Showing posts with label Stress. Show all posts
Showing posts with label Stress. Show all posts

New Explanation For Depression And Chronic Stress | UA Magazine

Major Depressive Disorder and chronic stress are both characterized by atrophy of neurons and loss of synapses (centers of neurotransmission that deliver neural impulses) in specific brain areas. It’s been recently shown that the prefrontal cortex of subjects with Major Depressive Disorder, analyzed postmortem, contains abnormally low expression levels of a protein called mTORC1, which controls protein synthesis during cell growth and synapses remodeling.
In line with this, it was also observed that in rats some antidepressants augment mTORC1 levels, and this is associated with increased synapses formation in the prefrontal cortex. But what controls mTORC1 expression in the brain? And more importantly, would it be possible to manipulate mTORC1 levels therapeutically to rescue neuronal function?

Stress and TORC1

In a study just published in Nature Medicine, Ota and colleagues from Yale University have identified a new mechanism that is at least in part responsible for the brain alterations caused by loss of mTORC1. The scientists focused on a gene called REDD1 whose product is known to inhibit mTORC1 function. They found that in individuals that were affected by Major Depressive Disorder, high levels of REDD1 correlated with low mTORC1 expression, suggesting a possible link between these two molecules.

An integrative review of factors associated with telomere length and implications for biobehavioral research.

Although telomere shortening occurs as a natural part of aging, there is now a robust body of research that suggests that there is a relationship between psychosocial, environmental, and behavioral factors and changes in telomere length. These factors need to be considered when integrating telomere measurement in biobehavioral research studies.
OBJECTIVES:

This article provides a brief summary of the known facts about telomere biology and an integrative review of current human research studies that assessed relationships between psychosocial, environmental, or behavioral factors and telomere length.
METHODS:

An integrative review was conducted to examine human research studies that focused on psychosocial, environmental, and behavioral factors affecting telomere length and telomerase activity using the electronic databases PubMed/Medline and CINAHL from 2003 to the present. In addition to the known individual factors that are associated with telomere length, the results of the integrative review suggest that perceived stress, childhood adversities, major depressive disorder, educational attainment, physical activity, and sleep duration should also be measured.
DISCUSSION:

Multiple factors have been shown to affect telomere length. To advance understanding of the role of telomere length in health and disease risk, it will be important to further elucidate the mechanisms that contribute to telomere shortening.
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Exposure to stress even before conception causes genetic changes to offspring

 " A female's exposure to distress even before she conceives causes changes in the expression of a gene linked to the stress mechanism in the body -- in the ovum and later in the brains of the offspring from when they are born, according to a new study on rats conducted by the University of Haifa."


Social stress and the inflamed brain: relevance to depression

 "The study, conducted in male rats, compared expression of 88 genes involved in signaling within the brain between socially stressed and non-stressed rats. It revealed more than 35 genes in stressed rats that had altered expression compared with non-stressed controls. Many of the genes that were differentially expressed were related to inflammation. Follow-up studies measuring protein levels revealed that Interleukin-1β and Monocyte chemotactic protein-1, inflammatory markers known to play a role in depression and heart disease, were suppressed in the brains of the resilient subset of rats and Interleukin-1β was increased in the vulnerable group. Dr. Wood measured the gene and protein levels under resting conditions 24 hours after just 5 daily 30-minute exposures to social stress."


Fetal exposure to excessive stress hormones in the womb linked to adult mood disorders

"Exposure of the developing fetus to excessive levels of stress hormones in the womb can cause mood disorders in later life and now, for the first time, researchers have found a mechanism that may underpin this process, according to research presented April 7 at the British Neuroscience Association Festival of Neuroscience (BNA2013) in London."


Chronic fatigue syndrome: System under stress

"ScienceDaily (Nov. 14, 2012) — Australian researchers have discovered for the first time that reduced heart rate variability -- or changes in heart beat timing -- best predicts cognitive disturbances, such as concentration difficulties commonly reported by people with chronic fatigue syndrome (CFS). This adds to the growing body of evidence linking autonomic nervous system imbalance to symptoms of this poorly understood disorder."

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Stress May Cause Illness By Methylating Genes: MNT

The researchers invited 76 participants in their sixties to undergo two types of stressful event: one was to to take part in a mock job interview, and the other was to solve arithmetic problems under observation. Both these tests are commonly used to produce stress under lab conditions.The participants gave blood samples before the tests, and also twice afterwards: one ten minutes after (post-test), and another 1.5 hours after (follow-up). From these the researchers could measure the amount of DNA methylation in the two genes.They found that the BDNF gene remained unaffected by any of the stress tests.But the OXTR gene showed methylation changes. There was an increase in methylation in a section of the OXTR gene in the post-test measure: this suggests the cells formed fewer receptors.

Depression And Chronic Inflammation Result From Childhood Adversity

Inflammation is the body's natural response to injury caused by invading pathogens, whether this be a sore throat due to bacteria from a cold, a wound that has become infected, or any other foreign pathogen that the body has to fight in order to get rid of it. Evidence is now growing that psychological traumas cause a similar response, although this type of inflammation can be destructive.

Sleep deprivation effect on the immune system mirrors physical stress

Severe sleep loss jolts the immune system into action, reflecting the same type of immediate response shown during exposure to stress, a new study reports.
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New study explains how stress can boost immune system

A study spearheaded by a Stanford University School of Medicine scientist has tracked the trajectories of key immune cells in response to short-term stress and traced, in great detail, how hormones triggered by such stress enhance immune readiness. The study, conducted in rats, adds weight to evidence that immune responsiveness is heightened, rather than suppressed as many believe, by the so-called "fight-or-flight" response.

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

PNAS: We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to down-regulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.
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Social stress affects immune system gene expression in monkeys

The ranking of a monkey within her social environment and the stress accompanying that status dramatically alters the expression of nearly 1,000 genes, a new scientific study reports. The research is the first to demonstrate a link between social status and genetic regulation in primates on a genome-wide scale, revealing a strong, plastic link between social environment and biology.

How stress influences disease: Research reveals inflammation as the culprit

Stress wreaks havoc on the mind and body. For example, psychological stress is associated with greater risk for depression, heart disease and infectious diseases. But, until now, it has not been clear exactly how stress influences disease and health.
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Stress making your blood pressure rise? Blame your immune system

If stress is giving you high blood pressure, blame the immune system. T cells, helpful for fighting infections, are also necessary for mice to show an increase in blood pressure after a period of psychological stress, scientists have found.
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