Neuroscience

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Posts tagged depression

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Low Strength Brain Stimulation May Be Effective for Depression
Brain stimulation treatments, like electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), are often effective for the treatment of depression. Like antidepressant medications, however, they typically have a delayed onset. For example, a patient may receive several weeks of regular ECT treatments before a full response is achieved.
Thus, there is an impetus to develop antidepressant treatments that act to rapidly improve mood.
Low field magnetic stimulation (LFMS) is one such potential new treatment with rapid mood-elevating effects, as reported by researchers at Harvard Medical School and Weill Cornell Medical College.
"LFMS is unlike any current treatment. It uses magnetic fields that are a fraction of the strength but at higher frequency than the electromagnetic fields used in TMS and ECT," explained first author Dr. Michael Rohan.
Indeed, the potential antidepressant properties of LFMS were discovered accidentally, while researchers were conducting an imaging study in healthy volunteers. This led Rohan and his colleagues to conduct a preliminary study in which they identified the imaging parameters that seemed to be causing the antidepressant effect.
They then designed and constructed a portable LFMS device, which delivers a low strength, high frequency, electromagnetic field waveform to the brain. The next step was to test the device in depressed patients, the results of which are published in the current issue of Biological Psychiatry.
A total of 63 currently depressed patients, diagnosed with either major depressive disorder or bipolar disorder, participated in the study and were randomized to receive a single 20-minute treatment of real LFMS or sham LFMS, where the device was on but the electromagnetic fields were inactive. Since neither the patients nor the researchers knew which treatment each person actually received, the true effect of the LFMS could be measured.
An immediate and substantial improvement in mood was observed in the patients who received real LFMS, compared to those who received the sham treatment. There were no reported side effects.
This finding suggests that LFMS may have the potential to provide immediate relief of depressed mood, perhaps even in emergency situations. It also confirms the success of the device’s design.
"The idea that weak electrical stimulation of the brain could produce beneficial effects on depression symptoms is somewhat surprising," said Dr. John Krystal, Editor of Biological Psychiatry. “Yet the data make a compelling case that this safe approach deserves further study.”
Rohan confirmed that additional research is underway to find the best parameters for LFMS use in the clinical treatment of depression. Further research will also be necessary to evaluate the effects of multiple compared to single treatments, and how long the antidepressant effects last following treatment.

Low Strength Brain Stimulation May Be Effective for Depression

Brain stimulation treatments, like electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), are often effective for the treatment of depression. Like antidepressant medications, however, they typically have a delayed onset. For example, a patient may receive several weeks of regular ECT treatments before a full response is achieved.

Thus, there is an impetus to develop antidepressant treatments that act to rapidly improve mood.

Low field magnetic stimulation (LFMS) is one such potential new treatment with rapid mood-elevating effects, as reported by researchers at Harvard Medical School and Weill Cornell Medical College.

"LFMS is unlike any current treatment. It uses magnetic fields that are a fraction of the strength but at higher frequency than the electromagnetic fields used in TMS and ECT," explained first author Dr. Michael Rohan.

Indeed, the potential antidepressant properties of LFMS were discovered accidentally, while researchers were conducting an imaging study in healthy volunteers. This led Rohan and his colleagues to conduct a preliminary study in which they identified the imaging parameters that seemed to be causing the antidepressant effect.

They then designed and constructed a portable LFMS device, which delivers a low strength, high frequency, electromagnetic field waveform to the brain. The next step was to test the device in depressed patients, the results of which are published in the current issue of Biological Psychiatry.

A total of 63 currently depressed patients, diagnosed with either major depressive disorder or bipolar disorder, participated in the study and were randomized to receive a single 20-minute treatment of real LFMS or sham LFMS, where the device was on but the electromagnetic fields were inactive. Since neither the patients nor the researchers knew which treatment each person actually received, the true effect of the LFMS could be measured.

An immediate and substantial improvement in mood was observed in the patients who received real LFMS, compared to those who received the sham treatment. There were no reported side effects.

This finding suggests that LFMS may have the potential to provide immediate relief of depressed mood, perhaps even in emergency situations. It also confirms the success of the device’s design.

"The idea that weak electrical stimulation of the brain could produce beneficial effects on depression symptoms is somewhat surprising," said Dr. John Krystal, Editor of Biological Psychiatry. “Yet the data make a compelling case that this safe approach deserves further study.”

Rohan confirmed that additional research is underway to find the best parameters for LFMS use in the clinical treatment of depression. Further research will also be necessary to evaluate the effects of multiple compared to single treatments, and how long the antidepressant effects last following treatment.

Filed under brain stimulation depression electromagnetic field antidepressants neuroscience science

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Tiny Molecule Could Help Diagnose and Treat Mental Disorders
Scientists “fingerprint” a culprit in depression, anxiety and other mood disorders
According to the World Health Organization, such mood disorders as depression affect some 10% of the world’s population and are associated with a heavy burden of disease. That is why numerous scientists around the world have invested a great deal of effort in understanding these diseases. Yet the molecular and cellular mechanisms that underlie these problems are still only partly understood.
The existing anti-depressants are not good enough: Some 60-70% of patients get no relief from them. For the other 30-40%, that relief is often incomplete, and they must take the drugs for a long period before feeling any effects. In addition, there are many side effects associated with the drugs. New and better drugs are clearly needed, an undertaking that requires, first and foremost, a better understanding of the processes and causes underlying the disorders.
The Weizmann Institute’s Prof. Alon Chen, together with his then PhD student Dr. Orna Issler, investigated the molecular mechanisms of the brain’s serotonin system, which, when misregulated, is involved in depression and anxiety disorders. Chen and his colleagues researched the role of microRNA molecules (small, non-coding RNA molecules that regulate various cellular activities) in the nerve cells that produce serotonin. They succeeded in identifying, for the first time, the unique “fingerprints” of a microRNA molecule that acts on the serotonin-producing nerve cells. Combining bioinformatics methods with experiments, the researchers found a connection between this particular microRNA, (miR135), and two proteins that play a key role in serotonin production and the regulation of its activities. The findings appeared today in Neuron.
The scientists noted that in the area of the brain containing the serotonin-producing nerve cells, miR135 levels increased when antidepressant compounds were introduced. Mice that were genetically engineered to produce higher-than-average amounts of the microRNA were more resistant to constant stress: They did not develop any of the behaviors associated with chronic stress, such as anxiety or depression, which would normally appear. In contrast, mice that expressed low levels of miR135 exhibited more of these behaviors; in addition, their response to antidepressants was weaker. In other words, the brain needs the proper miR135 levels – low enough to enable a healthy stress response and high enough to avoid depression or anxiety disorders and to respond to serotonin-boosting antidepressants. When this idea was tested on human blood samples, the researchers found that subjects who suffered from depression had unusually low miR135 levels in their blood. On closer inspection, the scientists discovered that the three genes involved in producing miR135 are located in areas of the genome that are known to be associated with risk factors for bipolar mood disorders.
These findings suggest that miR135 could be a useful therapeutic molecule – both as a blood test for depression and related disorders, and as a target whose levels might be raised in patients. Yeda Research and Development Co. Ltd., the technology transfer arm of the Weizmann Institute, has applied for a patent connected to these findings and recently licensed the rights to miCure Therapeutics to develop a drug and diagnostic method. After completing preclinical trials, the company hopes to begin clinical trials in humans.

Tiny Molecule Could Help Diagnose and Treat Mental Disorders

Scientists “fingerprint” a culprit in depression, anxiety and other mood disorders

According to the World Health Organization, such mood disorders as depression affect some 10% of the world’s population and are associated with a heavy burden of disease. That is why numerous scientists around the world have invested a great deal of effort in understanding these diseases. Yet the molecular and cellular mechanisms that underlie these problems are still only partly understood.

The existing anti-depressants are not good enough: Some 60-70% of patients get no relief from them. For the other 30-40%, that relief is often incomplete, and they must take the drugs for a long period before feeling any effects. In addition, there are many side effects associated with the drugs. New and better drugs are clearly needed, an undertaking that requires, first and foremost, a better understanding of the processes and causes underlying the disorders.

The Weizmann Institute’s Prof. Alon Chen, together with his then PhD student Dr. Orna Issler, investigated the molecular mechanisms of the brain’s serotonin system, which, when misregulated, is involved in depression and anxiety disorders. Chen and his colleagues researched the role of microRNA molecules (small, non-coding RNA molecules that regulate various cellular activities) in the nerve cells that produce serotonin. They succeeded in identifying, for the first time, the unique “fingerprints” of a microRNA molecule that acts on the serotonin-producing nerve cells. Combining bioinformatics methods with experiments, the researchers found a connection between this particular microRNA, (miR135), and two proteins that play a key role in serotonin production and the regulation of its activities. The findings appeared today in Neuron.

The scientists noted that in the area of the brain containing the serotonin-producing nerve cells, miR135 levels increased when antidepressant compounds were introduced. Mice that were genetically engineered to produce higher-than-average amounts of the microRNA were more resistant to constant stress: They did not develop any of the behaviors associated with chronic stress, such as anxiety or depression, which would normally appear. In contrast, mice that expressed low levels of miR135 exhibited more of these behaviors; in addition, their response to antidepressants was weaker. In other words, the brain needs the proper miR135 levels – low enough to enable a healthy stress response and high enough to avoid depression or anxiety disorders and to respond to serotonin-boosting antidepressants. When this idea was tested on human blood samples, the researchers found that subjects who suffered from depression had unusually low miR135 levels in their blood. On closer inspection, the scientists discovered that the three genes involved in producing miR135 are located in areas of the genome that are known to be associated with risk factors for bipolar mood disorders.

These findings suggest that miR135 could be a useful therapeutic molecule – both as a blood test for depression and related disorders, and as a target whose levels might be raised in patients. Yeda Research and Development Co. Ltd., the technology transfer arm of the Weizmann Institute, has applied for a patent connected to these findings and recently licensed the rights to miCure Therapeutics to develop a drug and diagnostic method. After completing preclinical trials, the company hopes to begin clinical trials in humans.

Filed under depression mood disorders serotonin microRNA miR135 antidepressants neuroscience science

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Researchers identify new compound to treat depression
There is new hope for people suffering from depression. Researchers have identified a compound, hydroxynorketamine (HNK), that may treat symptoms of depression just as effectively and rapidly as ketamine, without the unwanted side effects associated with the psychoactive drug, according to a study in the July issue of Anesthesiology, the official medical journal of the American Society of Anesthesiologists® (ASA®).  Interestingly, use of HNK may also serve as a future therapeutic approach for treating neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases, the authors note.
“The clinical use of ketamine therapy for depression is limited because the drug is administered intravenously and may produce adverse effects such as hallucinations and sedation to the point of anesthesia,” said Irving Wainer, Ph.D., senior investigator with the Intramural Research Program at the National Institute on Aging, Baltimore. “We found that the HNK compound significantly contributes to the anti-depressive effects of ketamine in animals, but doesn’t produce the sedation or anesthesia, which makes HNK an attractive alternative as an antidepressant in humans.”
HNK is one of several different compounds produced when ketamine, an anesthesia medicine-turned-antidepressant, is broken down (metabolized) in the body. Using a rat model, researchers tested HNK to see if the compound alone could produce the same beneficial effects attributed to ketamine without ketamine’s unwanted side effects. 
In the study, rats were given intravenous doses of ketamine, HNK and another compound produced by ketamine metabolism known as norketamine. The effect each had on stimulating certain cellular pathways of the rats’ brains was examined after 20, 30 and 60 minutes.  Brain tissue from drug-free rats was used as a control.
Researchers found the compound HNK, like ketamine, not only produced potent and rapid antidepressant effects, but also stimulated neuro-regenerative pathways and initiated the regrowth of neurons in rats’ brains. HNK also appears to have several advantages over ketamine in that it is 1,000 times more potent, does not act as an anesthetic agent, and can be taken by mouth, the authors report. 
Surprisingly, HNK was also found to reduce the production of D-serine, a chemical found in the body, overproduction of which is associated with neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. HNK’s ability to reduce the production of D-serine, while stimulating the regeneration of neuron connections in the brain, may present a potential new therapeutic approach to the treatment of these disorders. 
“HNK’s unique properties increase the possibility of the development of a self-administered, daily treatment that works quickly and can be taken at home for a variety of central nervous system diseases,” said Dr. Wainer.  “This is a very exciting discovery and we hope that the results of this study will enable future investigations into this potentially therapeutic and important compound.”
Dr. Wainer and several of the study’s authors are listed as co-inventors on a patent application for the use of ketamine compounds in the treatment of bipolar disorder and major depression. 

Researchers identify new compound to treat depression

There is new hope for people suffering from depression. Researchers have identified a compound, hydroxynorketamine (HNK), that may treat symptoms of depression just as effectively and rapidly as ketamine, without the unwanted side effects associated with the psychoactive drug, according to a study in the July issue of Anesthesiology, the official medical journal of the American Society of Anesthesiologists® (ASA®).  Interestingly, use of HNK may also serve as a future therapeutic approach for treating neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases, the authors note.

“The clinical use of ketamine therapy for depression is limited because the drug is administered intravenously and may produce adverse effects such as hallucinations and sedation to the point of anesthesia,” said Irving Wainer, Ph.D., senior investigator with the Intramural Research Program at the National Institute on Aging, Baltimore. “We found that the HNK compound significantly contributes to the anti-depressive effects of ketamine in animals, but doesn’t produce the sedation or anesthesia, which makes HNK an attractive alternative as an antidepressant in humans.”

HNK is one of several different compounds produced when ketamine, an anesthesia medicine-turned-antidepressant, is broken down (metabolized) in the body. Using a rat model, researchers tested HNK to see if the compound alone could produce the same beneficial effects attributed to ketamine without ketamine’s unwanted side effects. 

In the study, rats were given intravenous doses of ketamine, HNK and another compound produced by ketamine metabolism known as norketamine. The effect each had on stimulating certain cellular pathways of the rats’ brains was examined after 20, 30 and 60 minutes.  Brain tissue from drug-free rats was used as a control.

Researchers found the compound HNK, like ketamine, not only produced potent and rapid antidepressant effects, but also stimulated neuro-regenerative pathways and initiated the regrowth of neurons in rats’ brains. HNK also appears to have several advantages over ketamine in that it is 1,000 times more potent, does not act as an anesthetic agent, and can be taken by mouth, the authors report. 

Surprisingly, HNK was also found to reduce the production of D-serine, a chemical found in the body, overproduction of which is associated with neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases. HNK’s ability to reduce the production of D-serine, while stimulating the regeneration of neuron connections in the brain, may present a potential new therapeutic approach to the treatment of these disorders. 

“HNK’s unique properties increase the possibility of the development of a self-administered, daily treatment that works quickly and can be taken at home for a variety of central nervous system diseases,” said Dr. Wainer.  “This is a very exciting discovery and we hope that the results of this study will enable future investigations into this potentially therapeutic and important compound.”

Dr. Wainer and several of the study’s authors are listed as co-inventors on a patent application for the use of ketamine compounds in the treatment of bipolar disorder and major depression. 

Filed under hydroxynorketamine ketamine depression neurodegenerative diseases norketamine medicine science

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A tiny molecule may help battle depression

Levels of a small molecule found only in humans and in other primates are lower in the brains of depressed individuals, according to researchers at McGill University and the Douglas Institute. This discovery may hold a key to improving treatment options for those who suffer from depression.

image

Depression is a common cause of disability, and while viable medications exist to treat it, finding the right medication for individual patients often amounts to trial and error for the physician. In a new study to be published in the journal Nature Medicine, Dr. Gustavo Turecki, a psychiatrist at the Douglas and professor in the Faculty of Medicine, Department of Psychiatry at McGill, together with his team, discovered that the levels of a tiny molecule, miR-1202, may provide a marker for depression and help detect individuals who are likely to respond to antidepressant treatment.

“Using samples from the Douglas Bell-Canada Brain Bank, we examined brain tissues from individuals who were depressed and compared them with brain tissues from psychiatrically healthy individuals, says Turecki, who is also Director of the McGill Group for Suicide Studies, “We identified this molecule, a microRNA known as miR-1202, only found in humans and primates and discovered that it regulates an important receptor of the neurotransmitter glutamate”.

The team conducted a number of experiments that showed that antidepressants change the levels of this microRNA. “In our clinical trials with living depressed individuals treated with citalopram, a commonly prescribed antidepressant, we found lower levels in depressed individuals compared to the non-depressed individuals before treatment,” says Turecki. “Clearly, microRNA miR-1202 increased as the treatment worked and individuals no longer felt depressed.”

Antidepressant drugs are the most common treatment for depressive episodes, and are among the most prescribed medications in North America. “Although antidepressants are clearly effective, there is variability in how individuals respond to antidepressant treatment,” says Turecki, “We found that miR-1202 is different in individuals with depression and particularly, among those patients who eventually will respond to antidepressant treatment”.

The discovery may provide “a potential target for the development of new and more effective antidepressant treatments,” he adds.

(Source: mcgill.ca)

Filed under depression miR-1202 gene expression glutamate antidepressants neuroscience science

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(Image caption: Researchers at Cold Spring Harbor Laboratory have identified the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (green, left image), become hyperactive in depressed mice (right panel is close-up of left, yellow indicates activation). The team showed that this enhanced activity in fact causes depression.)
Dealing with stress – to cope or to quit?
We all deal with stress differently. For many of us, stress is a great motivator, spurring a renewed sense of vigor to solve life’s problems. But for others, stress triggers depression. We become overwhelmed, paralyzed by hopelessness and defeat. Up to 20% of us will struggle with depression at some point in life, and researchers are actively working to understand how and why this debilitating mental disease develops.
Today, a team of researchers at Cold Spring Harbor Laboratory (CSHL) led by Associate Professor Bo Li reveals a major insight into the neuronal basis of depression. They have identified the group of neurons in the brain that determines how a mouse responds to stress — whether with resilience or defeat.
For years, scientists have relied on brain imaging to look for neuronal changes during depression. They found that a region of the brain known as the medial prefrontal cortex (mPFC) becomes hyperactive in depressed people. This area of the brain is well known to play a role in the control of emotions and behavior, linking our feelings with our actions. But brain scans aren’t able to determine if increased activity in the mPFC causes depression, or if it is simply a byproduct of other neuronal changes. 
Dr. Li set out to identify the neuronal changes that underlie depression. In work published today in The Journal of Neuroscience,Li and his team, including Minghui Wang, Ph.D. and Zinaida Perova, Ph.D., used a mouse model for depression, known as “learned helplessness.” They combined this with a genetic trick to mark specific neurons that respond to stress. They discovered that neurons in the mPFC become highly excited in mice that are depressed. These same neurons are weakened in mice that aren’t deterred by stress – what scientists call resilient mice.
But the team still couldn’t be sure that enhanced signaling in the mPFC actually caused depression. To test this, they engineered mice to mimic the neuronal conditions they found in depressed mice. “We artificially enhanced the activity of these neurons using a powerful method known as chemical genetics,” says Li. “The results were remarkable: once-strong and resilient mice became helpless, showing all of the classic signs of depression.”
These results help explain how one promising new treatment for depression works and may lead to improvements in the treatment.
Doctors have had some success with deep brain stimulation (DBS), which suppresses the activity of neurons in a very specific portion of the brain. “We hope that our work will make DBS even more targeted and powerful,” says Li, “and we are working to develop additional strategies based upon the activity of the mPFC to treat depression.”
Next, Li is looking forward to exploring how the neurons in the mPFC become hyperactive in helpless mice. “These active neurons are surrounded by inhibitory neurons,” says Li. “Are the inhibitory neurons failing? Or are the active neurons somehow able to bypass their controls? These are some of the many open questions we are pursuing to understand the how depression develops.”

(Image caption: Researchers at Cold Spring Harbor Laboratory have identified the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (green, left image), become hyperactive in depressed mice (right panel is close-up of left, yellow indicates activation). The team showed that this enhanced activity in fact causes depression.)

Dealing with stress – to cope or to quit?

We all deal with stress differently. For many of us, stress is a great motivator, spurring a renewed sense of vigor to solve life’s problems. But for others, stress triggers depression. We become overwhelmed, paralyzed by hopelessness and defeat. Up to 20% of us will struggle with depression at some point in life, and researchers are actively working to understand how and why this debilitating mental disease develops.

Today, a team of researchers at Cold Spring Harbor Laboratory (CSHL) led by Associate Professor Bo Li reveals a major insight into the neuronal basis of depression. They have identified the group of neurons in the brain that determines how a mouse responds to stress — whether with resilience or defeat.

For years, scientists have relied on brain imaging to look for neuronal changes during depression. They found that a region of the brain known as the medial prefrontal cortex (mPFC) becomes hyperactive in depressed people. This area of the brain is well known to play a role in the control of emotions and behavior, linking our feelings with our actions. But brain scans aren’t able to determine if increased activity in the mPFC causes depression, or if it is simply a byproduct of other neuronal changes. 

Dr. Li set out to identify the neuronal changes that underlie depression. In work published today in The Journal of Neuroscience,Li and his team, including Minghui Wang, Ph.D. and Zinaida Perova, Ph.D., used a mouse model for depression, known as “learned helplessness.” They combined this with a genetic trick to mark specific neurons that respond to stress. They discovered that neurons in the mPFC become highly excited in mice that are depressed. These same neurons are weakened in mice that aren’t deterred by stress – what scientists call resilient mice.

But the team still couldn’t be sure that enhanced signaling in the mPFC actually caused depression. To test this, they engineered mice to mimic the neuronal conditions they found in depressed mice. “We artificially enhanced the activity of these neurons using a powerful method known as chemical genetics,” says Li. “The results were remarkable: once-strong and resilient mice became helpless, showing all of the classic signs of depression.”

These results help explain how one promising new treatment for depression works and may lead to improvements in the treatment.

Doctors have had some success with deep brain stimulation (DBS), which suppresses the activity of neurons in a very specific portion of the brain. “We hope that our work will make DBS even more targeted and powerful,” says Li, “and we are working to develop additional strategies based upon the activity of the mPFC to treat depression.”

Next, Li is looking forward to exploring how the neurons in the mPFC become hyperactive in helpless mice. “These active neurons are surrounded by inhibitory neurons,” says Li. “Are the inhibitory neurons failing? Or are the active neurons somehow able to bypass their controls? These are some of the many open questions we are pursuing to understand the how depression develops.”

Filed under stress prefrontal cortex depression deep brain stimulation animal model learned helplessness psychology neuroscience science

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Antidepressant use in pregnancy may be associated with structural changes in the infant brain

A new study by University of North Carolina at Chapel Hill researchers found that children of depressed mothers treated with a group of antidepressants called selective serotonin reuptake inhibitors (SSRIs) during pregnancy were more likely to develop Chiari type 1 malformations than were children of mothers with no history of depression.

However, the researchers cautioned, doctors treating pregnant women for depression should not change their prescribing practices based on the results of this study.

“Our results can be interpreted two ways,” said Rebecca Knickmeyer, PhD, assistant professor of psychiatry in the UNC School of Medicine and lead author of the study published May 19 in the journal Neuropsychopharmacology. “Either SSRIs increase risk for Chiari type 1 malformations, or other factors associated with SSRI treatment during pregnancy, such as severity of depression itself, increase risk. Additional research into the effects of depression during pregnancy, with and without antidepressant treatment is urgently needed.”

A Chiari type 1 malformation is a condition in which brain tissue in the cerebellum (a part of the brain that controls balance, motor systems, and some cognitive functions) extends into the spinal canal. About 5 percent of children have a Chiari type 1 malformation. Most do not have any problems because of it, but some develop symptoms such as headache and balance problems. In severe cases surgery may be necessary.

The study’s results are based on an analysis of magnetic resonance imaging (MRI) brain scans done on four groups of children at UNC Hospitals. Thirty-three children whose mothers were diagnosed with depression and took SSRI antidepressant medications, such as sertraline and fluoxetine, were compared to 66 children whose mothers had no history of depression. In addition, 30 children whose mothers were diagnosed with depression but did not take SSRIs were compared to 60 children whose mothers had no history of depression.

Eighteen percent of the children whose mothers took SSRIs during pregnancy had Chiari type 1 malformations, compared to 3 percent among children whose mothers had no history of depression. The rate of Chiari type 1 malformations was highest in children whose mothers reported a family history of depression in addition to treatment with SSRIs during pregnancy, suggesting an important role for genes as well as environment. Duration of SSRI exposure and SSRI exposure at conception also appeared to increase risk.

“These results raise many interesting questions, and there are many things we still don’t know,” said study co-author Samantha Meltzer-Brody, MD, MPH, associate professor of psychiatry in the UNC School of Medicine and director of UNC’s Perinatal Psychiatry Program. “For example, we do not know how many of these children will go on to develop symptoms of Chiari type 1 malformations. What we do know is that untreated depression can be very harmful for women and their babies, and so we strongly encourage pregnant women who are being treated for depression to continue with their treatment,” she said.

Knickmeyer said that a decision to use antidepressants during pregnancy must be based on the balance between risks and benefits and that it is critical that health care providers and the public get accurate information on this topic. She also noted that a diagnosis of Chiari Type 1 is often delayed due to the non-specific nature of the symptoms. Thus, it may be valuable for families in this situation to know about the results of this study.

In addition, “Chiari type 1 malformations are somewhat common, but very little is known about what causes them,” said study co-author J. Keith Smith, MD, PhD, professor and vice chair of clinical research in UNC’s Department of Radiology. “Studies like this could give us new insight into that question.”

Filed under antidepressants SSRIs chiari I malformations pregnancy depression neuroscience science

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Depression top cause of illness in world’s teens, WHO report
Depression is the top global cause of illness and disability for adolescents, with suicide the third-biggest cause of death, the World Health Organization said on Wednesday.
The finding is in a new report by the UN agency, which has pulled together a wealth of published evidence with direct consultations with 10 to 19-year-olds around the world to assess the health issues that affect them.
“The world has not paid enough attention to the health of adolescents,” says Flavia Bustreo, head of the WHO’s family, women and children’s health division.
Read more

Depression top cause of illness in world’s teens, WHO report

Depression is the top global cause of illness and disability for adolescents, with suicide the third-biggest cause of death, the World Health Organization said on Wednesday.

The finding is in a new report by the UN agency, which has pulled together a wealth of published evidence with direct consultations with 10 to 19-year-olds around the world to assess the health issues that affect them.

“The world has not paid enough attention to the health of adolescents,” says Flavia Bustreo, head of the WHO’s family, women and children’s health division.

Read more

Filed under depression mental illness adolescents health

463 notes

Psilocybin inhibits the processing of negative emotions in the brain

When emotions are processed in a negatively biased manner in the brain, an individual is at risk to develop depression. Psilocybin, the bioactive component of the Mexican magic mushroom, seems to intervene positively in the emotion-processing mechanism. Even a small amount of the natural substance attenuates the processing of negative emotions and brightens mood as shown by UZH researchers using imaging methods.

Emotions like fear, anger, sadness, and joy enable people to adjust to their environment and react flexibly to stress and strain and are vital for cognitive processes, physiological reactions, and social behaviour. The processing of emotions is closely linked to structures in the brain, i.e. to what is known as the limbic system. Within this system the amygdala plays a central role – above all it processes negative emotions like anxiety and fear. If the activity of the amygdala becomes unbalanced, depression and anxiety disorders may develop.

Researchers at the Psychiatric University Hospital of Zurich have now shown that psilocybin, the bioactive component in the Mexican magic mushroom, influences the amygdala, thereby weakening the processing of negative stimuli. These findings could “point the way to novel approaches to treatment” comments the lead author Rainer Krähenmann on the results which have now been published in the renowned medical journal “Biological Psychiatry”.

Psilocybin inhibits the processing of negative emotions in the amygdala

The processing of emotions can be impaired by various causes and elicit mental disorders. Elevated activity of the amygdala in response to stimuli leads to the neurons strengthening negative signals and weakening the processing of positive ones. This mechanism plays an important role in the development of depression and anxiety disorders. Psilocybin intervenes specifically in this mechanism as shown by Dr. Rainer Krähenmann’s research team of the Neuropsychopharmacology and Brain Imaging Unit led by Prof. Dr. Franz Vollenweider.

Psilocybin positively influences mood in healthy individuals. In the brain, this substance stimulates specific docking sites for the messenger serotonin. The scientists therefore assumed that psilocybin exerts its mood-brightening effect via a change in the serotonin system in the limbic brain regions. This could, in fact, be demonstrated using functional magnetic resonance imaging (fMRI). “Even a moderate dose of psilocybin weakens the processing of negative stimuli by modifying amygdala activity in the limbic system as well as in other associated brain regions”, continues Krähenmann. The study clearly shows that the modulation of amygdala activity is directly linked to the experience of heightened mood.

Next study with depressive patients

According to Krähenmann, this observation is of major clinical importance. Depressive patients in particular react more to negative stimuli and their thoughts often revolve around negative contents. Hence, the neuropharmacologists now wish to elucidate in further studies whether psilocybin normalises the exaggerated processing of negative stimuli as seen in neuroimaging studies of depressed patients - and may consequently lead to improved mood in these patients.

Rainer Krähenmann considers research into novel approaches to treatment very important, because current available drugs for the treatment of depression and anxiety disorders are not effective in all patients and are often associated with unwanted side effects.

(Source: mediadesk.uzh.ch)

Filed under psilocybin emotions amygdala serotonin depression neuroscience science

984 notes

Depression is detectable in the blood
Researchers at the MedUni Vienna have demonstrated the possibility of using a blood test to detect depression. While blood tests for mental illnesses have until recently been regarded as impossible, a recent study clearly indicates that, in principle, depression can in fact be diagnosed in this way and this could become reality in the not too distant future.
Serotonin transporter (SERT) is a protein in the cell membrane that facilitates the transport of the neurotransmitter serotonin (popularly known as the “happiness hormone”) into the cell. In the brain, serotonin transporter regulates neural depression networks. Depressive conditions can frequently be caused by a lack of serotonin. As a result, the serotonin transporter is also the point of action for the major antidepressant drugs.
The serotonin transporter, however, also occurs in large quantities in numerous other organs such as the intestines or blood. Recent studies have shown that the serotonin transporter in the blood works in exactly the same way as in the brain. In the blood, it ensures that blood platelets maintain the appropriate concentration of serotonin in the blood plasma.
Researchers at the MedUni Vienna have now used functional magnetic resonance imaging of the brain and pharmacological investigations to demonstrate that there is a close relationship between the speed of the serotonin uptake in blood platelets and the function of a depression network in the brain.
This network is termed the “default mode network” because it is primarily active at rest and processes content with strong self-reference. Findings from recent years have also demonstrated that it is actively suppressed during complex thought processes, which is essential for adequate levels of concentration. Interestingly, patients with depression find it difficult to suppress this network during thought processes, leading to negative thoughts and ruminations as well as poor concentration.
“This is the first study that has been able to predict the activity of a major depression network in the brain using a blood test. While blood tests for mental illnesses have until recently been regarded as impossible, this study clearly shows that a blood test is possible in principle for diagnosing depression and could become reality in the not too distant future,” explains study leader Lukas Pezawas from the Department of Biological Psychiatry at the University Department of Psychiatry and Psychotherapy within the MedUni Vienna. This result means that the diagnosis of depression through blood tests could become reality in the not too distant future.

Depression is detectable in the blood

Researchers at the MedUni Vienna have demonstrated the possibility of using a blood test to detect depression. While blood tests for mental illnesses have until recently been regarded as impossible, a recent study clearly indicates that, in principle, depression can in fact be diagnosed in this way and this could become reality in the not too distant future.

Serotonin transporter (SERT) is a protein in the cell membrane that facilitates the transport of the neurotransmitter serotonin (popularly known as the “happiness hormone”) into the cell. In the brain, serotonin transporter regulates neural depression networks. Depressive conditions can frequently be caused by a lack of serotonin. As a result, the serotonin transporter is also the point of action for the major antidepressant drugs.

The serotonin transporter, however, also occurs in large quantities in numerous other organs such as the intestines or blood. Recent studies have shown that the serotonin transporter in the blood works in exactly the same way as in the brain. In the blood, it ensures that blood platelets maintain the appropriate concentration of serotonin in the blood plasma.

Researchers at the MedUni Vienna have now used functional magnetic resonance imaging of the brain and pharmacological investigations to demonstrate that there is a close relationship between the speed of the serotonin uptake in blood platelets and the function of a depression network in the brain.

This network is termed the “default mode network” because it is primarily active at rest and processes content with strong self-reference. Findings from recent years have also demonstrated that it is actively suppressed during complex thought processes, which is essential for adequate levels of concentration. Interestingly, patients with depression find it difficult to suppress this network during thought processes, leading to negative thoughts and ruminations as well as poor concentration.

“This is the first study that has been able to predict the activity of a major depression network in the brain using a blood test. While blood tests for mental illnesses have until recently been regarded as impossible, this study clearly shows that a blood test is possible in principle for diagnosing depression and could become reality in the not too distant future,” explains study leader Lukas Pezawas from the Department of Biological Psychiatry at the University Department of Psychiatry and Psychotherapy within the MedUni Vienna. This result means that the diagnosis of depression through blood tests could become reality in the not too distant future.

Filed under blood test depression mental illness default mode network serotonin neuroscience science

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New study links inflammation in those with PTSD to changes in microRNA

With a new generation of military veterans returning home from Iraq and Afghanistan, post-traumatic stress disorder (PTSD) has become a prominent concern in American medical institutions and the culture at-large. Estimates indicate that as many as 35 percent of personnel deployed to Iraq and Afghanistan suffer from PTSD. New research from the University of South Carolina School of Medicine is shedding light on how PTSD is linked to other diseases in fundamental and surprising ways.

The rise in PTSD has implications beyond the impact of the psychiatric disorder and its immediate consequences, which include elevated suicide risk and inability to lead a normal life, that result in approximately $3 billion in lost productivity every year. Over time, these PTSD patients will continue to experience increased risks of a myriad of medical conditions like cardiovascular disease, diabetes, gastrointestinal disease, fibromyalgia, musculoskeletal disorders and others, all of which share chronic inflammation as a common underlying cause.

The mechanisms that trigger PTSD, and that cause PTSD patients to suffer from higher rates of chronic-inflammation-related medical conditions remain unknown. Additionally, PTSD is incurable, and though there are available treatments, they are often not completely effective. In an effort to get to the root of PTSD, and begin to understand the links between PTSD and the secondary diseases that often come with it, a team at the University of South Carolina School of Medicine is investigating PTSD through the lens of inflammation. They have recently published findings of a new study, “Dysregulation in microRNA Expression is Associated with Alterations in Immune Functions in Combat Veterans with Post-traumatic Stress Disorder,” in the journal PLOS ONE.

In this study, led by Drs. Prakash Nagarkatti and Mitzi Nagarkatti, the authors investigated microRNA profiles and tried to establish a link between the microRNA and inflammation in combat veterans of the Persian Gulf, Iraq and Afghanistan wars who are PTSD patients at the Dorn VA Medical Center. MicroRNA are small, noncoding RNA that can switch human genes on and off, effectively controlling gene expression. Some specific types of microRNA are known to regulate genes involved in inflammation, making them a kind of marker that can indicate when inflammation is present.

The microRNA role in PTSD has not been investigated previous to this study, which found that the PTSD patients had significant alterations in microRNA expression. The study analyzed 1163 microRNA and found that the expression of microRNA that regulate genes involved in inflammation were altered in PTSD patients. The alterations were found to be linked to heightened inflammation in these patients.

Dr. Mitzi Nagarkatti sums up the significance of this study as follows: “We are very excited about these results. Thus far, no one had looked at the role of microRNA in the blood of PTSD patients. Thus, our finding that the alterations in these small molecules are connected to higher inflammation seen in these patients is very interesting and helps establish the connection between war trauma and microRNA changes.”

In addition to the alterations in microRNA expression, the study also found that PTSD patients had higher levels of inflammation caused by certain types of immune cells called T cells. These T cells produced higher levels of inflammatory mediators called cytokines, specifically interferon-gamma and interleukin-17. This finding was especially interesting because one of the inflammation-associated microRNAs, miR-125a, which specifically targets increased production of interferon-gamma, was found to have decreased expression in the PTSD patients studied. Overall, these results suggested that trauma may cause alterations in the expression of microRNA which promote inflammation in PTSD patients.

Commenting on this, Dr. Prakash Nagarkatti said, “These studies form the foundation to further analyze the role of microRNA in PTSD. Trauma experienced during war may trigger changes in microRNA which may in turn cause various clinical disorders seen in PTSD patients. Our long-term goal is to identify whether PTSD patients express a unique signature profile of microRNA which can be used towards early detection, prevention and treatment of PTSD.”

(Source: eurekalert.org)

Filed under PTSD inflammation microRNA cytokines T cells miR-125a depression neuroscience science

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