Physical exercise may protect the brain from stress depression

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Physical exercise may protect the brain from stress depression 1

Posted on September 25, 2014 The “Cell” magazine, a study showed that a muscle gene can be activated by physical exercise, in order to protect the brains of mice against stress-induced depression. Triggered gene, called PGC-1α1, blocked inflammation in the brain may cause a (which causes depression) transmission metabolites. Learn why exercise can relieve symptoms and biochemical causes of depression patients part of this, the study collaborator, Jorge Ruas Karolinska Institute in Sweden, said:. “This study opens up a very interesting therapeutic potential.”

Previous studies have shown that physical exercise can prevent or improve the situation of many diseases, ranging from diabetes and obesity to mood disorders and depression disease. However, if improvement from cardiovascular effects, or muscle conditioning, or the benefits of social psychology, which has been neither clear.

In 2012, Ruas and his colleagues found that different forms of skeletal muscle PGC-1α gene will respond to different types of movement. The gene may be from two different transcription promoters: the resistance in response to a version of the training, such as weight lifting, and other, PGC-1α1 response to endurance activities. To understand the different variants of the gene, various mouse models studied to build a high expression of the different forms of the gene, and gene knockout lines. Ruas, explains, animal models also provide a means to separate from the influence of the invisible biochemical psychosocial impact of movement.

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In the new study, Ruas and his collaborators in transgenic mice expressing PGC-1α1, the control animals and humans analog trigger depression in chronic mild stress. After five weeks, the control group animals showed signs of behavioral anhedonia and despair, if not worked hard in the forced swim test. They also show some of the brain changes, including reduction in synaptic plasticity, glutamic acid, and lower levels of metabolic imbalance neurotrophic factor. However, in transgenic mice, neither depression nor depressive behavior anatomical landmarks.

Metabolic differences analysis revealed differences in animal tryptophan metabolism, Ruas said. “From the perspective of the brain, tryptophan metabolism is significant, because it uses the brain to produce serotonin, but for skeletal muscle, it would not make much sense.”

By digging deeper, they found that, PGC-1α1 gene regulation step tryptophan metabolism in the muscle, one of the metabolites, kynurenine (KYN), is converted to another form, kynurenic acid (KA). Previous studies have found that, KYN within the brain can cause inflammation, the inflammation associated with depression and schizophrenia-like symptoms. Outside the brain, liver stressful time in more tryptophan can be converted to KYN, and KYN can cross the blood – brain barrier, triggering an inflammatory response.

In mouse muscle, such as exercise-induced PGC-1α1 by elevated levels, the more KYN converted to KA, the latter can not cross the blood – brain barrier. To test for depression-like symptoms appear in their experiments are indeed the same time to control and transgenic mice were given KYN mediated by researchers KYN, and found that only the former group showed a gene expression associated with depression and changes in behavior.

These results suggest that, KYN converted by PGC-1α1 KA, may be related to stress-induced inflammation and depression-related key metabolic steps.

“It is important to remember that ‘pressure’ is not only stressful everyday life, including activation of cell stress response and external events,” collaborator Maria Lindskog said.

When the control mice after eight weeks of exercise, PGC-1α1 gene expression in skeletal muscle increases. Similar results appear in healthy adults after three weeks after the training program. Overall, the results indicate that “detoxifying effect muscles obtained in the absence of pressure conditions previously described,” Ruas said. “I do not think anyone will be able to think of this before changes in muscle and brain inflammation.”

“This is a non-drug mechanism of antidepressant action on interesting research,” University of Iowa neuroscientist Michael Lutter (not involved in the study) said.

Behavior at Emory University immunologist Andrew Miller said, adding that the movement or targeting PGC-1α1 drugs, is likely to be the only effective way to have signs of inflammation and KYN elevated depressive patients, such as those who also have early life stress, obesity, cancer, or other diseases. In healthy patients, the symptoms of brain KYN levels and no significant correlation between depression. “Exercise may be particularly suitable for those patients with depression increased inflammation in those,” Miller (not involved in the study) said. “These results allow us to enjoy sports therapy for selecting groups of individuals.”

“Certain aspects of looking for muscle metabolism may be associated with the development of mood disorders related,” Lutter said. “Could be more intimate than previously thought between the mind and body.”

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