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PostPosted: Fri Sep 07, 2007 2:29 pm    Post subject: Depression May Be World's Most Disabling Disease

Depression May Be World's Most Disabling Disease
By Steven Reinberg, HealthDay Reporter

posted: 07 September 2007 01:29 pm ET

(HealthDay News) -- When compared with other chronic diseases, depression may well be the most disabling disease in the world, a new global study finds.

People with chronic physical diseases such as angina, arthritis, asthma and diabetes also fare far worse if they also suffer from depression, the team of international researchers found.

For the full article:
PostPosted: Fri Jun 08, 2007 9:42 am    Post subject: Brain holds clues to bipolar disorder

University of Pittsburgh Medical Center
7 June 2007

Brain holds clues to bipolar disorder

PITTSBURGH, June 7 -- Looking into the brain is yielding vital clues to understanding, diagnosing and treating bipolar disorder, according to findings being presented today at the Seventh International Conference on Bipolar Disorder. Two studies, featured in a press briefing held at 12:15 p.m., Thursday, June 7, have helped to identify novel pathways and markers for diagnosis and treatment of the disease.

The first study, presented by Husseini K. Manji, M.D., chief of the Laboratory of Molecular Pathophysiology at the National Institute of Mental Health (NIMH), suggests that bipolar disorder arises from abnormalities in neuronal plasticity cascades – the complex machinery inside of nerve cells that regulates numerous processes inside the body. Using animal and cellular models, Dr. Manji and colleagues at NIMH showed that disruptions in these pathways resulted in many of the core symptoms of bipolar disorder and explained many other observations about the disease. The findings suggest a new avenue for treating the underlying cause of bipolar, rather than treating flare-ups of depression or mania, and also provide new targets, for improved medications many of which are being tested in clinical trials.

Mary Phillips, M.D., professor of psychiatry at the University of Pittsburgh School of Medicine and director of functional neuroimaging in emotional disorders at Western Psychiatric Institute and Clinic of UPMC, will discuss the emerging role of brain imaging techniques in psychiatry in general as well as in bipolar disorder. Using neuroimaging, Dr. Phillips has identified patterns of abnormalities in the neural systems that underlie emotional processing and cognitive control unique to the bipolar brain. Such abnormalities are valuable biomarkers for the illness and have the potential to help clinicians diagnose bipolar disorder earlier and more efficiently. Dr. Phillips also will present data illustrating how imaging can be used to identify biomarkers and how these markers can help clinicians determine which patients will respond best to certain treatments. Neuroimaging also can help predict which patients of those who are genetically predisposed to bipolar disorder will develop symptoms of the disease.
PostPosted: Tue May 08, 2007 8:10 am    Post subject: Genetic roots of bipolar disorder revealed by first genome-w

NIH/National Institute of Mental Health
8 May 2007

Genetic roots of bipolar disorder revealed by first genome-wide study of illness

Targeting enzyme produced by a specific gene may lead to better medications
The likelihood of developing bipolar disorder depends in part on the combined, small effects of variations in many different genes in the brain, none of which is powerful enough to cause the disease by itself, a new study shows. However, targeting the enzyme produced by one of these genes could lead to development of new, more effective medications. The research was conducted by scientists at the National Institutes of Health's National Institute of Mental Health (NIMH), with others from the Universities of Heidelberg and Bonn and a number of U.S. facilities collaborating in a major project called the NIMH Genetics Initiative.

The study is the first to scan virtually all of the variations in human genes to find those associated with bipolar disorder. Results were published online May 8 in Molecular Psychiatry by Amber E. Baum, PhD, lead researcher Francis J. McMahon, MD, and colleagues.

"This is an example of how advances in genetics research feed into practical applications. This research would not have been possible a very few years ago. We now have a new molecular target scientists can investigate in their search for better medications for bipolar disorder," said NIH Director Elias A. Zerhouni, MD.

About 5.7 million American adults have bipolar disorder, which also is called manic-depressive illness. Symptoms include extremes in mood, from pronounced over-excitement and elation, often coupled with severe irritability, to depression. Children also may have the condition, usually in a more severe form than adults.

"We're beginning to get a foothold on the genetics of this complex brain disorder," said NIMH Director Thomas R. Insel, MD.

Most people occasionally have mood swings, but the shifts that occur in bipolar disorder, and the changes in behavior and energy level that accompany them, are sometimes disabling. Lithium and the other mood-stabilizing medications used to treat the condition help many patients.

But some people do not respond to these medications, and clinicians need more options so that they can tailor treatments to each patient. People inherit different gene variations, which may influence whether or not they respond to a given medication. Identifying and targeting these variations could help scientists develop additional medication options that take these differences into account.

One of the genes the researchers correlated with the disorder, DGKH, is active in a biochemical pathway through which lithium is thought to exert its therapeutic effects. The gene produces an enzyme (diacylglycerol kinase eta) that functions at a point closer to the root of the lithium-sensitive pathway than does the protein that lithium is thought to target. Scientists can now try to develop more effective medications by focusing on new compounds that act on the DGKH enzyme or regulate how much of the enzyme is produced. The DGKH gene is on chromosome 13.

Several other genes detected in the study produce proteins involved in this and other biochemical pathways thought to play a role in bipolar disorder. Understanding the effects that variations of these genes have on brain-cell function could lead to explanations of how they contribute to the condition and how it might be better prevented or treated.

"Treatments that target just a few of these genes or the proteins they make could yield substantial benefits for patients. Lithium is still the primary treatment for bipolar disorder, but DGKH is a promising target for new treatments that might be more effective and better tolerated," McMahon said.

The finding was enabled by recent genetics technology that allows researchers to scan, in a single experiment, thousands of genes for variations. Everyone has the same genes, but variations in them influence whether or not a person gets a specific disease. In this study, researchers compared variations found in the scans of 413 adults who had bipolar disorder with variations found in the scans of 563 healthy adults.

By pooling the genetic material of the adults with bipolar disorder, the U.S. researchers were able to scan the entire group at a small fraction of the cost of scanning each person's material individually. The genetic material of the healthy group was pooled and scanned separately, again at a fraction of the cost of individual scans. The researchers then zeroed in on the gene variations that occurred more often in the people with bipolar disorder and examined them individually.

An important issue in genetics research is that findings correlating specific genes with specific diseases in one population may not apply to other populations. This study addressed that issue by focusing on US participants of European ancestry, then repeating the study in a large group of patients in Germany. Similar outcomes were found in both populations, strengthening the validity of the results. A subsequent study is examining whether the results apply to other populations, and will look for common variations among them.

The researchers will soon make the results of their scans available, on a website, to other scientists who are pursuing this line of research.

For more NIMH information about bipolar disorder, visit

Coauthors of this report, including contributors from the National Institute on Aging (also part of the National Institutes of Health), are listed below:

Amber E. Baum, Nirmala Akula, Imer Cardona, Michael Cabanero, and Winston Corona
(NIMH Genetic Basis of Mood and Anxiety Disorders Unit, Mood and Anxiety Disorders Program)

Ben Klemens
(NIMH Genetic Basis of Mood and Anxiety Disorders Unit, Mood and Anxiety Disorders Program; The Brookings Institution)

Thomas G Schulze
(University of Heidelberg)

Sven Cichon,
( University of Bonn)

Marcella Rietschel
(University of Heidelberg)

Markus Nöthen
(University of Bonn)

A. Georgi
(University of Heidelberg)

Johannes Schumacher
(University of Bonn)

M Schwarz
(University of Heidelberg)

R. Abou Jamra, S. Höfels, and P. Propping
(University of Bonn)

Jaya Satagopan
(Memorial Sloan-Kettering Cancer Center)

NIMH Genetics Initiative Bipolar Disorder Consortium
(Johns Hopkins University School of Medicine, Baltimore, MD; University of California, Irvine and San Diego, CA; University of Chicago, Chicago, IL; University of Pennsylvania, Philadelphia, PA; Laboratory of Clinical Science, National Institute of Mental Health Intramural Research Program, Rush University Medical Center, Chicago, IL; Washington University School of Medicine, St. Louis, MO; University of Iowa Medical School, Iowa City, IA; Indiana University School of Medicine, Indianapolis, IN)

Sevilla Detera-Wadleigh
(NIMH Genetic Basis of Mood and Anxiety Disorders Unit, Mood and Anxiety Disorders Program)

John Hardy
(National Institute on Aging, National Institutes of Health)

McMahon, Francis J.
(NIMH Genetic Basis of Mood and Anxiety Disorders Unit, Mood and Anxiety Disorders Program)

Baum AE, Akula N, Cabanero M, Cardona I, Corona W, Klemens B, Schulze TG, Cichon S, Rietschel M, Nöthen MM, Georgi A, Schumacher J, Schwarz M, Jamra RA, Höfels S, Propping P, Satagopan J, NIMH Genetics Initiative Bipolar Disorder Consortium, Detere-Wadleigh SD, Hardy J, McMahon F. A genome-wide association study implicates diacylglycerol kinase eta (DGKH) and several other genes in the etiology of bipolar disorder. Molecular Psychiatry, online ahead of print, May 8, 2007.

The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website:

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
PostPosted: Tue May 01, 2007 8:12 am    Post subject: Delayed treatment of childhood-onset bipolar disorder result

Elsevier Health Sciences
1 May 2007

Delayed treatment of childhood-onset bipolar disorder results in negative outcome in adults

Study published in the Journal of Pediatrics tracks patients untreated on average more than 16 years

In bipolar disorder, also called manic-depressive disorder, a person experiences mood changes that fluctuate between periods of abnormally high energy and extreme depression. Bipolar disorder is estimated to affect approximately 1-3% of adults, but also can affect children and adolescents. Untreated, this disorder is associated with greater risk of drug and alcohol addiction, of interpersonal relationship difficulties, of school and, later, work problems, of engaging in risky behaviors, and of suicide. A study published in the May issue of The Journal of Pediatrics shows that childhood-onset bipolar disorder is more common than believed and often goes unrecognized and untreated for long periods of time, leading to lower quality of life and greater difficulty in treatment.

480 adults in the United States who were diagnosed with bipolar disorder completed questionnaires and were interviewed about their courses of illness. These adults were studied at an average age of 42 and had been ill for an average time of more than 20 years. Researchers from the National Institute of Mental Health of the National Institutes of Health and from other institutions determined the age of onset of manic or depressive symptoms and the age of first treatment in this group. The duration of time from onset of illness to first pharmacological treatment for depression or mania was available for 420 patients. For those who experienced the onset of bipolar disorder in childhood (under 13 years old), the average time before first treatment was more than 16 years (Figure). They experienced more days depressed, more days in which both mania and depression occurred within a 24-hour period (ultradian cycling), and greater number of manic and depressive episodes throughout their lives. The patients also had an increased risk of substance abuse, a greater lifetime risk of suicide attempts, higher prevalence of lifetime anxiety disorders, and greater resistance to treatment.

22% to 28% of the adults studied experienced the onset of bipolar disorder prior to the age of 13. In the interval between onset of illness and initial treatment, patients are at risk of disability and comorbid conditions such as anxiety and substance abuse. Moreover, some children with bipolar disorder are diagnosed with ADHD or depression and receive treatment for long periods of time with only stimulants or antidepressants, rather than combination medications such as mood stabilizers or atypical antipsychotics, as recommended in most treatment guidelines for bipolar disorder. As stated by Dr. Russell Scheffer from the Medical College of Wisconsin in an editorial that accompanies the study, “The information contained in this report and additional mounting evidence suggest that early detection, diagnosis, and treatment are essential for determining effective treatment outcomes and, subsequently, quality of life for those affected with bipolar disorder.” Earlier recognition and treatment of bipolar disorder in children and adolescents could positively impact the course of illness.

The study is reported in “The Poor Prognosis of Childhood Onset Bipolar Disorder” by Gabriele Simon Leverich, Robert M Post, M.D., Paul E Keck Jr., M.D., Lori L Altshuler, M.D., Mark A Frye, M.D., Ralph W Kupka, M.D., Ph.D., Willem A Nolen, M.D., Ph.D., Trisha Suppes, M.D., Ph.D., Susan L McElroy, M.D., Heinz Grunze, M.D., Kirk D Denicoff, M.D., Maria KM Moravec, B.S., David Luckenbaugh, M.A. from the National Institute of Mental Health, National Institutes of Health, Maryland, University of Cincinnati College of Medicine, Ohio, Altrecht Institute for Mental Health Care and University Hospital Groningen, The Netherlands, University of Texas-Southwestern Medical Center, Texas, and Psychiatrische Klinik der LMU, Germany. The editorial is titled “Childhood Onset Bipolar Disorder: A Role for Early Recognition and Treatment” by Russell E. Scheffer, M.D. from the Medical College of Wisconsin, Milwaukee, Wisconsin. The article and editorial appear in The Journal of Pediatrics, Volume 150, Issue 5 (May 2007), published by Elsevier.
PostPosted: Thu Dec 28, 2006 9:54 am    Post subject: Good News About the Blues: Scientists Discover Gene Therapy

Good News About the Blues: Scientists Discover Gene Therapy for Depression

By Robin Lloyd
Special to LiveScience
posted: 28 December 2006
08:52 am ET

Scientists have discovered a new gene that makes mice happy, a finding that suggests another avenue of drugs for improving depression in humans.

The research represents the first time that depression has been eliminated genetically in any organism, said Guy Debonnel, a psychiatrist and professor at McGill University.

Debonnel and his colleagues achieved this effect by creating and breeding mice lacking a gene also found in humans that affects the transmission of the mood-modulating chemical serotinin.

Mice without the gene, called TREK-1, acted as if they had been treated with anti-depressants for at least three weeks, he said. By removing TREK-1 in mice, the animals performed as if they weren't depressed when confronted with five standard behavioral tests scientists use for depression in mice.

For the full article:
PostPosted: Tue Sep 26, 2006 9:24 pm    Post subject: Study explores 'manic' thinking

Association for Psychological Science
26 September 2006

Study explores 'manic' thinking

How fast thinking makes us happy, energized and self-confident
When people are made to think quickly, they report feeling happier as a result. They also say they are more energetic, more creative, more powerful, and more self-assured. In short, they reported a whole set of experiences associated with being "manic."

Fast thinking, or "racing thoughts," is most commonly known as a symptom of the clinical psychiatric disorder of mania (and of the manic part of bipolar disorder or "manic-depression"). But, according to Princeton University psychologist Emily Pronin, most healthy people also have experienced racing thoughts at some point in time--perhaps when they are excited about a new idea they have just learned, or when they are brainstorming with a group of people, or even when they lie in bed unable to fall asleep. Pronin and her Harvard colleague Daniel Wegner decided to explore whether inducing people to think fast might lead them to feel some of the other experiences also associated with the manic experience.

To examine this question, they experimentally manipulated the pace at which participants read a series of statements. Half of participants read the statements at a fast pace (about twice as fast as normal reading speed) and the other half read the statements at a slow pace (about twice as slow as normal reading speed). They then completed a questionnaire assessing their mood, energy level, self-esteem, etc., using standard psychological measures. As an added twist, some of the participants read statements that were very depressing in content (e.g., I want to go to sleep and never wake up) while others read statements that were very elating in content (e.g., Wow! I feel great!). The researchers found that regardless of the content of the statements, people felt happier, more energetic, more creative, more powerful, and more grandiose when they read the statements at a fast rather than a slow pace. In fact, the effect of thought speed was just as powerful as the effect of the content of the thoughts. In other words, the speed of people's cognitive processing was just as important as what they processed in determining their mood. Even thinking sad thoughts at a fast pace made people relatively happy.

The article, titled "Manic Thinking: Independent Effects of Thought Speed and Thought Content on Mood" appears in the September issue of Psychological Science, and was co-authored by Emily Pronin of Princeton University and Daniel Wegner of Harvard University.

The reported effect of fast thinking on mood could have important applications in both clinical (psychiatric) and normal populations. The authors note that simple manipulations of thought speed could perhaps be used to improve individuals' mood, self-esteem, feelings of creativity, feelings of power, and energy level. Such manipulations could be useful in everyday situations, where people would like a quick mood, energy, or self-esteem boost on a day they are feeling tired or downcast. Manipulations of thought speed might also prove useful as part of treating depression, which is characterized by slow thinking, and also by the absence of things like positive mood, energy, feelings of power, and self-esteem. The authors note that: "The results of our experiment suggest the intriguing possibility that even during moments when people feel stuck having depressed thoughts, interventions that accelerate the speed of such thoughts may serve to boost feelings of positive affect and energy."
PostPosted: Fri Sep 01, 2006 9:40 am    Post subject: Bipolar disorder exacts twice depression's toll in workplace

NIH/National Institute of Mental Health
1 September 2006

Bipolar disorder exacts twice depression's toll in workplace

Productivity lags even after mood lifts
Bipolar disorder costs twice as much in lost productivity as major depressive disorder, a study funded by the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) has found. Each U.S. worker with bipolar disorder averaged 65.5 lost workdays in a year, compared to 27.2 for major depression. Even though major depression is more than six times as prevalent, bipolar disorder costs the U.S. workplace nearly half as much – a disproportionately high $14.1 billion annually. Researchers traced the higher toll mostly to bipolar disorder's more severe depressive episodes rather than to its agitated manic periods. The study by Drs. Ronald Kessler, Philip Wang, Harvard University, and colleagues, is among two on mood disorders in the workplace published in the September 2006 issue of the American Journal of Psychiatry.

Their study is the first to distinguish the impact of depressive episodes due to bipolar disorder from those due to major depressive disorder on the workplace. It is based on one-year data from 3378 employed respondents to the National Co-morbidity Survey Replication, a nationally representative household survey of 9,282 U.S. adults, conducted in 2001-2003.

The researchers measured the persistence of the disorders by asking respondents how many days during the past year they experienced an episode of mood disorder. They judged the severity based on symptoms during a worst month. Lost work days due to absence or poor functioning on the job, combined with salary data, yielded an estimate of lost productivity due to the disorders.

Poor functioning while at work accounted for more lost days than absenteeism. Although only about 1 percent of workers have bipolar disorder in a year, compared to 6.4 percent with major depression, the researchers projected that bipolar disorder accounts for 96.2 million lost workdays and $14.1 billion in lost salary-equivalent productivity, compared to 225 million workdays and $36.6 billion for major depression annually in the United States.

About three-fourths of bipolar respondents had experienced depressive episodes over the past year, with about 63 percent also having agitated manic or hypomanic episodes. The bipolar-associated depressive episodes were much more persistent – affecting 134-164 days – compared to only 98 days for major depression. The bipolar-associated depressive episodes were also more severe. All measures of lost work performance were consistently higher among workers with bipolar disorder who had major depressive episodes than those who reported only manic or hypomanic episodes. The latter workers' lost performance was on a par with workers who had major depressive disorder.

"Major depressive episodes due to bipolar disorder are sometimes incorrectly treated as major depressive disorder," noted Wang. "Since antidepressants can trigger the onset of mania, workplace programs should first rule out the possibility that a depressive episode may be due to bipolar disorder."

Future effectiveness trials could gauge the return on investment for employers offering coordinated evaluations and treatment for both mood disorders, he said.

Also participating in the study were: Dr. Kathleen Merikangas, NIMH; Dr. Minnie Ames and Robert Jin, Harvard University; Dr. Howard Birnbaum, Paul Greenberg, Analysis Group Inc.; Dr. Robert Hirschfeld, University of Texas; Dr. Hagop Akiskal, University of California San Diego.

In a related NIMH-funded study in the same issue of the American Journal of Psychiatry, Drs. Debra Lerner, David Adler, and colleagues, Tufts University School of Medicine and Tufts-New England Medical Center, found that many aspects of job performance are impaired by depression and that the effects linger even after symptoms have improved.

The researchers tracked the job performance and productivity of 286 employed patients with depression and dysthymia, 93 with rheumatoid arthritis and 193 healthy controls recruited from primary care physician practices for 18 months. While job performance improved as depression symptoms waned, even "clinically improved" depressed patients performed worse than healthy controls on mental, interpersonal, time management, output and physical tasks. The arthritis patients showed greater impairment, compared to healthy controls, only for physical job demands.

Noting that 44 percent of the depressed patients were already taking antidepressants when they began the study and still met clinical criteria for depression – and that job performance continued to suffer despite some clinical improvement – the researchers recommended that the goal of depression treatment should be remission. They also suggest that health professionals pay more attention to recovery of work function and that workplace supports be developed, perhaps through employee assistance programs and worksite occupational health clinics, to help depressed patients better manage job demands.

Also participating in the study were: Dr. William Rogers, Dr. Hong Chang, Leueen Lapitsky, Tufts-New England Medical Center; Dr. Thomas McLaughlin, University of Massachusetts Medical School.

The National Institute on Drug Abuse (NIDA), Substance Abuse and Mental Health Services Administration (SAMHSA), Robert Wood Johnson Foundation and John W. Alden Trust provided supplemental funding.

The Tufts-New England Medical Center General Clinical Research Center is funded by the NIH's National Center for Research Resources.

EMBARGOED For release Sept. 1, 2006, 12:01 AM, ET

The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website,

The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports more than 85 percent of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to ensure the rapid dissemination of research information and its implementation in policy and practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at

NCRR provides laboratory scientists and clinical researchers with the environments and tools they need to understand, detect, treat, and prevent a wide range of diseases. With this support, scientists make biomedical discoveries, translate these findings to animal-based studies, and then apply them to patient-oriented research. Ultimately, these advances result in cures and treatments for both common and rare diseases. NCRR also connects researchers with one another, and with patients and communities across the nation. These connections bring together innovative research teams and the power of shared resources, multiplying the opportunities to improve human health. For more information, visit

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit
PostPosted: Wed May 31, 2006 6:59 am    Post subject: (Health) Bipolar Disorder

Source: NIH/National Institute of Mental Health

Posted: May 30, 2006

Fear Circuit Flares As Bipolar Youth Misread Faces

Youth with bipolar disorder misread facial expressions as hostile and show heightened neural reactions when they focus on emotional aspects of neutral faces, researchers at the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) have discovered. The study provides some of the first clues to the underlying workings of the episodes of mania and depression that disrupt friendships, school, and family life in up to one percent of children.

Brain scans showed that the left amygdala, a fear hub, and related structures, activated more in youth with the disorder than in healthy youth when asked to rate the hostility of an emotionally neutral face, as opposed to a non-emotional feature, such as nose width. The more patients misinterpreted the faces as hostile, the more their amygdala flared. Such a face-processing deficit could help account for the poor social skills, aggression, and irritability that characterizes the disorder in children, suggest Drs. Ellen Leibenluft, Brendan Rich, Daniel Pine, NIMH Mood and Anxiety Disorders Program, and colleagues, who report on their findings May 29, 2006 in the Proceedings of the National Academy of Sciences.

"Since children seem to have a more severe form of the disorder, they may provide a clearer window into the underlying illness process than adult onset cases," explained Leibenluft. "Our results suggest that children with bipolar disorder see emotion where other people don't. Our results also suggest that bipolar disorder likely stems from impaired development of specific brain circuits, as is thought to occur in schizophrenia and other mental illnesses."

Magnetic Resonance Imaging (MRI) studies have shown that, unlike in adults with the illness, the amygdala is consistently smaller in bipolar children than in healthy age-mates. Also, the NIMH researchers had found earlier that bipolar children falter at identifying facial emotion and have difficulty regulating their attention when frustrated.

Using functional MRI, the researchers measured brain activity in 22 bipolar youth and 21 healthy subjects while they rated faces. In addition to the amygdala, other parts of the emotion-regulating circuit – nucleus accumbens, putamen, and left prefrontal cortex – were also hyperactive in patients, compared to healthy peers, during the emotional tasks. Patients rated themselves as more afraid, and they rated the faces as more hostile, compared to healthy peers. The groups did not differ on nose width ratings, confirming that the differences were specific to perceiving emotional processes.

"By finding a brain imaging trait that may be more selective than current clinical criteria, this line of research might help us refine our definition of pediatric bipolar disorder," said NIMH Director Thomas Insel, M.D. "The researchers are following-up with imaging studies of children with bipolar spectrum disorders and healthy children who are at genetic risk for developing the disorder to see if they also have the same amygdala over-activation."

Also participating in the study were: Dr. Deborah Vinton, Dr. Rebecca Hommer, Dr. Stephen Fromm, Lisa Berghorst, NIMH; Dr. Roxann Roberson-Nay, Virginia Commonwealth University; Dr.Erin McClure, Georgia State University.


Questions to explore further this topic:

The Brain

What is bipolar disorder?

Videos on bipolar disorder

What are the types of bipolar disorder?

What are the symptoms of bipolar disorder?

Bipolar Disorder FAQs

What is depression?

What is the "bipolarity index"?

What is a "depression scale"?

Can children have bipolar disorder?

Biological Clocks and Bipolar Disorder

How is bipolar disorder treated?

The Historical Background of Lithium Therapy and Prophylaxis

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