFS and in distinguishing CFS symptoms from other diseases in the exam room.”

“We found that intolerance of exercise and intolerance to alcohol consumption were common to those diagnosed with CFS so this may help distinguish CFS from other conditions,” says study co-author Christian R. Timbol, MD, who worked with Baraniuk as a medical student before becoming an emergency medicine resident physician at Thomas Jefferson University Hospital in Philadelphia.

Chronic fatigue syndrome affects between 836,000 and 2.5 million Americans, according to a National Academy of Medicine review of over 9,000 articles covering 64 years of research.

This reviewers renamed the syndrome “Systemic Exertion Intolerance Disease” to emphasize the disability, post exertional malaise or exhaustion that follows mild exertion, cognitive dysfunction and orthostatic intolerance (blood pressure and heart rate changes that cause dizziness) that are the salient features of the illness.

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