CURRENT ASPECTS REGARDING THE RELEVANCE OF INFLAMMATION IN MAJOR DEPRESSIVE DISORDER

2019 
CURRENT ASPECTS REGARDING THE RELEVANCE OF INFLAMMATION IN MAJOR DEPRESSIVE DISORDER (Abstract): The World Health Organization predicts that depression, which already affects about 10% of the population in the United States, will be the world’s leading medical condition by 2030. The relationship between inflammation and depression has a bidirectional potential, but the underlying mechanisms are still less knowledgeable. In this way, the theory that argues that the inflammatory process is an etiologic factor in depression associated increased levels of inflammatory markers with decreased levels of serotonin, a neurotransmitter important in the pathogenesis of depression. An increase in serum levels of cytokines may lead to decreased availability of serotonin and other neurotransmitters, activation of the hypothalamic-pituitary-adrenal axis and increased oxidative stress in the brain. Depressive symptoms can cause a slight inflammatory response by triggering certain hormonal disorders in the HPA axis that leads to increased susceptibility to infections. Thus, inflammatory mechanisms may provide new paths for intervention and prevention of depressive affective disorders. Also, inflammation could explain the fairly widespread association of somatic-type diseases (such as cardiovascular disease) and diabetes, as well as mental disorders such as depression or schizophrenia. Cytokines have been shown to be related to many depression symptoms to a variety of the population. Examination of gene expression profiles provides insight into how altered gene activity is linked with exposure to stress. The expression of a gene may increase or decrease, and it represents the first step in the production of proteins that communicate changes in cell functions, including those that are involved in the immune systems’ response to the inflammation.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    0
    Citations
    NaN
    KQI
    []