Posts Tagged ‘mental health’

by Rachel Metz

There are about 45 million people in the US alone with a mental illness, and those illnesses and their courses of treatment can vary tremendously. But there is something most of those people have in common: a smartphone.

A startup founded in Palo Alto, California, by a trio of doctors, including the former director of the US National Institute of Mental Health, is trying to prove that our obsession with the technology in our pockets can help treat some of today’s most intractable medical problems: depression, schizophrenia, bipolar disorder, post-traumatic stress disorder, and substance abuse.

Mindstrong Health is using a smartphone app to collect measures of people’s cognition and emotional health as indicated by how they use their phones. Once a patient installs Mindstrong’s app, it monitors things like the way the person types, taps, and scrolls while using other apps. This data is encrypted and analyzed remotely using machine learning, and the results are shared with the patient and the patient’s medical provider.

The seemingly mundane minutiae of how you interact with your phone offers surprisingly important clues to your mental health, according to Mindstrong’s research—revealing, for example, a relapse of depression. With details gleaned from the app, Mindstrong says, a patient’s doctor or other care manager gets an alert when something may be amiss and can then check in with the patient by sending a message through the app (patients, too, can use it to message their care provider).

For years now, countless companies have offered everything from app-based therapy to games that help with mood and anxiety to efforts to track smartphone activities or voice and speech for signs of depression. But Mindstrong is different, because it’s considering how users’ physical interactions with the phones—not what they do, but how they do it—can point to signs of mental illness. That may lead to far more accurate ways to track these problems over time. If Mindstrong’s method works, it could be the first that manages to turn the technology in your pocket into the key to helping patients with a wide range of chronic brain disorders—and may even lead to ways to diagnose them before they start.

Digital fingerprints
Before starting Mindstrong, Paul Dagum, its founder and CEO, paid for two Bay Area–based studies to figure out whether there might be a systemic measure of cognitive ability—or disability—hidden in how we use our phones. One hundred and fifty research subjects came into a clinic and underwent a standardized neurocognitive assessment that tested things like episodic memory (how you remember events) and executive function (mental skills that include the ability to control impulses, manage time, and focus on a task)—the kinds of high-order brain functions that are weakened in people with mental illnesses.

The assessment included neuropsychological tests that have been used for decades, like a so-called timed trail-­tracing test, where you have to connect scattered letters and numbers in the proper order—a way to measure how well people can shift between tasks. People who have a brain disorder that weakens their attention may have a harder time with this.

Subjects went home with an app that measured the ways they touched their phone’s display (swipes, taps, and keyboard typing), which Dagum hoped would be an unobtrusive way to log these same kinds of behavior on a smartphone. For the next year, it ran in the background, gathering data and sending it to a remote server. Then the subjects came back for another round of neurocognitive tests.

As it turns out, the behaviors the researchers measured can tell you a lot. “There were signals in there that were measuring, correlating—predicting, in fact, not just correlating with—the neurocognitive function measures that the neuropsychologist had taken,” Dagum says.

For instance, memory problems, which are common hallmarks of brain disorders, can be spotted by looking at things including how rapidly you type and what errors you make (such as how frequently you delete characters), as well as by how fast you scroll down a list of contacts. (Mindstrong can first determine your baseline by looking at how you use your handset and combining those characteristics with general measures.) Even when you’re just using the smartphone’s keyboard, Dagum says, you’re switching your attention from one task to another all the time—for example, when you’re inserting punctuation into a sentence.

He became convinced the connections presented a new way to investigate human cognition and behavior over time, in a way that simply isn’t possible with typical treatment like regularly visiting a therapist or getting a new medication, taking it for a month, and then checking back in with a doctor. Brain-disorder treatment has stalled in part because doctors simply don’t know that someone’s having trouble until it’s well advanced; Dagum believes Mindstrong can figure it out much sooner and keep an eye on it 24 hours a day.

In 2016, Dagum visited Verily, Alphabet’s life sciences company, where he pitched his work to a group including Tom Insel, a psychiatrist who had spent 13 years as director of the National Institute of Mental Health before he joined Verily in 2015.

Verily was trying to figure out how to use phones to learn about depression or other mental health conditions. But Insel says that at first, what Dagum presented—more a concept than a show of actual data—didn’t seem like a big deal. “The bells didn’t go off about what he had done,” he says.

Over several meetings, however, Insel realized that Dagum could do something he believed nobody in the field of mental health had yet been able to accomplish. He had figured out smartphone signals that correlated strongly with a person’s cognitive performance—the kind of thing usually possible only through those lengthy lab tests. What’s more, he was collecting these signals for days, weeks, and months on end, making it possible, in essence, to look at a person’s brain function continuously and objectively. “It’s like having a continuous glucose monitor in the world of diabetes,” Insel says.

Why should anyone believe that what Mindstrong is doing can actually work? Dagum says that thousands of people are using the app, and the company now has five years of clinical study data to confirm its science and technology. It is continuing to perform numerous studies, and this past March it began working with patients and doctors in clinics.

In its current form, the Mindstrong app that patients see is fairly sparse. There’s a graph that updates daily with five different signals collected from your smartphone swipes and taps. Four of these signals are measures of cognition that are tightly tied to mood disorders (such as the ability to make goal-based decisions), and the other measures emotions. There’s also an option to chat with a clinician.

For now, Insel says, the company is working mainly with seriously ill people who are at risk of relapse for problems like depression, schizophrenia, and substance abuse. “This is meant for the most severely disabled people, who are really needing some innovation,” he says. “There are people who are high utilizers of health care and they’re not getting the benefits, so we’ve got to figure out some way to get them something that works better.” Actually predicting that a patient is headed toward a downward spiral is a harder task, but Dagum believes that having more people using the app over time will help cement patterns in the data.

There are thorny issues to consider, of course. Privacy, for one: while Mindstrong says it protects users’ data, collecting such data at all could be a scary prospect for many of the people it aims to help. Companies may be interested in, say, including it as part of an employee wellness plan, but most of us wouldn’t want our employers anywhere near our mental health data, no matter how well protected it may be.

Spotting problems before they start
A study in the works at the University of Michigan is looking at whether Mindstrong may be beneficial for people who do not have a mental illness but do have a high risk for depression and suicide. Led by Srijan Sen, a professor of psychiatry and neuroscience, the study tracks the moods of first-year doctors across the country—a group that is known to experience intense stress, frequent sleep deprivation, and very high rates of depression.

Participants log their mood each day and wear a Fitbit activity tracker to log sleep, activity, and heart-rate data. About 1,500 of the 2,000 participants also let a Mindstrong keyboard app run on their smartphones to collect data about the ways they type and figure out how their cognition changes throughout the year.

Sen hypothesizes that people’s memory patterns and thinking speed change in subtle ways before they realize they’re depressed. But he says he doesn’t know how long that lag will be, or what cognitive patterns will be predictive of depression.

Insel also believes Mindstrong may lead to more precise diagnoses than today’s often broadly defined mental health disorders. Right now, for instance, two people with a diagnosis of major depressive disorder might share just one of numerous symptoms: they could both feel depressed, but one might feel like sleeping all the time, while the other is hardly sleeping at all. We don’t know how many different illnesses are in the category of depression, Insel says. But over time Mindstrong may be able to use patient data to find out. The company is exploring how learning more about these distinctions might make it possible to tailor drug prescriptions for more effective treatment.

Insel says it’s not yet known if there are specific digital markers of, say, auditory hallucinations that someone with schizophrenia might experience, and the company is still working on how to predict future problems like post-traumatic stress disorder. But he is confident that the phone will be the key to figuring it out discreetly. “We want to be able to do this in a way that just fits into somebody’s regular life,” he says.

https://www.technologyreview.com/s/612266/the-smartphone-app-that-can-tell-youre-depressed-before-you-know-it-yourself/

Advertisements

merlin_144488709_dd45e03b-d06e-4037-9c40-c8353cdb464b-superJumbo

By Moises Velasquez-Manoff

The man was 23 when the delusions came on. He became convinced that his thoughts were leaking out of his head and that other people could hear them. When he watched television, he thought the actors were signaling him, trying to communicate. He became irritable and anxious and couldn’t sleep.

Dr. Tsuyoshi Miyaoka, a psychiatrist treating him at the Shimane University School of Medicine in Japan, eventually diagnosed paranoid schizophrenia. He then prescribed a series of antipsychotic drugs. None helped. The man’s symptoms were, in medical parlance, “treatment resistant.”

A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

At first glance, the idea seems bizarre — what does the immune system have to do with the brain? — but it jibes with a growing body of literature suggesting that the immune system is involved in psychiatric disorders from depression to bipolar disorder.

The theory has a long, if somewhat overlooked, history. In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.

Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.

One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.

Modern doctors have also observed that people who suffer from certain autoimmune diseases, like lupus, can develop what looks like psychiatric illness. These symptoms probably result from the immune system attacking the central nervous system or from a more generalized inflammation that affects how the brain works.

Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.

Admittedly, these diseases are exceedingly rare, but their existence suggests there could be other immune disorders of the brain and nervous system we don’t know about yet.

Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance. “The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past. Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

Which brings us back to Dr. Miyaoka’s patient. There are other possible explanations for his recovery. Dr. Andrew McKeon, a neurologist at the Mayo Clinic in Rochester, Minn., a center of autoimmune neurology, points out that he could have suffered from a condition called paraneoplastic syndrome. That’s when a cancer patient’s immune system attacks a tumor — in this case, the leukemia — but because some molecule in the central nervous system happens to resemble one on the tumor, the immune system also attacks the brain, causing psychiatric or neurological problems. This condition was important historically because it pushed researchers to consider the immune system as a cause of neurological and psychiatric symptoms. Eventually they discovered that the immune system alone, unprompted by malignancy, could cause psychiatric symptoms.

Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia. Once he had the same immune system, he developed similar psychiatric symptoms.

The bigger question is this: If so many syndromes can produce schizophrenia-like symptoms, should we examine more closely the entity we call schizophrenia?

Some psychiatrists long ago posited that many “schizophrenias” existed — different paths that led to what looked like one disorder. Perhaps one of those paths is autoinflammatory or autoimmune.

If this idea pans out, what can we do about it? Bone marrow transplant is an extreme and risky intervention, and even if the theoretical basis were completely sound — which it’s not yet — it’s unlikely to become a widespread treatment for psychiatric disorders. Dr. Yolken says that for now, doctors treating leukemia patients who also have psychiatric illnesses should monitor their psychiatric progress after transplantation, so that we can learn more.

And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

Dr. Yolken and colleagues recently explored this idea with a different tool: probiotics, microbes thought to improve immune function. He focused on patients with mania, which has a relatively clear immunological signal. During manic episodes, many patients have elevated levels of cytokines, molecules secreted by immune cells. He had 33 mania patients who’d previously been hospitalized take a probiotic prophylactically. Over 24 weeks, patients who took the probiotic (along with their usual medications) were 75 percent less likely to be admitted to the hospital for manic attacks compared with patients who didn’t.

The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.

Watershed moments occasionally come along in medical history when previously intractable or even deadly conditions suddenly become treatable or preventable. They are sometimes accompanied by a shift in how scientists understand the disorders in question.

We now seem to have reached such a threshold with certain rare autoimmune diseases of the brain. Not long ago, they could be a death sentence or warrant institutionalization. Now, with aggressive treatment directed at the immune system, patients can recover. Does this group encompass a larger chunk of psychiatric disorders? No one knows the answer yet, but it’s an exciting time to watch the question play out.

evolution-personality-neurosciencenews

How and why human-unique characteristics such as highly social behavior, languages and complex culture have evolved is a long-standing question. A research team led by Tohoku University in Japan has revealed the evolution of a gene related to such human-unique psychiatric traits.

PhD candidate Daiki Sato and Professor Masakado Kawata have discovered SLC18A1 (VMAT1), which encodes vesicular monoamine transporter 1, as one of the genes evolved through natural selection in the human lineage. VMAT1 is mainly involved in the transport of neurochemicals, such as serotonin and dopamine in the body, and its malfunction leads to various psychiatric disorders. VMAT1 has variants consisting of two different amino acids, threonine (136Thr) and isoleucine (136Ile), at site 136.

Several studies have shown that these variants are associated with psychiatric disorders, including schizophrenia, bipolar disorder, anxiety, and neuroticism (a personality trait). It has been known that individuals with 136Thr tend to be more anxious and more depressed and have higher neuroticism scores. They showed that other mammals have 136Asn at this site but 136Thr had been favored over 136Asn during human evolution. Moreover, the 136Ile variant had originated nearly at the Out-of-Africa migration, and then, both 136Thr and 136Ile variants have been positively maintained by natural selection in non-African populations.

The study by Sato and Kawata indicates that natural selection has possibly shaped our psychiatric traits and maintained its diversity. The results provide two important implications for human psychiatric evolution. First, through positive selection, the evolution from Asn to Thr at site 136 on SLC18A1 was favored by natural selection during the evolution from ancestral primates to humans, although individuals with 136Thr are more anxious and have more depressed minds.

Second, they showed that the two variants of 136Thr and 136Ile have been maintained by natural selection using several population genetic methods. Any form of natural selection that maintains genetic diversity within populations is called “balancing selection”. Individual differences in psychiatric traits can be observed in any human population, and some personality traits are also found in non-human primates. This suggests the possibility that a part of genetic diversity associated with personality traits and/or psychiatric disorders are maintained by balancing selection, although such selective pressure is often weak and difficult to detect.

https://neurosciencenews.com/personality-psychiatry-genetics-9820/

largest-ever-study-of-genetic-links-to-depression-and-anxiety-launched-309700

The NIHR and King’s College London are calling for 40,000 people diagnosed with depression or anxiety to enrol online for the Genetic Links to Anxiety and Depression (GLAD) Study and join the NIHR Mental Health Bioresource.

Researchers hope to establish the largest ever database of volunteers who can be called up to take part in research exploring the genetic factors behind the two most common mental health conditions – anxiety and depression.

[youtube=https://youtu.be/wzgvS8gU2Ss\

The GLAD study will make important strides towards better understanding of these disorders and provide a pool of potential participants for future studies, reducing the time-consuming process of recruiting patients for research.

Research has shown 30-40% of the risk for both depression and anxiety is genetic and 60-70% due to environmental factors. Only by having a large, diverse group of people available for studies will researchers be able to determine how genetic and environmental triggers interact to cause anxiety and depression.

Leader of the GLAD study and the NIHR Mental Health BioResource, Dr Gerome Breen of King’s College London, said: “It’s a really exciting time to become involved in mental health research, particularly genetic research which has made incredible strides in recent years – we have so far identified 46 genetic links for depression and anxiety.

“By recruiting 40,000 volunteers willing to be re-contacted for research, the GLAD Study will take us further than ever before. It will allow researchers to solve the big unanswered questions, address how genes and environment act together and help develop new treatment options.”

The GLAD Study, a collaboration between the NIHR BioResource and King’s College London, has been designed to be particularly accessible, with a view to motivating more people to take part in mental health research.

Research psychologist and study lead Professor Thalia Eley, King’s College London, said: “We want to hear from all different backgrounds, cultures, ethnic groups and genders, and we are especially keen to hear from young adults. By including people from all parts of the population, what we learn will be relevant to everyone. This is a unique opportunity to participate in pioneering medical science.”

https://www.nihr.ac.uk/news/nihr-launches-largest-ever-study-of-genetic-links-to-depression-and-anxiety/9201

mayosi-banner-x
The 51-year-old University of Cape Town researcher had been suffering from depression, and his death has prompted reflection on being a black academic in South Africa.

Bongani Mayosi, a prominent cardiologist and dean of the Faculty of Health Sciences at the University of Cape Town in South Africa, died of suicide on July 27. He was 51.

“In the last two years he has battled with depression and on that day [Friday] took the desperate decision to end his life,” his family said in a statement at the time, News24 reports. “We are still struggling to come to terms with this devastating loss.”

Born in 1967, Mayosi grew up under apartheid in the Transkei region of South Africa. Homeschooled by his mother as a child, he later studied medicine at the University of KwaZulu-Natal, incorporating a year of research to qualify for a BMedSci degree. In 1998, he won a fellowship to join the PhD program in the department of cardiovascular medicine at the University of Oxford.

Upon returning to South Africa a few years later, Bongani worked on a number of projects, including searching for the genetic mutations underpinning arrhythmogenic cardiomyopathy to identifying risk factors involved in cardiovascular disease. In 2006, at 38 years old, he became the first black person to chair the Department of Medicine at the University of Cape Town (UCT).

His career over the next decade would be marked by several awards recognizing his contributions to cardiology. In 2007, he was named one of the top 25 “influential leaders in healthcare in South Africa,” and, two years later, received the Order of Mapungubwe, South Africa’s highest honor. In 2017, he was elected to the US National Academy of Medicine.

Becoming dean in 2016, Mayosi was responsible for handling part of the university’s response to a tumultuous period of student unrest across the country. In a letter published on News24, the university’s vice chancellor Mamokgethi Phakeng writes that during that period, Mayosi’s “office was occupied for about two weeks in 2016. He had to manage pressure coming from many different directions, including from staff and students.” Over the next two years, Mayosi suffered from depression and took time off from his position; he resigned twice, but was persuaded to change his mind.

Mayosi’s death has led colleagues to examine the external forces that might have contributed to his desperation. In early August, Johannesburg’s City Press and other outlets reported that UCT had instigated an inquiry into the circumstances surrounding Mayosi’s death following calls from concerned colleagues and the university’s Black Academic Caucus. In a statement on Facebook on August 2, the Caucus wrote that “it is hard for us to exclude the UCT working environment from the tragic death of our colleague, and indeed others, including students.” Many researchers and activists also highlighted challenges Mayosi faced as a black academic in South Africa.

Matshidiso Moeti, the African regional director for the World Health Organization—where Mayosi had chaired the African Advisory Committee on Health Research & Development—was one of many health officials and researchers to send condolences after news of Mayosi’s death. “We will always cherish him for his diligence and immense contribution to the development of the WHO strategy for strengthening the use of evidence, information and research for policy-making in the African Region,” she wrote.

Cardiologists Hugh Watkins of the University of Oxford and Ntobeko Ntusi of UCT write in a memorial published yesterday (September 11) in Circulation that “one of the most striking impressions from his funeral, attended by thousands of mourners who remembered him with awe and love, was the abundant evidence of his commitment to bring others with him, nurture talent, and provide the sorts of opportunity from which he had benefited. . . . We speak for many in saying that we are in awe of what Bongani achieved.”

https://www.the-scientist.com/news-opinion/celebrated-cardiologist-bongani-mayosi-dies-64787?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=65896990&_hsenc=p2ANqtz-_Xn_C3066EAlU479N7jk9yk0YpvAneSzSm7Ae9hwdounQSXC6y1NB1SlSwEHpKfuJXV3J_nz64REq0mTIGy6GuyMPE0Q&_hsmi=65896990

anewmapofthe
A 3-D rendering of the serotonin system in the left hemisphere of the mouse brain reveals two groups of serotonin neurons in the dorsal raphe that project to either cortical regions (blue) or subcortical regions (green) while rarely crossing into the other’s domain.

As Liqun Luo was writing his introductory textbook on neuroscience in 2012, he found himself in a quandary. He needed to include a section about a vital system in the brain controlled by the chemical messenger serotonin, which has been implicated in everything from mood to movement regulation. But the research was still far from clear on what effect serotonin has on the mammalian brain.

“Scientists were reporting divergent findings,” said Luo, who is the Ann and Bill Swindells Professor in the School of Humanities and Sciences at Stanford University. “Some found that serotonin promotes pleasure. Another group said that it increases anxiety while suppressing locomotion, while others argued the opposite.”

Fast forward six years, and Luo’s team thinks it has reconciled those earlier confounding results. Using neuroanatomical methods that they invented, his group showed that the serotonin system is actually composed of at least two, and likely more, parallel subsystems that work in concert to affect the brain in different, and sometimes opposing, ways. For instance, one subsystem promotes anxiety, whereas the other promotes active coping in the face of challenges.

“The field’s understanding of the serotonin system was like the story of the blind men touching the elephant,” Luo said. “Scientists were discovering distinct functions of serotonin in the brain and attributing them to a monolithic serotonin system, which at least partly accounts for the controversy about what serotonin actually does. This study allows us to see different parts of the elephant at the same time.”

The findings, published online on August 23 in the journal Cell, could have implications for the treatment of depression and anxiety, which involves prescribing drugs such as Prozac that target the serotonin system – so-called SSRIs (selective serotonin reuptake inhibitors). However, these drugs often trigger a host of side effects, some of which are so intolerable that patients stop taking them.

“If we can target the relevant pathways of the serotonin system individually, then we may be able to eliminate the unwanted side effects and treat only the disorder,” said study first author Jing Ren, a postdoctoral fellow in Luo’s lab.

Organized projections of neurons

The Stanford scientists focused on a region of the brainstem known as the dorsal raphe, which contains the largest single concentration in the mammalian brain of neurons that all transmit signals by releasing serotonin (about 9,000).

The nerve fibers, or axons, of these dorsal raphe neurons send out a sprawling network of connections to many critical forebrain areas that carry out a host of functions, including thinking, memory, and the regulation of moods and bodily functions. By injecting viruses that infect serotonin axons in these regions, Ren and her colleagues were able to trace the connections back to their origin neurons in the dorsal raphe.

This allowed them to create a visual map of projections between the dense concentration of serotonin-releasing neurons in the brainstem to the various regions of the forebrain that they influence. The map revealed two distinct groups of serotonin-releasing neurons in the dorsal raphe, which connected to cortical and subcortical regions in the brain.

“Serotonin neurons in the dorsal raphe project to a bunch of places throughout the brain, but those bunches of places are organized,” Luo said. “That wasn’t known before.”

Two parts of the elephant

In a series of behavioral tests, the scientists also showed that serotonin neurons from the two groups can respond differently to stimuli. For example, neurons in both groups fired in response to mice receiving rewards like sips of sugar water but they showed opposite responses to punishments like mild foot shocks.

“We now understand why some scientists thought serotonin neurons are activated by punishment, while others thought it was inhibited by punishment. Both are correct – it just depends on which subtype you’re looking at,” Luo said.

What’s more, the group found that the serotonin neurons themselves were more complex than originally thought. Rather than just transmitting messages with serotonin, the cortical-projecting neurons also released a chemical messenger called glutamate – making them one of the few known examples of neurons in the brain that release two different chemicals.

“It raises the question of whether we should even be calling these serotonin neurons because neurons are named after the neurotransmitters they release,” Ren said.

Taken together, these findings indicate that the brain’s serotonin system is not made up of a homogenous population of neurons but rather many subpopulations acting in concert. Luo’s team has identified two groups, but there could be many others.

In fact, Robert Malenka, a professor and associate chair of psychiatry and behavioral sciences at Stanford’s School of Medicine, and his team recently discovered a group of serotonin neurons in the dorsal raphe that project to the nucleus accumbens, the part of the brain that promotes social behaviors.

“The two groups that we found don’t send axons to the nucleus accumbens, so this is clearly a third group,” Luo said. “We identified two parts of the elephant, but there are more parts to discover.”

https://medicalxpress.com/news/2018-08-brain-serotonin.html

Buds-1024x683

For what is thought to be the largest study of its kind, the researchers analyzed brain scans of 31,227 people aged 9 months–105 years.

In a paper that now features in the Journal of Alzheimer’s Disease, they describe how they identified “patterns of aging” from the brain scans.

These were done using single photon emission computed tomography (SPECT) and came from people with psychiatric conditions such as attention deficit hyperactivity disorder (ADHD), schizophrenia, and bipolar disorder. They were all attending a psychiatric clinic that was based at several locations.

Each participant underwent two SPECT brain scans — one during a resting state, and another during completion of “a concentration task” — giving a total of 62,454 scans.

The scientists found that they could predict a person’s age from the pattern of blood flow in their brain.

Brain circulation varied over lifespan
They observed that blood flow varied from childhood into older age throughout the lifespan. They also saw that brain aging was more visible in scans of men and those with schizophrenia, anxiety, bipolar disorder, and ADHD.

Brain aging was also more strongly associated with use of cannabis and alcohol.

“Based on one of the largest brain imaging studies ever done,” says lead study author Dr. Daniel G. Amen, a psychiatrist and founder of Amen Clinics in Costa Mesa, CA, “we can now track common disorders and behaviors that prematurely age the brain.”

He suggests that improving the treatment of these disorders could “slow or even halt the process of brain aging.”

https://www.medicalnewstoday.com/articles/322852.php