Posts Tagged ‘schizophrenia’


In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

They say the results advance the hope that supplementing with broccoli sprout extract, which contains high levels of the chemical sulforaphane, may someday provide a way to lower the doses of traditional antipsychotic medicines needed to manage schizophrenia symptoms, thus reducing unwanted side effects of the medicines.

“It’s possible that future studies could show sulforaphane to be a safe supplement to give people at risk of developing schizophrenia as a way to prevent, delay or blunt the onset of symptoms,” adds Akira Sawa, M.D., Ph.D., professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and director of the Johns Hopkins Schizophrenia Center.

Schizophrenia is marked by hallucinations, delusions and disordered thinking, feeling, behavior, perception and speaking. Drugs used to treat schizophrenia don’t work completely for everyone, and they can cause a variety of undesirable side effects, including metabolic problems increasing cardiovascular risk, involuntary movements, restlessness, stiffness and “the shakes.”

In a study described in the Jan. 9 edition of the journal JAMA Psychiatry, the researchers looked for differences in brain metabolism between people with schizophrenia and healthy controls. They recruited 81 people from the Johns Hopkins Schizophrenia Center within 24 months of their first psychosis episode, which can be a characteristic symptom of schizophrenia, as well as 91 healthy controls from the community. The participants were an average of 22 years old, and 58% were men.

The researchers used a powerful magnet to measure and compare five regions in the brain between the people with and without psychosis. A computer analysis of 7-Tesla magnetic resonance spectroscopy (MRS) data identified individual chemical metabolites and their quantities.

The researchers found on average 4% significantly lower levels of the brain chemical glutamate in the anterior cingulate cortex region of the brain in people with psychosis compared to healthy people.

Glutamate is known for its role in sending messages between brain cells, and has been linked to depression and schizophrenia, so these findings added to evidence that glutamate levels have a role in schizophrenia.

Additionally, the researchers found a significant reduction of 3% of the chemical glutathione in the brain’s anterior cingulate cortex and 8% in the thalamus. Glutathione is made of three smaller molecules, and one of them is glutamate.

Next, the researchers asked how glutamate might be managed in the brain and whether that management is faulty in disease. They first looked at how it’s stored. Because glutamate is a building block of glutathione, the researchers wondered if the brain might use glutathione as a way to store extra glutamate. And if so, the researchers questioned if they could use known drugs to shift this balance to either release glutamate from storage when there isn’t enough, or send it into storage if there is too much.

In another study, described in the Feb. 12 issue of the journal PNAS, the team used the drug L-Buthionine sulfoximine in rat brain cells to block an enzyme that turns glutamate into glutathione, allowing it to be used up. The researchers found that theses nerves were more excited and fired faster, which means they were sending more messages to other brain cells. The researchers say shifting the balance this way is akin to shifting the brain cells to a pattern similar to one found in the brains of people with schizophrenia. Next, the researchers wanted to see if they could do the opposite and shift the balance to get more glutamate stored in the form of glutathione. They used the chemical sulforaphane found in broccoli sprouts, which is known to turn on a gene that makes more of the enzyme that sticks glutamate with another molecule to make glutathione. When they treated rat brain cells with glutathione, it slowed the speed at which the nerve cells fired, meaning they were sending fewer messages. The researchers say this pushed the brain cells to behave less like the pattern found in brains with schizophrenia.

“We are thinking of glutathione as glutamate stored in a gas tank,” says Thomas Sedlak, M.D., Ph.D., assistant professor of psychiatry and behavioral sciences. “If you have a bigger gas tank, you have more leeway on how far you can drive, but as soon as you take the gas out of the tank it’s burned up quickly. We can think of those with schizophrenia as having a smaller gas tank.”

Because sulforaphane changed the glutamate imbalance in the rat brains and affected how messages were transmitted between the rat brain cells, the researchers wanted to test whether sulforaphane could change glutathione levels in healthy people’s brains and see if this could eventually be a strategy for people with mental disorders. For their study, published in April 2018 in Molecular Neuropsychiatry, the researchers recruited nine healthy volunteers (four women, five men) to take two capsules with 100 micromoles daily of sulforaphane in the form of broccoli sprout extract for seven days.

The volunteers reported that a few of them were gassy and some had stomach upset when eating the capsules on an empty stomach, but overall the sulforaphane was relatively well tolerated.

The researchers used MRS again to monitor three brain regions for glutathione levels in the healthy volunteers before and after taking sulforaphane. They found that after seven days, there was about a 30% increase in average glutathione levels in the subjects’ brains. For example, in the hippocampus, glutathione levels rose an average of 0.27 millimolar from a baseline of 1.1 millimolar after seven days of taking sulforaphane.

The scientists say further research is needed to learn whether sulforaphane can safely reduce symptoms of psychosis or hallucinations in people with schizophrenia. They would need to determine an optimal dose and see how long people must take it to observe an effect. The researchers caution that their studies don’t justify or demonstrate the value of using commercially available sulforaphane supplements to treat or prevent schizophrenia, and patients should consult their physicians before trying any kind of over-the-counter supplement. Versions of sulforaphane supplementsare sold in health food stores and at vitamin counters, and aren’t regulated by the U.S. Food and Drug Administration.

“For people predisposed to heart disease, we know that changes in diet and exercise can help stave off the disease, but there isn’t anything like that for severe mental disorders yet,” says Sedlak. “We are hoping that we will one day make some mental illness preventable to a certain extent.”

Sulforaphane is found in a variety of cruciferous vegetables, and was first identified as a “chemoprotective” substance decades ago by Paul Talalay and Jed Fahey at Johns Hopkins.

According to the World Health Organization, schizophrenia affects about 21 million people worldwide.

https://www.eurekalert.org/pub_releases/2019-05/jhm-bsc050619.php

ummary: Study identifies 104 high-risk genes for schizophrenia. One gene considered high-risk is also suspected in the development of autism.

Source: Vanderbilt University

Using a unique computational framework they developed, a team of scientist cyber-sleuths in the Vanderbilt University Department of Molecular Physiology and Biophysics and the Vanderbilt Genetics Institute (VGI) has identified 104 high-risk genes for schizophrenia.

Their discovery, which was reported April 15 in the journal Nature Neuroscience, supports the view that schizophrenia is a developmental disease, one which potentially can be detected and treated even before the onset of symptoms.

“This framework opens the door for several research directions,” said the paper’s senior author, Bingshan Li, PhD, associate professor of Molecular Physiology and Biophysics and an investigator in the VGI.

One direction is to determine whether drugs already approved for other, unrelated diseases could be repurposed to improve the treatment of schizophrenia. Another is to find in which cell types in the brain these genes are active along the development trajectory.

Ultimately, Li said, “I think we’ll have a better understanding of how prenatally these genes predispose risk, and that will give us a hint of how to potentially develop intervention strategies. It’s an ambitious goal … (but) by understanding the mechanism, drug development could be more targeted.”

Schizophrenia is a chronic, severe mental disorder characterized by hallucinations and delusions, “flat” emotional expression and cognitive difficulties.

Symptoms usually start between the ages of 16 and 30. Antipsychotic medications can relieve symptoms, but there is no cure for the disease.

Genetics plays a major role. While schizophrenia occurs in 1% of the population, the risk rises sharply to 50% for a person whose identical twin has the disease.

Recent genome-wide association studies (GWAS) have identified more than 100 loci, or fixed positions on different chromosomes, associated with schizophrenia. That may not be where high-risk genes are located, however. The loci could be regulating the activity of the genes at a distance — nearby or very far away.

To solve the problem, Li, with first authors Rui Chen, PhD, research instructor in Molecular Physiology and Biophysics, and postdoctoral research fellow Quan Wang, PhD, developed a computational framework they called the “Integrative Risk Genes Selector.”

The framework pulled the top genes from previously reported loci based on their cumulative supporting evidence from multi-dimensional genomics data as well as gene networks.

Which genes have high rates of mutation? Which are expressed prenatally? These are the kinds of questions a genetic “detective” might ask to identify and narrow the list of “suspects.”

The result was a list of 104 high-risk genes, some of which encode proteins targeted in other diseases by drugs already on the market. One gene is suspected in the development of autism spectrum disorder.

Much work remains to be done. But, said Chen, “Our framework can push GWAS a step forward … to further identify genes.” It also could be employed to help track down genetic suspects in other complex diseases.

Also contributing to the study were Li’s lab members Qiang Wei, PhD, Ying Ji and Hai Yang, PhD; VGI investigators Xue Zhong, PhD, Ran Tao, PhD, James Sutcliffe, PhD, and VGI Director Nancy Cox, PhD.

Chen also credits investigators in the Vanderbilt Center for Neuroscience Drug Discovery — Colleen Niswender, PhD, Branden Stansley, PhD, and center Director P. Jeffrey Conn, PhD — for their critical input.

Funding: The study was supported by the Vanderbilt Analysis Center for the Genome Sequencing Program and National Institutes of Health grant HG009086.

https://neurosciencenews.com/high-risk-schizophrenia-genes-12021/

In a small study of patients referred to the Johns Hopkins Early Psychosis Intervention Clinic (EPIC), researchers report that about half the people referred to the clinic with a schizophrenia diagnosis did not actually have schizophrenia. People who reported hearing voices or having anxiety were the ones more likely to be misdiagnosed, according to the study published in the Journal of Psychiatric Practice.

The researchers say that therapies can vary widely for people with schizophrenia, bipolar disorder, major depression or other serious types of mental illness, and that misdiagnosis can lead to inappropriate or delayed treatment.

The findings, the researchers say, suggest that second opinions at a specialised schizophrenia clinic after initial diagnosis are wise efforts to reduce the risk of misdiagnosis, and ensure prompt and appropriate patient treatment.

“Because we’ve shined a spotlight in recent years on emerging and early signs of psychosis, diagnosis of schizophrenia is like a new fad, and it’s a problem especially for those who are not schizophrenia specialists because symptoms can be complex and misleading,” says Krista Baker, LCPC, Johns Hopkins Medicine, Baltimore, Maryland. “Diagnostic errors can be devastating for people, particularly the wrong diagnosis of a mental disorder,” she adds.

According to the National Institute of Mental Health, schizophrenia affects an estimated 0.5% of the world population, and is more common in men. It typically arises in the late adolescences, 20s and even as late as the early 30s in women. Symptoms such as disordered thinking, hallucinations, delusions, reduced emotions and unusual behaviours can be disabling, and drug treatments often create difficult side effects.

The new study was prompted in part by anecdotal evidence among healthcare providers in Baker’s specialty clinic that a fair number of people were being seen who were misdiagnosed. These patients usually had other mental illnesses, such as depression.

To see if there was rigorous evidence of such a trend, the researchers looked at patient data from 78 cases referred to EPIC for consultation between February 2011 and July 2017. Patients were an average age of 19, and about 69% were men, 74% were white, 12% African American and 14% were another ethnicity. Patients were referred to the clinic by general psychiatrists, outpatient psychiatric centres, primary care physicians, nurse practitioners, neurologists or psychologists.

Each consultation by the clinic took 3 to 4 hours, and included interviews with the patient and the family, physical exams, questionnaires, and medical and psychosocial histories.

Of the patients referred to the clinic, 54 people came with a predetermined diagnosis of a schizophrenia spectrum disorder. Of those, 26 received a confirmed diagnosis of a schizophrenia spectrum disorder following their consultation with the EPIC team, which is composed of clinicians and psychiatrists. Of the 54 cases, 51% were rediagnosed by clinic staff as having anxiety or mood disorders. Anxiety symptoms were prominent in 14 of the misdiagnosed patients.

One of the other most common symptoms that the researchers believe may have contributed to misdiagnosis of schizophrenia was hearing voices, as almost all incorrectly diagnosed patients reported auditory hallucinations.

“Hearing voices is a symptom of many different conditions, and sometimes it is just a fleeting phenomenon with little significance,” says Russell L. Margolis, MD, Johns Hopkins Schizophrenia Center, Johns Hopkins University School of Medicine, Baltimore, Maryland. “At other times when someone reports ‘hearing voices’ it may be a general statement of distress rather than the literal experience of hearing a voice. The key point is that hearing voices on its own doesn’t mean a diagnosis of schizophrenia.”

In speculating about other reasons why there might be so many misdiagnoses, the researchers say that it could be due to overly simplified application of criteria listed in the Diagnostic Statistical Manual of Mental Disorders, a standard guide to the diagnosis of psychiatric disorders.

“Electronic medical record systems, which often use pull-down diagnostic menus, increase the likelihood of this type of error,” says Dr. Margolis, who refers to the problem as “checklist psychiatry.”

“The big take-home message from our study is that careful consultative services by experts are important and likely underutilised in psychiatry,” says Dr. Margolis. “Just as a primary care clinician would refer a patient with possible cancer to an oncologist or a patient with possible heart disease to a cardiologist, it’s important for general mental health practitioners to get a second opinion from a psychiatry specialty clinic like ours for patients with confusing, complicated or severe conditions. This may minimise the possibility that a symptom will be missed or overinterpreted.”

Dr. Margolis cautioned that the study was limited to patients evaluated in 1 clinic. Nonetheless, he was encouraged by the willingness of so many patients, their families and their clinicians to ask for a second opinion from the Johns Hopkins clinic. If further study confirms their findings, it would lend support to the belief by the Johns Hopkins team that overdiagnosis may be a national problem, because they see patients from across the country who travel to Johns Hopkins for an opinion. They hope to examine the experience of other specialty consultation clinics in the future.

Reference: doi: 10.1097/PRA.0000000000000363

SOURCE: Johns Hopkins Medicine

https://dgnews.docguide.com/reported-symptoms-anxiety-hearing-voices-most-common-reasons-misdiagnosis-schizophrenia?overlay=2&nl_ref=newsletter&pk_campaign=newsletter&nl_eventid=20124

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.

Mit-Dopamine-Tracking_0

By Anne Trafton

Dopamine, a signaling molecule used throughout the brain, plays a major role in regulating our mood, as well as controlling movement. Many disorders, including Parkinson’s disease, depression, and schizophrenia, are linked to dopamine deficiencies.

MIT neuroscientists have now devised a way to measure dopamine in the brain for more than a year, which they believe will help them to learn much more about its role in both healthy and diseased brains.

“Despite all that is known about dopamine as a crucial signaling molecule in the brain, implicated in neurologic and neuropsychiatric conditions as well as our abilty to learn, it has been impossible to monitor changes in the online release of dopamine over time periods long enough to relate these to clinical conditions,” says Ann Graybiel, an MIT Institute Professor, a member of MIT’s McGovern Institute for Brain Research, and one of the senior authors of the study.

Michael Cima, the David H. Koch Professor of Engineering in the Department of Materials Science and Engineering and a member of MIT’s Koch Institute for Integrative Cancer Research, and Rober Langer, the David H. Koch Institute Professor and a member of the Koch Institute, are also senior authors of the study. MIT postdoc Helen Schwerdt is the lead author of the paper, which appears in the Sept. 12 issue of Communications Biology.

Long-term sensing

Dopamine is one of many neurotransmitters that neurons in the brain use to communicate with each other. Traditional systems for measuring dopamine — carbon electrodes with a shaft diameter of about 100 microns — can only be used reliably for about a day because they produce scar tissue that interferes with the electrodes’ ability to interact with dopamine.

In 2015, the MIT team demonstrated that tiny microfabricated sensors could be used to measure dopamine levels in a part of the brain called the striatum, which contains dopamine-producing cells that are critical for habit formation and reward-reinforced learning.

Because these probes are so small (about 10 microns in diameter), the researchers could implant up to 16 of them to measure dopamine levels in different parts of the striatum. In the new study, the researchers wanted to test whether they could use these sensors for long-term dopamine tracking.

“Our fundamental goal from the very beginning was to make the sensors work over a long period of time and produce accurate readings from day to day,” Schwerdt says. “This is necessary if you want to understand how these signals mediate specific diseases or conditions.”

To develop a sensor that can be accurate over long periods of time, the researchers had to make sure that it would not provoke an immune reaction, to avoid the scar tissue that interferes with the accuracy of the readings.

The MIT team found that their tiny sensors were nearly invisible to the immune system, even over extended periods of time. After the sensors were implanted, populations of microglia (immune cells that respond to short-term damage), and astrocytes, which respond over longer periods, were the same as those in brain tissue that did not have the probes inserted.

In this study, the researchers implanted three to five sensors per animal, about 5 millimeters deep, in the striatum. They took readings every few weeks, after stimulating dopamine release from the brainstem, which travels to the striatum. They found that the measurements remained consistent for up to 393 days.

“This is the first time that anyone’s shown that these sensors work for more than a few months. That gives us a lot of confidence that these kinds of sensors might be feasible for human use someday,” Schwerdt says.

Paul Glimcher, a professor of physiology and neuroscience at New York University, says the new sensors should enable more researchers to perform long-term studies of dopamine, which is essential for studying phenomena such as learning, which occurs over long time periods.

“This is a really solid engineering accomplishment that moves the field forward,” says Glimcher, who was not involved in the research. “This dramatically improves the technology in a way that makes it accessible to a lot of labs.”

Monitoring Parkinson’s

If developed for use in humans, these sensors could be useful for monitoring Parkinson’s patients who receive deep brain stimulation, the researchers say. This treatment involves implanting an electrode that delivers electrical impulses to a structure deep within the brain. Using a sensor to monitor dopamine levels could help doctors deliver the stimulation more selectively, only when it is needed.

The researchers are now looking into adapting the sensors to measure other neurotransmitters in the brain, and to measure electrical signals, which can also be disrupted in Parkinson’s and other diseases.

“Understanding those relationships between chemical and electrical activity will be really important to understanding all of the issues that you see in Parkinson’s,” Schwerdt says.

The research was funded by the National Institute of Biomedical Imaging and Bioengineering, the National Institute of Neurological Disorders and Stroke, the Army Research Office, the Saks Kavanaugh Foundation, the Nancy Lurie Marks Family Foundation, and Dr. Tenley Albright.

https://news.mit.edu/2018/brain-dopamine-tracking-sensors-0912

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

By Bahar Gholipour

Schizophrenia may have a special fingerprint in the brain, even before its symptoms fully emerge. Now, a new method of analyzing this fingerprint — found within the folds of the brain — could help predict which young adults at high risk for schizophrenia will go on to develop the illness, a new study suggests.

The method, which was based on MRI scans of the brain, looked at the correlation between the amount of folding in different brain areas, which can reflect the strength of underlying connections between those areas. Using this method, the researchers could predict the outcome of 79 high-risk individuals with 80 percent accuracy, they reported yesterday (April 25) in the journal JAMA Psychiatry.

These findings need to be confirmed in larger future studies before the method can be used to in the clinic, the researchers said. And even then, a simple brain scan on its own won’t be enough to predict the future — it has to be used in conjunction with other symptoms for which a person is seeking help. But the goal is to find what clues from the brain’s structure could help clinicians better identify and treat patients before they experience full-blown schizophrenia and drop out of schools or lose their jobs due to a psychotic episode, said study investigator Dr. Lena Palaniyappan, an associate professor of psychiatry at Western University in Ontario, Canada.

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What the Folds of Your Brain Could Tell You About Schizophrenia Risk
A simplified representation of the folds in different brain regions.
Credit: University Psychiatric Clinics Basel
Schizophrenia may have a special fingerprint in the brain, even before its symptoms fully emerge. Now, a new method of analyzing this fingerprint — found within the folds of the brain — could help predict which young adults at high risk for schizophrenia will go on to develop the illness, a new study suggests.

The method, which was based on MRI scans of the brain, looked at the correlation between the amount of folding in different brain areas, which can reflect the strength of underlying connections between those areas. Using this method, the researchers could predict the outcome of 79 high-risk individuals with 80 percent accuracy, they reported yesterday (April 25) in the journal JAMA Psychiatry.

These findings need to be confirmed in larger future studies before the method can be used to in the clinic, the researchers said. And even then, a simple brain scan on its own won’t be enough to predict the future — it has to be used in conjunction with other symptoms for which a person is seeking help. But the goal is to find what clues from the brain’s structure could help clinicians better identify and treat patients before they experience full-blown schizophrenia and drop out of schools or lose their jobs due to a psychotic episode, said study investigator Dr. Lena Palaniyappan, an associate professor of psychiatry at Western University in Ontario, Canada. [10 Things You Didn’t Know About the Brain]

Schizophrenia is a mental disorder characterized by psychotic episodes involving delusional thoughts and distorted perception. It is often preceded by subtle symptoms: A teenager who is withdrawn and suspicious, has anxiety, depression or sleep problems, and who experiences subtle changes in thinking and perception may be deemed by a doctor to be at high risk for developing schizophrenia in the next two or three years. But having these symptoms, which overlap with those of many other mental health conditions, doesn’t mean one will surely go on to develop schizophrenia — in fact, just about a third of individuals with these symptoms do.

“It’s really hard to know who is going to develop schizophrenia and who is not,” Palaniyappan told Live Science.

A wrinkle in the brain

Compared with other animals, the surface of the human brain is especially wrinkly — likely as a solution to fit a large brain inside a small skull. The patterns of folds in the brain’s surface, called the cortex, are determined before birth and change very little after the first or second year of life.

Previous studies of people with conditions such as schizophrenia and autism have detected local differences in folding patterns. For example, they have found a smoother surface in one brain region or a more wrinkled one in another, when comparing people with these conditions to the general population.

Palaniyappan and his colleagues examined all the brain regions and the relationship between their folding patterns. The idea is that the degree of folding would be similar between two brain areas if they are strongly interconnected. So, if an individual doesn’t show the same folding patterns as everyone else, it may suggest a problem in the wiring beneath the brain’s surface.

“Imagine two brain regions have a strong wire between them. If you cut the wire off, both of these regions would not be properly folded,” Palaniyappan said.

Sorting through scans

The team collected MRI brain scans from a group of people in Switzerland, who were on average 24 years old. The participants included 79 people with symptoms suggesting a high risk of schizophrenia and 44 healthy control subjects.

Then, the researchers followed the participants for four years and found 16 people in the high-risk group developed schizophrenia.

Looking back at the brain scans, the researchers found that 80 percent of the time, the relationship between folding patterns could correctly identify who developed schizophrenia and who didn’t. Those who did seemed to have a disorganized brain network — the folds of their cortical regions didn’t go hand in hand as much as the folds in the controls and in the high-risk people who didn’t develop the illness.

The earlier patients with schizophrenia receive psychotherapy or medication, the better they fare, according to a 2005 review of 30 studies published in the American Journal of Psychiatry. Early intervention may even change the course of the illness. One study published last year in Nature Neuropsychopharmacology, for instance, found a longer period of untreated symptoms was associated with weaker connectivity in the brain, especially in areas associated with responding to antipsychotic medications.

https://www.livescience.com/62414-brain-folds-schizophrenia.html