During the second world war, the physicist Enrico Fermi asked General Leslie Groves of the US Army how many generals might be called "great" and why. Groves replied that any general who won five major battles in a row might be called great, and that about three in every hundred would qualify.
Fermi countered that if opposing forces are roughly equal, the odds are one in two that a general will win one battle, one in four that he will win two battles in a row, one in eight for three battles, one in 16 for four battles, and one in 32 for five battles in a row. "So you are right, General, about three in a hundred. Mathematical probability, not genius."1
There's an analogue of Fermi's "great general": the "great scientific discovery", or at least, as a case study, "the great genetic scientific discovery" as reported in the press. The discovery of genes for a certain behaviour, for schizophrenia, for happiness, always get good press coverage, usually based on publication in a respected scientific journal such as Science or Nature.
The research paper will include a statistic: the probability that the finding could have occurred by chance. The probability will have been sufficiently low that a reviewer for the journal was impressed and therefore recommended publication. Typically this probability or "P-value" will be less than 0.05, or 5%, which means the odds are less than one in 20 that the observed genetic correlation could have occurred by chance.
READ MORE @ GUARDIAN"
Showing posts with label serotonin. Show all posts
Showing posts with label serotonin. Show all posts
Monday, November 9, 2009
Friday, October 2, 2009
Antidepressant improves recovery from spine injury
A common antidepressant combined with an intensive treadmill training program helped people with partial spinal cord injuries walk better and faster, U.S. researchers said on Sunday.
They said Forest Laboratories' antidepressant Lexapro or escitalopram, which affects a message-carrying brain chemical called serotonin, helps strengthen remaining nerve connections along the spine, giving patients with spinal cord injuries more ability to control their muscles during training.
"The drug is enhancing the effects of the therapy," said George Hornby, a research scientist at the Rehabilitation Institute of Chicago, who is presenting his findings at the Society for Neuroscience's meeting in Chicago.
"The drug on its own isn't a miracle drug. What you need is the drug plus the training," Hornby said in a telephone interview.
The findings are the first in humans and builds on studies in animals that found giving serotonin-like drugs after spinal cord injuries can promote recovery of walking when paired with an intensive training program.
READ MORE @ REUTERS
They said Forest Laboratories' antidepressant Lexapro or escitalopram, which affects a message-carrying brain chemical called serotonin, helps strengthen remaining nerve connections along the spine, giving patients with spinal cord injuries more ability to control their muscles during training.
"The drug is enhancing the effects of the therapy," said George Hornby, a research scientist at the Rehabilitation Institute of Chicago, who is presenting his findings at the Society for Neuroscience's meeting in Chicago.
"The drug on its own isn't a miracle drug. What you need is the drug plus the training," Hornby said in a telephone interview.
The findings are the first in humans and builds on studies in animals that found giving serotonin-like drugs after spinal cord injuries can promote recovery of walking when paired with an intensive training program.
READ MORE @ REUTERS
Monday, August 24, 2009
Touted "Depression Risk Gene" May Not Add to Risk After All
A gene variation long thought to increase a person’s risk for major depression when paired with stressful life events may actually have no effect, according to a new analysis. The result challenges a common approach to studying depression risk factors.
Most mental disorders are thought to be caused by a combination of many genetic risk factors interacting with environmental triggers. Finding the exact combinations of factors, however, has been a significant challenge. Advances during the past decade have led to powerful tools for studying how genes and the environment interact to affect the risk for disease. In 2003, these advances allowed scientists to show that variation in a gene called the serotonin transporter gene affected the risk of major depression in people who had a number of stressful life events over a 5-year period.
Serotonin is a chemical messenger that helps brain cells communicate. The serotonin transporter directs serotonin from the space between brain cells back into the cell for reuse. Since the most widely prescribed class of medication for treating major depression acts by blocking this protein, it’s been a prime suspect in mood and anxiety disorders.
READ MORE @ NIH Research Matters
Most mental disorders are thought to be caused by a combination of many genetic risk factors interacting with environmental triggers. Finding the exact combinations of factors, however, has been a significant challenge. Advances during the past decade have led to powerful tools for studying how genes and the environment interact to affect the risk for disease. In 2003, these advances allowed scientists to show that variation in a gene called the serotonin transporter gene affected the risk of major depression in people who had a number of stressful life events over a 5-year period.
Serotonin is a chemical messenger that helps brain cells communicate. The serotonin transporter directs serotonin from the space between brain cells back into the cell for reuse. Since the most widely prescribed class of medication for treating major depression acts by blocking this protein, it’s been a prime suspect in mood and anxiety disorders.
READ MORE @ NIH Research Matters
Thursday, October 16, 2008
Treatment on a plate - A dietary approach to treating addiction seems worth investigating
PEOPLE are programmed for addiction. Their brains are designed so that actions vital for propagating their genes—such as eating and having sex—are highly rewarding. Those reward pathways can, however, be subverted by external chemicals (in other words, drugs) and by certain sorts of behaviour such as gambling.
In recent years, neuroscientists have begun to understand how these reward pathways work and, in particular, the role played by message-carrying molecules called neurotransmitters. These molecules, notably serotonin, dopamine and gamma-aminobutyric acid (GABA), hop between nerve cells, carrying signals as they go. Some drugs mimic their actions. Others enhance them. Either way, the body tends, as a result, to give up making them. At that point the person needs the drug as a substitute for the missing transmitter. In other words, he is an addict.
READ MORE @ THE ECONOMIST
In recent years, neuroscientists have begun to understand how these reward pathways work and, in particular, the role played by message-carrying molecules called neurotransmitters. These molecules, notably serotonin, dopamine and gamma-aminobutyric acid (GABA), hop between nerve cells, carrying signals as they go. Some drugs mimic their actions. Others enhance them. Either way, the body tends, as a result, to give up making them. At that point the person needs the drug as a substitute for the missing transmitter. In other words, he is an addict.
READ MORE @ THE ECONOMIST
Thursday, September 4, 2008
Brain's Serotonin May Explain Seasonal Mood Changes
Fluctuations in the actions of the serotonin transporter, which helps regulate the mood-altering neurotransmitter serotonin, may help explain seasonal affective disorder and related mood changes, researchers say.
In places where the weather changes with the seasons, people commonly feel happier and more energetic when the days are bright and sunny and more depressed and fatigued during the dark of winter. Scientists believe this is related to variations in brain levels of serotonin, a neurotransmitter involved in regulating functions such as mating, feeding, energy balance, and sleep.
READ MORE @ WASHINGTON POST
In places where the weather changes with the seasons, people commonly feel happier and more energetic when the days are bright and sunny and more depressed and fatigued during the dark of winter. Scientists believe this is related to variations in brain levels of serotonin, a neurotransmitter involved in regulating functions such as mating, feeding, energy balance, and sleep.
READ MORE @ WASHINGTON POST
Tuesday, July 8, 2008
Some Antidepressants Work Quickly
pillsA single antidepressant tablet makes a depressed person see the world in a more positive light just four hours after swallowing it, suggests a new study.
Dr Philip Cowen, professor of pharmacology at the Department of Psychiatry at the University of Oxford, told delegates at the Royal College of Psychiatrists’ Annual Meeting in London that antidepressant medication starts to work far faster than most clinicians assume.
“Depressed people interpret the world in a negative way,” he said. “They become stuck in this state. Negativity causes depression and depression causes negativity and, whatever happens, events will be interpreted in a negative way.”
Antidepressants elevate mood, which in turn leads to a depressed person becoming more positive and interpreting things that happen to them in a positive way. Prof Cowen said: “Antidepressants change biases. People who take them begin to see the world in a positive light,” said Prof Cowen
But it does not take weeks for this change to happen. Prof Cowen and his colleagues gave 30 depressed people one single 4mg dose of reboxetine – which inhibits the update of both serotonin and noradrenaline in the brain – and compared them with 30 ‘controls’ who were given a placebo or dummy pil
RAD MORE @ PSYCHCENTRAL
Dr Philip Cowen, professor of pharmacology at the Department of Psychiatry at the University of Oxford, told delegates at the Royal College of Psychiatrists’ Annual Meeting in London that antidepressant medication starts to work far faster than most clinicians assume.
“Depressed people interpret the world in a negative way,” he said. “They become stuck in this state. Negativity causes depression and depression causes negativity and, whatever happens, events will be interpreted in a negative way.”
Antidepressants elevate mood, which in turn leads to a depressed person becoming more positive and interpreting things that happen to them in a positive way. Prof Cowen said: “Antidepressants change biases. People who take them begin to see the world in a positive light,” said Prof Cowen
But it does not take weeks for this change to happen. Prof Cowen and his colleagues gave 30 depressed people one single 4mg dose of reboxetine – which inhibits the update of both serotonin and noradrenaline in the brain – and compared them with 30 ‘controls’ who were given a placebo or dummy pil
RAD MORE @ PSYCHCENTRAL
Monday, July 7, 2008
Head fake - How Prozac sent the science of depression in the wrong direction
PROZAC IS ONE of the most successful drugs of all time. Since its introduction as an antidepressant more than 20 years ago, Prozac has been prescribed to more than 54 million people around the world, and prevented untold amounts of suffering.
But the success of Prozac hasn't simply transformed the treatment of depression: it has also transformed the science of depression. For decades, researchers struggled to identify the underlying cause of depression, and patients were forced to endure a series of ineffective treatments. But then came Prozac. Like many other antidepressants, Prozac increases the brain's supply of serotonin, a neurotransmitter. The drug's effectiveness inspired an elegant theory, known as the chemical hypothesis: Sadness is simply a lack of chemical happiness. The little blue pills cheer us up because they give the brain what it has been missing.
There's only one problem with this theory of depression: it's almost certainly wrong, or at the very least woefully incomplete. Experiments have since shown that lowering people's serotonin levels does not make them depressed, nor does it does not make them depressed, nor does it worsen their symptoms if they are already depressed.
READ MORE @ BOSTON GLOBE
But the success of Prozac hasn't simply transformed the treatment of depression: it has also transformed the science of depression. For decades, researchers struggled to identify the underlying cause of depression, and patients were forced to endure a series of ineffective treatments. But then came Prozac. Like many other antidepressants, Prozac increases the brain's supply of serotonin, a neurotransmitter. The drug's effectiveness inspired an elegant theory, known as the chemical hypothesis: Sadness is simply a lack of chemical happiness. The little blue pills cheer us up because they give the brain what it has been missing.
There's only one problem with this theory of depression: it's almost certainly wrong, or at the very least woefully incomplete. Experiments have since shown that lowering people's serotonin levels does not make them depressed, nor does it does not make them depressed, nor does it worsen their symptoms if they are already depressed.
READ MORE @ BOSTON GLOBE
Saturday, June 7, 2008
New research explores role of serotonin
Findings provide insight into clinical disorders characterised by low serotonin level, such as depression, obsessive compulsive disorder and severe anxiety
New research by scientists at the University of Cambridge suggests that the neurotransmitter serotonin, which acts as a chemical messenger between nerve cells, plays a critical role in regulating emotions such as aggression during social decision-making.
Serotonin has long been associated with social behaviour, but its precise involvement in impulsive aggression has been controversial. Though many have hypothesised the link between serotonin and impulsivity, this is one of the first studies to show a causal link between the two.
Their findings highlight why some of us may become combative or aggressive when we haven't eaten. The essential amino acid necessary for the body to create serotonin can only be obtained through diet. Therefore, our serotonin levels naturally decline when we don't eat, an effect the researchers took advantage of in their experimental technique.
The research also provides insight into clinical disorders characterised by low serotonin levels, such as depression and obsessive compulsive disorder (OCD), and may help explain some of the social difficulties associated with these disorders.
This research, funded by the Wellcome Trust and the Medical Research Council, suggests that patients with depression and anxiety disorders may benefit from therapies that teach them strategies for regulating emotions during decision making, particularly in social scenarios.
READ MORE @ EUREKALERT
New research by scientists at the University of Cambridge suggests that the neurotransmitter serotonin, which acts as a chemical messenger between nerve cells, plays a critical role in regulating emotions such as aggression during social decision-making.
Serotonin has long been associated with social behaviour, but its precise involvement in impulsive aggression has been controversial. Though many have hypothesised the link between serotonin and impulsivity, this is one of the first studies to show a causal link between the two.
Their findings highlight why some of us may become combative or aggressive when we haven't eaten. The essential amino acid necessary for the body to create serotonin can only be obtained through diet. Therefore, our serotonin levels naturally decline when we don't eat, an effect the researchers took advantage of in their experimental technique.
The research also provides insight into clinical disorders characterised by low serotonin levels, such as depression and obsessive compulsive disorder (OCD), and may help explain some of the social difficulties associated with these disorders.
This research, funded by the Wellcome Trust and the Medical Research Council, suggests that patients with depression and anxiety disorders may benefit from therapies that teach them strategies for regulating emotions during decision making, particularly in social scenarios.
READ MORE @ EUREKALERT
Thursday, June 5, 2008
Eating And Weight Gain Not Necessarily Linked, Study Shows
You may not be what you eat after all. A new study shows that increased eating does not necessarily lead to increased fat. The finding in the much-studied roundworm opens the possibility of identifying new targets for drugs to control weight, the researchers say.
The discovery reveals that the neurotransmitter serotonin, already known to control appetite and fat build-up, actually does so through two separate signaling channels. One set of signals regulates feeding, and a separate set of signals regulates fat metabolism. The worm, known scientifically as Caenorhabdtis elegans, shares half of its genes with humans and is often a predictor of human traits.
The signaling pathways are composed of a series of molecular events triggered by neurons in the brain that ultimately "instruct" the body to burn or store fat.
READ MORE @ SCIENCE DAILY
The discovery reveals that the neurotransmitter serotonin, already known to control appetite and fat build-up, actually does so through two separate signaling channels. One set of signals regulates feeding, and a separate set of signals regulates fat metabolism. The worm, known scientifically as Caenorhabdtis elegans, shares half of its genes with humans and is often a predictor of human traits.
The signaling pathways are composed of a series of molecular events triggered by neurons in the brain that ultimately "instruct" the body to burn or store fat.
READ MORE @ SCIENCE DAILY
Monday, February 18, 2008
Sex differences in the brain's serotonin system
A new thesis from he Swedish medical university Karolinska Institutet shows that the brain’s serotonin system differs between men and women. The scientists who conducted the study think that they have found one of the reasons why depression and chronic anxiety are more common in women than in men.
Serotonin is a brain neurotransmitter that is critical to the development and treatment of depression and chronic anxiety, conditions that, for reasons still unknown, are much more common in women than in men. A research group at Karolinska Institutet has now shown using a PET scanner that women and men differ in terms of the number of binding sites for serotonin in certain parts of the brain.
Their results, which are to be presented in a doctoral thesis by Hristina Jovanovic at the end of February, show that women have a greater number of the most common serotonin receptors than men. They also show that women have lower levels of the protein that transports serotonin back into the nerve cells that secrete it. It is this protein that the most common antidepressants (SSRIs) block.
“We don’t know exactly what this means, but the results can help us understand why the occurrence of depression differs between the sexes and why men and women sometimes respond differently to treatment with antidepressant drugs,” says associate professor Anna-Lena Nordström, who led the study.
The group has also shown that the serotonin system in healthy women differs from that in women with serious premenstrual mental symptoms. These results suggest that the serotonin system in such women does not respond as flexibly to the hormone swings of the menstrual cycle as that in symptom-free women.
READ MORE @ EUREKALERT
Serotonin is a brain neurotransmitter that is critical to the development and treatment of depression and chronic anxiety, conditions that, for reasons still unknown, are much more common in women than in men. A research group at Karolinska Institutet has now shown using a PET scanner that women and men differ in terms of the number of binding sites for serotonin in certain parts of the brain.
Their results, which are to be presented in a doctoral thesis by Hristina Jovanovic at the end of February, show that women have a greater number of the most common serotonin receptors than men. They also show that women have lower levels of the protein that transports serotonin back into the nerve cells that secrete it. It is this protein that the most common antidepressants (SSRIs) block.
“We don’t know exactly what this means, but the results can help us understand why the occurrence of depression differs between the sexes and why men and women sometimes respond differently to treatment with antidepressant drugs,” says associate professor Anna-Lena Nordström, who led the study.
The group has also shown that the serotonin system in healthy women differs from that in women with serious premenstrual mental symptoms. These results suggest that the serotonin system in such women does not respond as flexibly to the hormone swings of the menstrual cycle as that in symptom-free women.
READ MORE @ EUREKALERT
Monday, February 11, 2008
Growing Up to Prozac: Drug makes new neurons mature faster
Peter Pan won't be pleased to hear the latest theory about how Prozac works. A new study shows that the antidepressant stimulates growth of neurons in the hippocampus and speeds the young brain cells toward maturity. The maturation process could be the mechanism by which the drug relieves depression.
Fluoxetine, the drug commonly known as Prozac, has been used to treat depression since the 1980s. Prozac and other SSRIs (selective serotonin reuptake inhibitors) block the ability of the neurons to take up serotonin, thereby raising levels of the active neurotransmitter in the brain. When people with depression begin taking such drugs, serotonin levels in the brain increase rapidly, but it often takes 2 to 4 weeks before they begin to feel better.
The new study, published Feb. 6 in the Journal of Neuroscience, suggests that the lag is due to the time it takes for serotonin to stimulate new neurons to grow, mature, and integrate into brain circuits.
René Hen, a neuroscientist at Columbia University, and his colleagues tested the long-term effects of Prozac treatment on a specially bred strain of nervous mice.
READ MORE @ SCIENCE NEWS
Fluoxetine, the drug commonly known as Prozac, has been used to treat depression since the 1980s. Prozac and other SSRIs (selective serotonin reuptake inhibitors) block the ability of the neurons to take up serotonin, thereby raising levels of the active neurotransmitter in the brain. When people with depression begin taking such drugs, serotonin levels in the brain increase rapidly, but it often takes 2 to 4 weeks before they begin to feel better.
The new study, published Feb. 6 in the Journal of Neuroscience, suggests that the lag is due to the time it takes for serotonin to stimulate new neurons to grow, mature, and integrate into brain circuits.
René Hen, a neuroscientist at Columbia University, and his colleagues tested the long-term effects of Prozac treatment on a specially bred strain of nervous mice.
READ MORE @ SCIENCE NEWS
Monday, January 21, 2008
Height link to suicide attempts
Men are less likely to attempt suicide if they are tall, research has shown.
A study in the Journal of Epidemiology and Community Health examined the suicide and death figures for 320,000 Swedish men born between 1973 and 1980.
It found that short babies - those less than 47cm in length at birth - were more likely to attempt suicide as adults, regardless of their eventual height.
Short birth length more than doubled the risk of violent suicide, defined as the use of guns or knives, jumping from a height or in front of vehicles, or drowning.
But short men who were born a normal length were also affected.
The study found they were 56% more likely to take their own lives than tall men.
The authors of the study suggested the brain chemical serotonin, which is crucial to brain development, could be the reason for their findings.
Low serotonin levels can trigger impulsive, aggressive and suicidal behaviour, and can be caused by premature birth and other factors affecting growth in the womb.
READ MORE @ THE PRESS ASSOCIATION
A study in the Journal of Epidemiology and Community Health examined the suicide and death figures for 320,000 Swedish men born between 1973 and 1980.
It found that short babies - those less than 47cm in length at birth - were more likely to attempt suicide as adults, regardless of their eventual height.
Short birth length more than doubled the risk of violent suicide, defined as the use of guns or knives, jumping from a height or in front of vehicles, or drowning.
But short men who were born a normal length were also affected.
The study found they were 56% more likely to take their own lives than tall men.
The authors of the study suggested the brain chemical serotonin, which is crucial to brain development, could be the reason for their findings.
Low serotonin levels can trigger impulsive, aggressive and suicidal behaviour, and can be caused by premature birth and other factors affecting growth in the womb.
READ MORE @ THE PRESS ASSOCIATION
Wednesday, January 2, 2008
Some Antipsychotic Drugs May Be Missing Their Mark
Drugs that treat depression, schizophrenia and other psychotic conditions and that target a particular protein on brain cells might not be triggering the most appropriate response in those cells, new research suggests.
The study by researchers at The Ohio State University Medical Center examined the serotonin 2A receptor, a protein on brain cells sensitive to the neurotransmitter serotonin.
This study examined the early chemical events that happen inside neurons when the 2A receptor is stimulated by serotonin and by a synthetic hallucinogenic agent that is thought to mimic serotonin.
The findings, published online in the early edition of the Proceedings of the National Academy of Sciences with an accompanying editorial, show that although both compounds combine with and activate this receptor, they trigger different chemical pathways inside the neuron.
READ MORE @ SCIENCE DAILY
The study by researchers at The Ohio State University Medical Center examined the serotonin 2A receptor, a protein on brain cells sensitive to the neurotransmitter serotonin.
This study examined the early chemical events that happen inside neurons when the 2A receptor is stimulated by serotonin and by a synthetic hallucinogenic agent that is thought to mimic serotonin.
The findings, published online in the early edition of the Proceedings of the National Academy of Sciences with an accompanying editorial, show that although both compounds combine with and activate this receptor, they trigger different chemical pathways inside the neuron.
READ MORE @ SCIENCE DAILY
Wednesday, December 26, 2007
An active ingredient in treating mild depression
Study supports findings that exercise can help beat the blues and might reduce need for medication.
This fall, we ran a series of articles called Healthwatch that examined the latest medical studies making the news. The series provoked a lot of discussion, and readers asked for more, so medical journalist Evra Taylor Levy and emergency physician Eddy Lang are back, helping to make sense of sometimes contradictory medical research. Healthwatch runs every other week as a regular Gazette feature. The writers invite you to join them in their online forum. See details on Page D3.
- - -
It's no secret that the holidays and transition into a new year spell depression for many people experiencing loneliness, difficult life events or loss. With this, our end-of-the-year edition of Healthwatch, we bring you an uplifting study that looks at a way of beating some kinds of depression without medication.
Worldwide, depression is the leading cause of years lived with disability. During their lifetime, about five to 12 per cent of men and 10 to 25 per cent of women will have at least one major depressive episode. Interestingly, mood disorders often begin in adolescence, making early diagnosis especially important to offset years of unhappy, impaired living. Additionally, Canadian winters mean reduced sunlight and shorter days, which have been implicated in an increased prevalence of depression at this time of the year.
Symptoms of depression
It has been reported that half of the people who have clinical depression don't know it, so recognizing its symptoms is essential and the first step toward treatment. While not a complete list, symptoms include: persistent sadness; pessimism; feelings of guilt; loss of interest and pleasure in activities; helplessness or hopelessness; difficulty concentrating; insomnia or oversleeping; apathy; anxiety; thoughts of suicide or death.
READ MORE @ MONTREAL GAZETTE
This fall, we ran a series of articles called Healthwatch that examined the latest medical studies making the news. The series provoked a lot of discussion, and readers asked for more, so medical journalist Evra Taylor Levy and emergency physician Eddy Lang are back, helping to make sense of sometimes contradictory medical research. Healthwatch runs every other week as a regular Gazette feature. The writers invite you to join them in their online forum. See details on Page D3.
- - -
It's no secret that the holidays and transition into a new year spell depression for many people experiencing loneliness, difficult life events or loss. With this, our end-of-the-year edition of Healthwatch, we bring you an uplifting study that looks at a way of beating some kinds of depression without medication.
Worldwide, depression is the leading cause of years lived with disability. During their lifetime, about five to 12 per cent of men and 10 to 25 per cent of women will have at least one major depressive episode. Interestingly, mood disorders often begin in adolescence, making early diagnosis especially important to offset years of unhappy, impaired living. Additionally, Canadian winters mean reduced sunlight and shorter days, which have been implicated in an increased prevalence of depression at this time of the year.
Symptoms of depression
It has been reported that half of the people who have clinical depression don't know it, so recognizing its symptoms is essential and the first step toward treatment. While not a complete list, symptoms include: persistent sadness; pessimism; feelings of guilt; loss of interest and pleasure in activities; helplessness or hopelessness; difficulty concentrating; insomnia or oversleeping; apathy; anxiety; thoughts of suicide or death.
READ MORE @ MONTREAL GAZETTE
Sunday, December 2, 2007
One Gene Variant Puts Stressed Women At Risk For Depression; Has Opposite Effect In Men
A common variation in genes puts women who are under chronic stress at risk for increased depressive symptoms, but has the exact opposite effect in men, according to new findings from Duke University Medical Center researchers.
The researchers analyzed two independent samples of healthy individuals for the presence of a genetic variant that regulates levels of serotonin — a neurotransmitter that is linked to health in numerous ways, including emotion regulation.
One version of the gene puts women who are under chronic stress at risk for more severe depressive symptoms. But among men, the same gene variant appeared to be protective against depression. In fact, men with the opposite gene variant were the ones who experienced more depressive symptoms when under chronic stress.
READ MORE @ SCIENCE DAILY
The researchers analyzed two independent samples of healthy individuals for the presence of a genetic variant that regulates levels of serotonin — a neurotransmitter that is linked to health in numerous ways, including emotion regulation.
One version of the gene puts women who are under chronic stress at risk for more severe depressive symptoms. But among men, the same gene variant appeared to be protective against depression. In fact, men with the opposite gene variant were the ones who experienced more depressive symptoms when under chronic stress.
READ MORE @ SCIENCE DAILY
Saturday, December 1, 2007
Novel Antidepressant Agomelatin Targets Melatonin and Serotonin Receptors: Presented at CPA
The soon-to-be-available antidepressant agomelatin offers excellent efficacy with great tolerability and sleep improvements to boot.
Raymond W. Lam, MD, Professor and Head of Clinical Neuroscience, Department of Psychiatry, Faculty of Medicine, University of British Columbia, Vancouver, Canada, presented the latest findings on this agent here at the 57th Annual Conference of the Canadian Psychiatric Association (CPA).
Agomelatin is a new antidepressant with a novel mechanism of action. It acts as an agonist to both the melatonin receptors MT1 and MT2. It is also an antagonist to the 5HT2C serotonin receptor. It also appears to have no other action in any other receptor site, and over 80 sites have been studied so far, said Dr. Lam.
Both the M1 and M2 receptors are known to be involved in regulation of circadian rhythms. Stimulation of M1 has a positive effect on sleep by attenuating the alerting signal produced by the suprachiasmatic nucleus (SCN) in the brain. M2 has a phase-shifting effect on circadian rhythms. Antagonism of the 5HT2C increases the activity of dopamine and noradrenalin in the frontal cortex, which can have both anxiolytic and antidepressant effects. It also promotes slow wave sleep or deep, restorative sleep.
READ MORE @ DOCTOR'S GUIDE
Raymond W. Lam, MD, Professor and Head of Clinical Neuroscience, Department of Psychiatry, Faculty of Medicine, University of British Columbia, Vancouver, Canada, presented the latest findings on this agent here at the 57th Annual Conference of the Canadian Psychiatric Association (CPA).
Agomelatin is a new antidepressant with a novel mechanism of action. It acts as an agonist to both the melatonin receptors MT1 and MT2. It is also an antagonist to the 5HT2C serotonin receptor. It also appears to have no other action in any other receptor site, and over 80 sites have been studied so far, said Dr. Lam.
Both the M1 and M2 receptors are known to be involved in regulation of circadian rhythms. Stimulation of M1 has a positive effect on sleep by attenuating the alerting signal produced by the suprachiasmatic nucleus (SCN) in the brain. M2 has a phase-shifting effect on circadian rhythms. Antagonism of the 5HT2C increases the activity of dopamine and noradrenalin in the frontal cortex, which can have both anxiolytic and antidepressant effects. It also promotes slow wave sleep or deep, restorative sleep.
READ MORE @ DOCTOR'S GUIDE
Friday, August 17, 2007
Antidepressant Gatekeeper - Structural and functional studies point to tricyclics' mechanism of action
AN IMPORTANT CLASS of drugs-tricyclic antidepressants (TCAs)—binds in a surprising place. That finding, based on studies with a bacterial protein, could influence the design of new drugs for depression.
According to two new studies, TCAs seal off a molecular passageway in a bacterial counterpart of human neurotransmitter transporter proteins (Nature, DOI: 10.1038/nature06038 and Science, DOI: 10.1126/science.1147614). The work indicates a molecular mechanism of action for this compound class.
Since the 1950s, TCAs such as desipramine (Norpramin and Pertofrane) have been prescribed to treat symptoms of depression. They prevent reuptake of serotonin and norepinephrine by binding to corresponding membrane-spanning neurotransmitter transporter proteins
READ MORE @ CHEMICAL & ENGINEERING NEWS
According to two new studies, TCAs seal off a molecular passageway in a bacterial counterpart of human neurotransmitter transporter proteins (Nature, DOI: 10.1038/nature06038 and Science, DOI: 10.1126/science.1147614). The work indicates a molecular mechanism of action for this compound class.
Since the 1950s, TCAs such as desipramine (Norpramin and Pertofrane) have been prescribed to treat symptoms of depression. They prevent reuptake of serotonin and norepinephrine by binding to corresponding membrane-spanning neurotransmitter transporter proteins
READ MORE @ CHEMICAL & ENGINEERING NEWS
Tuesday, July 10, 2007
Plagued by midsummer SADness
Seasonal Affective Disorder is normally banished by the sunshine, but this year it is lingering on, reports Chloe Rhodes
Now is the winter of our discontent. The fact that it's July is irrelevant.
Flooding, freak hail and attempted terrorist attacks have blighted what is usually our sunniest and most carefree time of year, while grey skies and incessant showers have turned midsummer into one long, gloomy February afternoon.
Everyone gets fed up when bad weather drags on, but for some people, including me, the lack of sunshine has a bigger impact.
One in 50 of us is thought to suffer from Seasonal Affective Disorder (SAD), the symptoms of which include lethargy, anxiety, irritability, loss of libido and depression. One in eight experiences a milder version known as winter blues, and both usually occur in the months between October and March, when daylight hours are reduced.
READ MORE @ TELEGRAPH
Now is the winter of our discontent. The fact that it's July is irrelevant.
Flooding, freak hail and attempted terrorist attacks have blighted what is usually our sunniest and most carefree time of year, while grey skies and incessant showers have turned midsummer into one long, gloomy February afternoon.
Everyone gets fed up when bad weather drags on, but for some people, including me, the lack of sunshine has a bigger impact.
One in 50 of us is thought to suffer from Seasonal Affective Disorder (SAD), the symptoms of which include lethargy, anxiety, irritability, loss of libido and depression. One in eight experiences a milder version known as winter blues, and both usually occur in the months between October and March, when daylight hours are reduced.
READ MORE @ TELEGRAPH
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