They also had lower levels of the two genes involved in making brain circuits. These differences might change how different neurons communicate in the brain and could render SSRIs ineffective, the researchers said. Senior author Rusty Gage, president of the Salk Institute for Biological Studies, said: "With each new study, we move closer to a fuller understanding of the complex neural circuitry underlying neuropsychiatric diseases, including major depression.
This paper, along with another we recently published, not only provides insights into this common treatment but also suggests that other drugs, such as serotonergic antagonists, could be additional options for some patients. Gage added, "These results contribute to a new way of examining, understanding and addressing depression. Valentina Mosienko, a neuroscientist at Britain's University of Exeter College of Medicine and Health, told Newsweek, "This study is the first to offer a new model to study serotonergic neurons by deriving them from skin cells of patients non- and responsive to antidepressant treatment.
She said normalizing the length of serotonergic neurons in patients with major depressive disorders could one day become a treatment for depression. Ullrich Bartsch, a research fellow at Britain's University of Bristol, told Newsweek , "This study allowed a rare glimpse of very fundamental properties of neurons that produce the neurotransmitter serotonin in the brain.
Scientists report a discovery that may explain why this is the case. Depression is one of the most common mental health disorders in the United States, affecting around In most cases of depression, psychotherapy, antidepressant medications such as selective serotonin reuptake inhibitors , or a combination of both are prescribed to help treat symptoms.
However, only one third of people with depression benefit from the antidepressant that they are prescribed. Therefore, the most effective treatment is currently identified through a process of trial and error until the right fit is found. One way to develop tailored treatments would be to distinguish biomarkers that determine whether a person would respond to a certain medication or not.
Although research in this area has been promising, no significant predictors have yet been identified due, in part, to three issues. Although antidepressants are meant to help you feel better, in some cases an antidepressant may combine with other medications you are taking or foods you are eating and lead to serotonin syndrome , an uncommon condition involving an overabundance of serotonin in the body, the Cleveland Clinic states.
Symptoms to watch out for, Lim says, include fever, aches, shakes, sweats, fatigue, irritability, a bad headache , confusion, agitation, restlessness, dizziness, difficulty seeing or walking, muscle twitching, muscle tension, or jaw clenching. Typically, serotonin syndrome happens within days or weeks of starting an antidepressant or after a dose increase, says Lim.
The most common factors that affect your risk of serotonin syndrome, per the Cleveland Clinic, are:. As a result, a medication that once worked well at quelling your sadness, anxiety, and other symptom no longer has that power. Sometimes, Hullett says, increasing the dose under supervision by your doctor may help. In other cases, trying a different medication or treatment is helpful.
Specific warning signs to watch for include feeling agitated or restless, pacing or constant movement, hand wringing, or feeling generally out of control. Thomas says. Options include another depression medication or the addition of counseling, psychotherapy, mood-boosting cardio exercise, or light therapy to your treatment regimen. Out of a total of over 30, genes on the microarray, she discovered approximately genes related to stress and genes related to depression, with an overlap of only five genes between the two.
Most animal models that are used by scientists to test antidepressants are based on the hypothesis that stress causes depression. That is one key reason why current antidepressants aren't doing a great job, Redei noted. She is now looking at the genes that differ in the depressed rat to narrow down targets for drug development. She said another reason current antidepressants are often ineffective is that they aim to boost neurotransmitters based on the popular molecular explanation of depression, which is that it's the result of decreased levels of the neurotransmitters serotonin, norepinephrine and dopamine.
But that's wrong, Redei said. In the second part of the study, Redei found strong indications that depression actually begins further up in the chain of events in the brain. The biochemical events that ultimately result in depression actually start in the development and functioning of neurons. Her animal model of depression did not show dramatic differences in the levels of genes controlling neurotransmitters functions.
Jelena Radulovic, M. Materials provided by Northwestern University.
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