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Genetics

A Genetic Variant You May Have Inherited From Neanderthals Reduces the Risk of Severe COVID-19 – SciTechDaily

New research has found that a group of genes that reduces the risk of developing severe COVID-19 by around 20% is inherited from Neanderthals. Credit: Bjorn Oberg, Karolinska Institutet

DNA variants passed on to modern humans from Neanderthals can increase as well as decrease our ability to fight SARS-CoV-2, a new PNAS study finds.

SARS-CoV-2, the virus that causes COVID-19, impacts people in different ways after infection. Some experience only mild or no symptoms at all while others become sick enough to require hospitalization and may develop respiratory failure and die.

Now, researchers at the Okinawa Institute of Science and Technology Graduate University (OIST) in Japan and the Max Planck Institute for Evolutionary Anthropology in Germany have found that a group of genes that reduces the risk of a person becoming seriously ill with COVID-19 by around 20% is inherited from Neanderthals.

Of course, other factors such as advanced age or underlying conditions such as diabetes have a significant impact on how ill an infected individual may become, said Professor Svante Pbo, who leads the Human Evolutionary Genomics Unit at OIST. But genetic factors also play an important role and some of these have been contributed to present-day people by Neanderthals.

Last year, Professor Svante Pbo and his colleague Professor Hugo Zeberg reported in Nature that the greatest genetic risk factor so far identified, doubling the risk to develop severe COVID-19 when infected by the virus, had been inherited from Neanderthals.

Their latest research builds on a new study, published in December last year from the Genetics of Mortality in Critical Care (GenOMICC) consortium in the UK, which collected genome sequences of 2,244 people who developed severe COVID-19. This UK study pinpointed additional genetic regions on four chromosomes that impact how individuals respond to the virus.

Now, in a study published recently in Proceedings of the National Academy of Sciences (PNAS), Professor Pbo and Professor Zeberg show that one of the newly identified regions carries a variant that is almost identical to those found in three Neanderthals a ~50,000-year-old Neanderthal from Croatia, and two Neanderthals, one around 70,000 years old and the other around 120,000 years old, from Southern Siberia.

Surprisingly, this second genetic factor influences COVID-19 outcomes in the opposite direction to the first genetic factor, providing protection rather than increasing the risk to develop severe COVID-19. The variant is located on chromosome 12 and reduces the risk that an individual will require intensive care after infection by about 22%.

Its quite amazing that despite Neanderthals becoming extinct around 40,000 years ago, their immune system still influences us in both positive and negative ways today, said Professor Pbo.

To try to understand how this variant affects COVID-19 outcomes, the research team took a closer look at the genes located in this region. They found that three genes in this region, called OAS, code for enzymes that are produced upon viral infection and in turn activate other enzymes that degrade viral genomes in infected cells.

It seems that the enzymes encoded by the Neanderthal variant are more efficient, reducing the chance of severe consequences to SARS-CoV-2 infections, Professor Pbo explained.

The researchers also studied how the newly discovered Neanderthal-like genetic variants changed in frequency after ending up in modern humans some 60,000 years ago.

To do this, they used genomic information retrieved by different research groups from thousands of human skeletons of varying ages.

They found that the variant increased in frequency after the last Ice Age and then increased in frequency again during the past millennium. As a result, today it occurs in about half of people living outside Africa and in around 30% of people in Japan. In contrast, the researchers previously found that the major risk variant inherited from Neanderthals is almost absent in Japan.

The rise in the frequency of this protective Neanderthal variant suggests that it may have been beneficial also in the past, maybe during other disease outbreaks caused by RNA viruses, said Professor Pbo.

Reference: A genomic region associated with protection against severe COVID-19 is inherited from Neandertals by Hugo Zeberg and Svante Pbo, 16 February 2021, Proceedings of the National Academy of Sciences.DOI: 10.1073/pnas.2026309118

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A Genetic Variant You May Have Inherited From Neanderthals Reduces the Risk of Severe COVID-19 - SciTechDaily

Genetics

Don’t Suffer in The Cold? Turns Out There’s a Genetic Mutation For That – ScienceAlert

Most of us living on planet Earth have to make it through some amount of cold weather for at least part of the year, and new research has identified a specific genetic mutation that makes a fifth of us more resilient to cold conditions.

The genetic mutation in question stops the production of the protein -actinin-3, which is important for skeletal muscle fibre: The protein is only found in fast-twitch (or white) fibres and not in slow-twitch (or red) fibres.

Based on the new study's results, people without -actinin-3 have a higher proportion of slow-twitch fibres, and one of the consequences is that the body tends to conserve energy by building up muscle tone through contractions rather than shivering.

"This suggests that people lacking -actinin-3 are better at keeping warm and, energy-wise, at enduring a tougher climate, but there hasn't been any direct experimental evidence for this before," says physiologist Hkan Westerblad, from the Karolinska Institutet in Sweden.

"We can now show that the loss of this protein gives a greater resilience to cold and we've also found a possible mechanism for this."

The researchers recruited 42 men to sit in 14-degree Celsius (57.2-degree Fahrenheit) water while their temperatures and muscles were measured. The chilly immersion lasted 20 minutes at a time with 10-minute breaks, for up to two hours in total.

The proportion of participants who could keep their body temperature above 35.5 degrees Celsius (95.9 degrees Fahrenheit) was higher in those with the -actinin-3 mutation versus those without 69 percent of volunteers versus 30 percent.

In other words, the genetic mutation appeared to help these participants to conserve energy more efficiently and build up a greater resilience to the cold.

The team also conducted follow-up experiments in mice with the same mutation in order to check whether having this mutation could have something to do with increasing brown fat stores a well-known heat-generating tissue in mammals but that didn't turn out to be the case.

People lacking -actinin-3 might be better braced for a cold water swim or a bout of wintry weather, but it could also leave them more vulnerable to obesity and type-2 diabetes if they're inactive, the researchers say. It might also increase the risk of falling as they get older, as fast-twitch fibres handle speedy muscle movements.

"The mutation probably gave an evolutionary advantage during the migration to a colder climate, but in today's modern society this energy-saving ability might instead increase the risk of [these] diseases, which is something we now want to turn our attention to," says Westerblad.

As previous research has shown, -actinin-3 deficiency has increased across the population as humans have moved from warmer to colder climes, although questions remain about whether this mutation is present at birth and affects infant mortality.

It's also interesting to note that athletes who excel at sports involving explosiveness and strength (such as sprinting) are more likely to not have this lack of -actinin-3, while for endurance sports the stats are reversed.

As for future research, the team is keen to look at how this might all work at the molecular level, as well as how it could affect muscle disease. For now, it's an important new discovery about this genetic mutation and the allele or gene form associated with it.

"These findings provide a mechanism for the increase in [these gene variants'] frequency as modern humans migrated from Africa to the colder climates of central and northern Europe over 50,000 years ago," conclude the researchers in their published paper.

The research has been published in the American Journal of Human Genetics.

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Don't Suffer in The Cold? Turns Out There's a Genetic Mutation For That - ScienceAlert

Neuroscience

The neuroscience of hate – Sapulpa Times

Scientists in recent years have begun to establish the neural coordinates for complex emotional concepts such as hate. Functional magnetic resonance imaging (fMRI) is giving researchers an understanding of the way these intense emotions begin to emerge in the brain.

In 2008, Semir Zeki, a neurobiologist at University College Londons Laboratory of Neurobiology, conducted a study last year that performed fMRIs on 17 adults as they looked at images of people whom they hated. Certain areas in the right putamen, medial frontal gyrus, medial insula, and the premotor cortex were activated.

The scientists noted that components of this hate circuit are also involved in commencing aggressive behavior, However, hatred exhibits different brain patterns than do the feelings of aggression itself, as well as fear, anger, and danger. The researchers postulated that activity in these areas indicate that the brain is primed for violence.

Hate can come from positive emotions, such as romantic love, as in the case of a jilted lover. Not surprisingly, love appears to deactivate areas associated with judgment, whereas hatred activates areas in the frontal cortex that are thought to be involved in evaluating another person and anticipate his or her behavior.

According to the authors of the study, there are striking similarities between love and hate. The regions of the putamen and insula that are switched on by hate are also the same as those for romantic love. This linkage may account for why love and hate are so closely linked to each other in life.

Psychologically speaking, hatred and violence against another classification of people is an extension and distortion of our natural human tendency to classify us from them. From an evolutionary standpoint, group membership or tribalism was necessary for human survival.

Related: The neuroscience of of love

In-group/out-group categorizations are made within milliseconds in the brain, and, when coupled with negative stereotypes, can result in feelings of fear, revulsion, and dehumanization.

Scientific studies have demonstrated that viewing pictures of people from a different race or culture activates the amygdala, which is an area of the brain linked with creating fear. Seeing or thinking about an out-group like the homeless or people who use drugs can also attenuate activity in the medial prefrontal cortex, an area associated with social cognition and empathy. This decreased activity gives rise to feelings of dehumanization. In other words, seeing the other group as less than human, which creates an increased risk for violence.

Rebecca Saxe, a professor of cognitive neuroscience, and associate department head at the Department of Brain and Cognitive Sciences at MIT, stated that violence between groups can occur when resources are considered to be limited. In those scenarios, protecting ones own group and its resources at the expense of another group, even through the use of physical force, is deemed imperative. Even when the resources at stake are not commodities but existential ideals and fundamental values, feelings of hate for the opposing group can develop.

In a lecture given at Harvard in 2019, Saxe said: If we think that the survival, autonomy, and dignity of our ideals is a scarce resource in a zero-sum conflict with the survival, autonomy, and dignity of another group, then it could be my obligation to destroy the other group.

Saxe further stated: Hate is a mixing of both intense dislike with moral contempt and disgust. The moral motive of extreme violence in which the other must be destroyed [is] to make a better, more just world for that which I hold most dear. She has concluded that hate and violence are not caused by sociopathic tendencies but the extreme culmination of perceiving an existential threat to ones in-group.

Listening to hate speech can increase prejudice toward an out-group and even prime the brain for violent actions. According to Arizona State University psychologist Arthur Glenberg, Words themselves are enough to trigger simulations in motor, perceptual and emotional neural systems. Your brain creates a sense of being there: The motor system is primed for action and the emotional system motivates those actions.

How is it possible to control hate if the drive to hate is located in a primitive and unconscious part of the brain? The higher-order brain structures, like the ventromedial prefrontal cortex (vmPFC), among others, allow us to choose anger and hatred or to let it go.

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The neuroscience of hate - Sapulpa Times

Neuroscience

5 compelling reasons to listen to the neuroscience to build a healthy workplace – CEOWORLD magazine

An innovative, creative, financially thriving workplace that supports excellent teamwork and workforce wellbeing is critical and yet can be elusive.

Recent advances in technology have changed our understanding of the brain, giving us practical insights into ways to elevate performance, productivity, workplace learning, culture and the wellbeing of employees, all necessary ingredients in building a thriving workplace.

Neuroscientists have proven that our brain is continually shaped by and adapting to our thoughts, interactions, experiences, and environment. The responsiveness of the brain, called neuroplasticity, can be intentionally optimised to support organisational success and a healthy workplace.

Understanding a little about the brain can be game-changing in achieving organisational success. The executive brain, located behind our forehead, is the source of our best thinking and psychological functioning. It enables us to be proactive, strategic, reflective, creative, make our best decisions and be mentally and psychologically agile. The executive brain is more available to us when we feel physically and psychologically safe, valued, connected and fulfilled.

The more primitive, or reptilian, parts of our brain, are vital for survival, continually scanning our environment to protect us from threats. When we feel unsafe, disconnected, devalued, or invalidated, the reptilian brain takes over, making it harder to access our best thinking. At these times well operate in self-protective mode, which can be through being reactive, aggressive, competitive or withdrawn. Were generally less considered in our actions and words.

How can the neuroscience guide us to build a healthy workplace?

If we want to build a healthy workplace, the neuroscience clearly directs us to feed the executive brain, rather than the reptilian brain of employees. This is achieved through our daily workplace interactions and behaviours, which can have a profound impact on brain functioning. Behaviours that are positive and feed the executive brain are above the line, negative behaviours feed the reptilian brain, and are below the line.

Above-the-line behaviours are acceptable, healthy and responsible from a human, psychological and interpersonal perspective. They feed the executive brain, are good for people, bringing out employees capacity to think, learn and relate effectively. Above-the-line behaviours generate positivity, kindness, appreciation, goodwill, respect, openness to learning, authenticity, trust and connection.

Below-the-line behaviours are not acceptable, healthy or responsible from a psychological and human perspective. They feed the reptilian brain, are not in the best interests of people, diminishing performance, productivity and employees mental health. Incivility, sarcasm, defensiveness, shaming, excluding, ignoring, bitching, unnecessary criticism, bullying, harassment and discrimination are examples of below-the-line behaviours.

If we listen to the neuroscience and feed the executive brain and not the reptilian brain, were far more likely to achieve:

Recent advances in neuroscience challenge us to critically evaluate how interpersonal behaviours directly influence workplace functioning and on building a healthy workplace.

Written by Michelle Bihary.

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5 compelling reasons to listen to the neuroscience to build a healthy workplace - CEOWORLD magazine

Neuroscience

Irregular Sleep Connected to Bad Moods and Depression, Study Shows – Michigan Medicine

An irregular sleep schedule can increase a persons risk of depression over the long term as much as getting fewer hours of sleep overall, or staying up late most nights, a new study suggests.

Even when it comes to just their mood the next day, people whose waking time varies from day to day may find themselves in as much of a foul mood as those who stayed up extra late the night before, or got up extra early that morning, the study shows.

The study, conducted by a team from Michigan Medicine, the University of Michigans academic medical center, uses data from direct measurements of the sleep and mood of more than 2,100 early-career physicians over one year. Its published in npj Digital Medicine.

The interns, as they are called in their first year of residency training after medical school, all experienced the long intense work days and irregular work schedules that are the hallmark of this time in medical training. Those factors, changing from day to day, altered their ability to have regular sleep schedules.

SEE ALSO: Health Care Workers Struggled With Mood, Sleep in First Months of COVID-19 Pandemic

The new paper is based on data gathered by tracking the interns sleep and other activity through commercial devices worn on their wrists, and asking them to report their daily mood on a smartphone app and take quarterly tests for signs of depression.

Those whose devices showed they had variable sleep schedules were more likely to score higher on standardized depression symptom questionnaires, and to have lower daily mood ratings. Those who regularly stayed up late, or got the fewest hours of sleep, also scored higher on depression symptoms and lower on daily mood. The findings add to whats already known about the association between sleep, daily mood and long-term risk of depression.

The advanced wearable technology allows us to study the behavioral and physiological factors of mental health, including sleep, at a much larger scale and more accurately than before, opening up an exciting field for us to explore, says Yu Fang, M.S.E., lead author of the new paper and a research specialist at the Michigan Neuroscience Institute. Our findings aim not only to guide self-management on sleep habits but also to inform institutional scheduling structures.

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Fang is part of the team from the Intern Health Study, led by Srijan Sen, M.D., Ph.D., that has been studying the mood and depression risk of first-year medical residents for more than a decade. The study collected an average of two weeks of data from before the doctors intern years began, and an average of nearly four months of monitoring through their intern year.

For the new paper, the team worked with Cathy Goldstein, M.D., M.S., an associate professor of neurology and physician in the Sleep Disorders Center at Michigan Medicine.

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Irregular Sleep Connected to Bad Moods and Depression, Study Shows - Michigan Medicine

Neuroscience

The Efficacy of Transdermal Rivastigmine in Mild to Moderate Alzheimer | CIA – Dove Medical Press

Chathuri Yatawara,1 Fatin Zahra Zailan,1 Esther Vanessa Chua,1 Linda Lay Hoon Lim,1 Eveline Silva,1 Joanna Sihan Wang,1 Adeline Ng,1 Kok Pin Ng,1 Nagaendran Kandiah1 3

1Department of Neurology, National Neuroscience Institute, Singapore, Singapore; 2Duke-NUS Medical School, Singapore, Singapore; 3Lee Kong Chian School of Medicine-Imperial College London, Nanyang Technological University, Singapore, Singapore

Correspondence: Nagaendran KandiahNational Neuroscience Institute, Level 3, Clinical Staff Office, 11 Jalan Tan Tock Seng, Singapore, 308433, SingaporeTel +65 6357 7171Fax +65 6357 7137Email Nagaendran.Kandiah@singhealth.com.sg

Background: Rivastigmine is used to treat cognitive impairment in Alzheimers disease (AD); however, the efficacy of Rivastigmine in patients with AD and concomitant small vessel cerebrovascular disease (svCVD) remains unclear. We investigated the effectiveness of Rivastigmine Patch in patients with AD and svCVD.Methods: In this open-label study, 100 patients with AD and MRI confirmed svCVD received 9.5mg/24 hours Rivastigmine transdermal treatment for 24 weeks. The primary outcome was global cognition indexed using the ADAS-Cog. Secondary outcomes included clinical-rated impression of change (indexed using (ADCSCGIC), activities of daily living (indexed using ADCS-ADL) and side effects.Results: Overall, performance on the ADAS-Cog after 24 weeks deteriorated by 1.78 (SD = 5.29) points. Fifty-two percent of the sample demonstrated improvement or remained stable, while 48% demonstrated worsening of ADAS-Cog scores. Of the 52%, significant improvement (2 or more-point decline) on the ADAS-Cog was observed in 25% of the sample, with a mean change of 5.08 (SD = 3.11). A decline on the ADAS-Cog was observed in 48% of the sample, with a mean change of 6 (SD = 2.98) points. Cognitive outcome did not interact with severity of svCVD. ADCS-ADL scores remained stable from baseline to week 24 and ADCSCGIC reports indicated that 81% of the patients remained stable after treatment. Side effects were reported by 16% of the patients, with contact dermatitis being the most common.Conclusion: Our findings suggest that Rivastigmine may have a role in the management of patients having AD and concomitant mild-severe svCVD, with minimal side effects.

Keywords: rivastigmine, Alzheimers disease, small vessel cerebrovascular disease, treatment

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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The Efficacy of Transdermal Rivastigmine in Mild to Moderate Alzheimer | CIA - Dove Medical Press

Neuroscience

Folks Can Have Real-Life Conversations While Dreaming, Study Finds – HealthDay News

THURSDAY, Feb. 18, 2021 (HealthDay News) -- If you've ever had a "lucid dream" -- one in which you're aware you're dreaming -- new research just might jolt you awake.

Not only is it possible during these vivid dreams to perceive questions, but to answer them, too -- at least sometimes.

That's the tantalizing takeaway from four independent studies that used different methods to communicate with sleeping volunteers, including some who were experienced in the art of lucid dreaming.

"When we started the project, we predicted that two-way communication would be possible because there have been all these previous studies of lucid dreamers using eye signals to communicate out of dreams," said study lead author Karen Konkoly, a doctoral student at Northwestern University in Evanston, Ill., who noted that there's also literature on things from the real world being incorporated into dreams.

But depending on someone to recount his or her dreams is notoriously inaccurate. So researchers in the United States, France, Germany and the Netherlands devised separate experiments to see whether they could communicate with slumbering volunteers and get a response back.

As Konkoly and others predicted, the answer is yes -- at least sometimes.

In one experiment, a researcher asked the sleeping volunteer, "What's eight minus six?" Without missing a beat, the volunteer responded with two left-right eye movements, indicating the answer is two.

Slumbering volunteers could also respond by contracting muscles in their faces.

"We worried that one reason the experiment wouldn't work is because we would present somebody with a math problem, like five minus two, and they would hear 'slime climbs on you,' " Konkoly said. "We were worried that it wouldn't get in, it would be really distorted too much for them to actually answer it."

That wasn't a problem at all.

Many volunteers were able to hear what was said transposed over their dream or they could hear it even though the dream was going on, she said.

"There's a cool example from the French team where it seemed like God was speaking to them or like a narrator in a movie," Konkoly said. "And then, the German team, they just used tones and lights and Morse code. And, so, they had more interesting incorporation. The lights in the room were flashing, a fishbowl was flashing. The clouds were flashing. But when we just asked people math problems, the incorporation seemed to be pretty direct."

Besides Northwestern, researchers were from Sorbonne University in France, Osnabruck University in Germany and Radboud University Medical Center in the Netherlands. They worked with 36 volunteers. Some were experienced lucid dreamers; some were not.

The studies revealed that dreaming volunteers could do simple math, follow instructions, answer yes-or-no questions and tell the difference between different sensory stimuli such as light and sound.

The correct responses were observed 18.4% of the time.

Researchers placed electrodes on participants' faces and head to monitor their brain waves, eye movements and chin muscles to confirm they were asleep and in the stage of sleep known as REM sleep. REM sleep is short for Rapid Eye Movement, the deepest of five stages of sleep.

Researchers also asked for their dream reports after they woke up.

The combination of results from these four separate teams most convincingly affirms that this communication is possible, Konkoly said.

The findings were published Feb. 18 in the journal Current Biology.

Dream research is still a field with many unknowns. Other studies have had sleepers recall their dreams after waking, but that can be flawed, with many of the details forgotten, Konkoly said.

Questions about REM sleep and dreams have been set aside by some researchers in years past while more focus was placed on other aspects of sleep, Konkoly said.

But lucid dreaming can be used to practice a skill or work on a problem, Konkoly said. Giving people more support for their dream content in real time might be an option, she said.

Some people use lucid dreaming for confronting nightmares, Konkoly said, but sometimes a lucid dreamer will forget what they want to do or get scared so the experience doesn't go the way they want.

"You can envision two-way nightmare therapy where you have a therapist on the other side saying, 'No, it's OK,' " said Konkoly, who works in Ken Paller's Cognitive Neuroscience Laboratory at Northwestern. Paller is a study co-author.

One of the procedures used in the study was developed by Michelle Carr, now at the University of Rochester. She was a student of Tore Nielsen, director of the Dream and Nightmare Laboratory at Sacre-Coeur Hospital in Montreal, who said he was encouraged to see it being used in new research.

"The given knowledge about dreaming is that it's all in the brain -- it's independent of everything else, there's active inhibition of all the sensory systems and it's all just the brain sort of creating stories for itself, and that's not a view that I've subscribed to much," Nielsen said.

This study offers evidence that at least sometimes during lucid dreams, and even in those the sleeper is unaware of at the time, people are able to perceive things and then do "higher-level operations on that information that they received," he said.

This opens the doors a little more to understanding dreaming, Nielsen said.

"It is providing us with a new methodology for studying dreams," he said. "So, we're going to be able to get in there and influence dreams and measure what's happening in the dream experience much more closely than we have been able to. This is a big step for research."

More information

The U.S. National Institute of Neurological Disorders and Stroke has more on the anatomy of sleep.

SOURCES: Karen Konkoly, graduate student researcher, Department of Psychology and Cognitive Neuroscience Laboratory, Northwestern University, Evanston, Ill.; Tore Nielsen, PhD, MSc, professor, psychiatry, University of Montreal, and director, Dream and Nightmare Laboratory, Sacre-Coeur Hospital, Montreal, Canada; Current Biology, Feb. 18, 2021

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Folks Can Have Real-Life Conversations While Dreaming, Study Finds - HealthDay News

Neuroscience

PPD Awarded US Army Study to Help Develop Post-Traumatic Stress Disorder Drugs – Business Wire

WILMINGTON, N.C.--(BUSINESS WIRE)--PPD, Inc. (Nasdaq: PPD), a leading global contract research organization, has been awarded Defense Health Agency funds to support a five-year Research Project Award (RPA) to develop and execute an adaptive platform clinical research trial of drug interventions to treat post-traumatic stress disorder (PTSD). PPD will work with U.S. Medical Research Development Command (USAMRDC) U.S. Army Medical Materiel Development Activitys (USAMMDA) Warfighter Brain Health Project Management Office (WBH PMO) to test the effectiveness and safety of at least two pharmacotherapeutic drug candidates for the treatment of PTSD in U.S. military active duty personnel and veterans.

The RPA is part of the Medical Technology Enterprise Consortium (MTEC) that is under an Other Transaction Authority with the USAMRDC. As an MTEC member, PPD supports ongoing efforts to expand and grow additional important public health research programs like PTSD for the Department of Defense and U.S. Army.

PTSD is a major unmet medical need, particularly for the men and women who serve in the U.S. military, said Stephen Peroutka, M.D., Ph.D., vice president and global therapeutic area head of neuroscience for PPD and former chief of neurology at the Palo Alto VA Medical Center. Our adaptive platform trial will offer an innovative, cost-effective and much-needed approach to PTSD drug development, with an end goal of delivering efficacious drugs to treat this major unmet medical need. We appreciate and are honored to have this opportunity to support active duty service members and veterans in the effort to develop life-changing drugs for those who face this illness.

The adaptive platform trial design PPD plans to utilize will provide the WBH PMO with increased efficiency and a streamlined development process for the clinical program. The trial design facilitates evaluating multiple experimental treatment options simultaneously, adding new treatments over time, terminating ineffective treatments and graduating promising treatments to the next stage of development.

The PPD neuroscience clinical and medical experts who will be responsible for the studies are former VA attending psychiatrists and physicians who have treated PTSD in active-duty service members and veterans. At the same time, the leader of PPDs government and public health services team who oversees the companys team of experts focused on this illness is a retired Army veteran who has direct experience with those who suffer from PTSD.

PTSD is a mental health condition that affects about 8 million American adults during a given year. Some people develop the disorder after experiencing or witnessing a life-threatening event, such as military combat, a natural disaster, a car accident or a sexual assault. The number of veterans suffering from PTSD varies by service era, but up to 30% of war veterans have had PTSD in their lifetimes, according to the VAs National Center for PTSD. Currently, there are only two drugs approved by the FDA to treat PTSD, both of which were introduced nearly two decades ago.

About PPD

PPD is a leading global contract research organization providing comprehensive, integrated drug development, laboratory and lifecycle management services. Our customers include pharmaceutical, biotechnology, medical device, academic and government organizations. With offices in 46 countries and more than 26,000 professionals worldwide, PPD applies innovative technologies, therapeutic expertise and a firm commitment to quality to help customers bend the cost and time curve of drug development and optimize value in delivering life-changing therapies to improve health. For more information, visit http://www.ppd.com.

This news release contains forward-looking statements. These statements often include words such as expect, believe, project, forecast, estimate, target and other similar expressions. Although we believe these forward-looking statements are based on reasonable assumptions at the time they are made, you should be aware that many factors could affect our actual financial results, and therefore actual results might differ materially from those expressed in the forward-looking statements. Factors that might materially affect such forward-looking statements include, but are not limited to, the fragmented and highly competitive nature of the drug development services industry; changes in trends in the biopharmaceutical industry; our ability to keep pace with rapid technological changes that could make our services less competitive or obsolete; political, economic and/or regulatory influences and changes; and other factors disclosed under the Risk Factors section in our periodic reports filed with the Securities and Exchange Commission (SEC), including our latest Annual Report on Form 10-K and Quarterly Report on Form 10-Q, which is available on our website at https://investors.ppd.com or the SECs website at http://www.sec.gov. We assume no obligation and disclaim any duty to revise or update any forward-looking statements, or make any new forward-looking statement, whether as a result of new information, future events or otherwise, except as required by applicable law.

The views and conclusions contained herein are those of the authors and should not be interpreted as necessarily representing the official policies or endorsements, either expressed or implied, of the U.S. Government.

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PPD Awarded US Army Study to Help Develop Post-Traumatic Stress Disorder Drugs - Business Wire

Neuroscience

Growing Evidence That Mentally Ill Youths Become Less Healthy Adults – Duke Today

DURHAM, N.C. -- A new pair of studies from a Duke research teams long-term work in New Zealand make the case that mental health struggles in early life can lead to poorer physical health and advanced aging in adulthood.

But because mental health problems peak early in life and can be identified, the researchers say that more investment in prompt mental health care could be used to prevent later diseases and lower societal healthcare costs.

The same people who experience psychiatric conditions when they are young go on to experience excess age-related physical diseases and neurodegenerative diseases when they are older adults, explained Terrie Moffitt, the Nannerl O. Keohane professor of psychology and neuroscience at Duke, who is the senior author on both studies.

The findings in a paper appearing Feb. 17 in JAMA Psychiatry come from the long-term Dunedin Study, which has tested and monitored the health and wellbeing of a thousand New Zealanders born in 1972 and 73 from their birth to past age 45.

In middle age, the study participants who had a history of youthful psychopathology were aging at a faster pace, had declines in sensory, motor and cognitive functions, and were rated as looking older than their peers. This pattern held even after the data were controlled for health factors such as overweight, smoking, medications and prior physical disease. Their young mental health issues included mainly anxiety, depression, and substance abuse, but also schizophrenia.

You can identify the people at risk for physical illnesses much earlier in life, said Jasmin Wertz, a postdoctoral researcher at Duke who led the study. If you can improve their mental health in childhood and adolescence, its possible that you might intervene to improve their later physical health and aging.

A related study by the same team that appeared in JAMA Network Open in January used a different approach and looked at 30 years of hospital records for 2.3 million New Zealanders aged 10 to 60 from 1988 to 2018. It also found a strong connection between early-life mental health diagnoses and later-life medical and neurological illnesses.

That analysis, led by former Duke postdoctoral researcher Leah Richmond-Rakerd, showed that young individuals with mental disorders were more likely to develop subsequent physical diseases and to die earlier than people without mental disorders. People with mental illnesses experienced more hospitalizations for physical conditions, spent more time in hospitals and accumulated more healthcare costs over the subsequent 30 years.

"Our healthcare system often divides treatment between the brain and the body, but integrating the two could benefit population health, said Richmond-Rakerd, who is now an assistant professor of psychology at the University of Michigan.

Investing more resources in treating young peoples mental-health problems is a window of opportunity to prevent future physical diseases in older adults, Moffitt said. Young people with mental health problems go on to become very costly medical patients in later life.

In a 2019 commentary for JAMA Psychiatry, Moffitt and her research partner Avshalom Caspi, the Edward M. Arnett professor of psychology and neuroscience at Duke, made the argument that mental health providers have an opportunity to forestall later health problems and other social costs by intervening in the lives of younger people. Their body of work is showing that mental disorders can be reliably predicted from childhood risk factors such as poverty, maltreatment, low IQ, poor self-control and family mental health issues. And because populations in the developed world are becoming more dominated by older people, the time to make those investments in prevention is now, they said.

These studies were supported by the U.S. National Institute on Aging, the U.S. National Institute of Child Health and Development, and the UK Medical Research Council. Additional support came from the Jacobs Foundation, the Lundbeck Foundation and the New Zealand Health Research Council (R01-AG032282, R01-AG049789, MR/P005918, P30 AG028716, P30 AG034424, 15-265, R288-2018-380, P2C HD065563). The Dunedin Multidisciplinary Health and Development Study is supported by the New Zealand Health Research Council and New Zealand Ministry of Business, Innovation, and Employment.

CITATIONS: Association of History of Psychopathology With Accelerated Aging at Midlife, Jasmin Wertz, Avshalom Caspi, Antony Ambler, Jonathan Broadbent, Robert J. Hancox, HonaLee Harrington, Renate M. Houts, Joan H. Leung, Richie Poulton, Suzanne C. Purdy, Sandhya Ramrakha, Line Jee Hartmann Rasmussen, Leah S. Richmond-Rakerd, Peter R. Thorne, Graham A. Wilson, Terrie E. Moffitt. JAMA-Psychiatry, Feb. 17, 2021. DOI: 10.1001/jamapsychiatry.2020.4626

"Longitudinal Associations of Mental Disorders With Physical Diseases and Mortality Among 2.3 Million New Zealand Citizens," Leah S. Richmond-Rakerd, Stephanie DSouza, Barry J. Milne, Avshalom Caspi, Terrie E. Moffitt. JAMA Network Open, Jan. 13, 2021. DOI: 10.1001/jamanetworkopen.2020.33448

Psychiatrys Opportunity to Prevent the Rising Burden of Age-related Disease, Terrie Moffitt, Avshalom Caspi. JAMA-Psychiatry, March 27, 2019. DOI: 10.1001/jamapsychiatry.2019.0037

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Growing Evidence That Mentally Ill Youths Become Less Healthy Adults - Duke Today

Neuroscience

Demystifying the teenage brain – The Bay’s News First – SunLive

At 31-years-old, I am still a teenager. That is, at least, according to the popular neuroscience educator Nathan Wallis.

He informs me that as a male middle child, still under the age of 32, I could still be in the midst of my own adolescence.

It might explain the mood swings and predilection to video games.

You are actually an adolescent yourself then, Nathan insists. You wont have an adult brain until you are about 32.

Nathan suggests his teen brain lasted well into conventional adulthood.

I was sort of 33 when I thought: I sort of get this whole grown up thing now and how to be an adult and what I want to do with my life.

Before that I very much felt like I was 15 and pretending to be an adult.

Nathan is leading a seminar called The Teen Brain at Tauranga Girls College this month with the aim of demystifying some of the myths surrounding teenage brain development.

He has grown-up children himself and is now enjoying life as a grandfather, so he knows all too well about the trials of raising a teenager.

As he explains, for much of a childs teenage years the frontal cortex part of the brain is shut for renovations.

The whole brain isnt shut or theyd be dead! Nathan jokes, but their ability to control emotions, their ability to organise themselves, is supposed to go backwards. Adolescence is, essentially, brain number four, the frontal cortex, and it is shut for renovations for about three years.

With words such as frontal cortex and neuroscience flying around, the seminar sounds complex, but Nathan believes he has developed a way of cutting through the jargon and making the talk accessible to anyone with a brain.

A big part of what the seminar is about is demystifying it. Taking out the big words and saying this is this.

It is surprisingly and incredibly simple for what the topic is, which is complicated neuroscience.

Nathan believes the talk will be beneficial to anyone - parents, teens, those who work with teens, or perhaps those who have suffered trauma in their youth may find the seminar helpful. He will also touch on the topic of alcohol and marijuanas impact on the teenage brain.

The promise of a top tip for parents might be worth the admission fee alone.

I can teach parents in 10 minutes how to be in the top percentage of communicators, he says. If they do that they will vastly improve the quality of their relationship with their teenagers.

The Teen Brain seminar takes place at 7.30pm on February 28 at Tauranga Girls College. For more information, visit: http://www.nathanwallis.com

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Demystifying the teenage brain - The Bay's News First - SunLive