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An interesting new study into the symptoms of depression



     Are researchers really onto something here? Having lived with depression for many years, I know about the complexities of the depressive symptoms. Maybe there is some benefit to isolating these symptoms and treating them. However, I am not certain that this research study brings anything new to the table. What do you think?

A new way to look at depressive symptoms 
October 22, 2015, LEUVEN, Belgium--

​A new study suggests that the current approach to diagnosing depression should be reassessed to reflect how a person’s particular symptoms interconnect. “Depression is a complex, extremely heterogeneous system of interacting symptoms,” lead author Dr Eiko Fried said in a release. “We may want to focus treatment efforts on the symptoms driving a patient’s depression.”

Based on evaluations of 3,463 people, Fried and an international team of researchers created a network of 28 depression symptoms to determine which were most closely related (for example, insomnia may link to fatigue which contributes to difficulty concentrating). Some criteria in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5)—used to identify major depression as well as depressive episodes in bipolar disorder—made the list of “most central symptoms.” Others were deemed less important than symptoms which are not in the criteria, including anxiety.

NEW Research study shows new path to reduce depression




Study further links immune response, serotonin signaling

by Bill Snyder | Thursday, Nov. 5, 2015, 8:43 AM

​Vanderbilt University scientists are a step closer to understanding how inflammation in the body can affect mood and behavior.
Their latest discovery, reported this week in the journal Translational Psychiatry, provides further evidence that a signaling pathway involved in the body’s immune response to infection and other stressors can regulate the brain’s control of the neurotransmitter serotonin.
                                                                                           Randy Blakely, Ph.D.

“The inflammatory pathway that we have identified is likely one by which serotonin signaling is regulated in general,” said Randy Blakely, Ph.D., who led the research team. “By targeting this pathway, we might come up with better medications to treat disorders where manipulation of serotonin signaling has proved beneficial, as in depression.”
For the better part of a decade, Blakely and his colleagues have investigated the p38alpha MAPK signaling pathway. MAPKs, or mitogen-activated protein kinases, are enzymes that regulate the body’s response to infection and other stress stimuli, among other roles.
The latest findings add to an increasing body of evidence that the p38alpha MAPK pathway links the body’s immune response to regulation of the brain serotonin transporter. The transporter, which eliminates serotonin from the synapse, or gap between nerve cells, is the target for a major class of anti-depressants.
Selective serotonin reuptake inhibitors or SSRIs like Prozac increase the brain’s supply of serotonin by blocking the transporter. But it can take weeks to achieve a therapeutic effect, and not everyone responds to them.
Using genetic mouse models they developed, Blakely and his colleagues showed that the MAPK pathway acts in serotonin neurons to communicate signs of infection in the periphery. That leads to an elevation in serotonin transporter activity and multiple serotonin-linked behaviors.
“The net consequence of p38alpha MAPK activation is … we get elevated transporter activity that can drain away the serotonin,” said Blakely, the Allan D. Bass Professor of Pharmacology and Psychiatry.
The impact on behavior was profound. When an inflammatory response was produced by peripheral injection of a piece of bacteria in mice, their serotonin neurons showed rapid activation of the p38alpha MAPK pathway. The animals also exhibited depressive-like behaviors, including signs of heightened anxiety and despair.
But when, in the current study, the p38alpha MAPK pathway was genetically “knocked out,” specifically in serotonin neurons, these behaviors were extinguished. The inflammatory agent had no effect. The animals were, as Blakely described them, “resilient.”
This “is a response to an acute inflammatory agent,” Blakely cautioned. It says nothing about what may occur in chronic inflammatory states. “That’s something we’re eager to pursue with the same kind of genetic approach,” he said.
At the same time, “I doubt that (this MAPK pathway) has evolved only to respond to inflammation,” he said.
Since the p38alpha MAPK pathway has the ability to turn up and turn down the activity of the serotonin transporter, “maybe if we targeted the way (it) regulates the transporter as opposed to blocking the transporter itself, we might have a better antidepressant,” Blakely said.
Blakely is director of the Vanderbilt/NIMH Silvio O. Conte Center for Neuroscience Research, which is supported by the National Institute of Mental Health, part of the National Institutes of Health (NIH). First author of the study was Nicole Baganz, Ph.D., a postdoctoral fellow in the Blakely lab.
The research was supported in part by NIH grants NS007491, MH094527 and MH096972, the Brain and Behavioral Research Foundation and the Institute for Psychiatric Neuroscience.
Media Inquiries: 
Bill Snyder, (615) 322-4747  


Larry Drain encourages us to choose life




Choose life… Insure Tennessee

by hopeworkscommunity

Choose life. When in doubt, when you are not sure... When there is a question choose life.

The question of Insure Tennessee is a question of whether or not we will choose life. It is not a question of a better way to choose life. It is not a question of not this but that. As more and more stories pour in it is obvious. For thousands of Tennessean it is increasingly each day a question of life or death... a question of life or needless and preventable suffering... a future of hope or one bound by despair. It is not about finding an answer. It is about the common sense and political will to grab the one (the only one) in front of us and stop the unnecessary misery that defines the lives of so many vulnerable Tennesseans.

Chattanooga voted last night to choose life. Their city council voted overwhelmingly in favor of a resolution supporting Insure Tennessee. They joined a growing movement of cities and towns saying they support their neighbors, their friends, their families. No one should have to unnecessarily suffer or suffer as a direct result of governmental policy. Insure Tennessee.

The movement is growing. Thanks to the leadership of people like Pam Weston in East Tennessee and Meryl and Randall Rice in West Tennessee and the stories and words of more and more Tennesseans the movement is growing. It is the growing crescendo of more and more ordinary Tennesseans saying "CHOOSE LIFE!!!!!"

Imagine a flood, a hurricane in Tennessee. The waters are rising.. People are dying.... Many are on top of their houses waiting for a miracle.. a boat... a something... someone who cares.... hope. The government has boats. But they decide to wait. "Let's make sure this is a good idea..."

The waters still rise. For some it is too late. For others it will soon be too late. Action matters. The hurricane is here for thousands of Tennesseans. And they are on top of their houses waiting.

Join the movement to choose life. Talk to your local government. Ask them to join Chattanooga and the other towns and counties that have acted.

Today. Today please choose life.

Insure Tennessee

Larry Drain ~


Keep on keeping on!