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Neuroinflammation
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=== Activation of cyclical neuroinflammation: A self-perpetuating cycle === When a patient gets an infection, the body attempts to return homeostasis. The immune system has regulatory structures called toll-like receptors (TLRs). High amounts of stress or a previous injury can predispose an individual’s TLRs to be more sensitive, releasing inflammatory molecules more readily in response to an immune stressor.<ref>{{Cite journal | last = Gárate | first = Iciar | last2 = Garcia-Bueno | first2 = Borja | last3 = Madrigal | first3 = Jose Luis Muñoz | last4 = Caso | first4 = Javier Rubén | last5 = Alou | first5 = Luis | last6 = Gomez-Lus | first6 = Marisa L. | last7 = Micó | first7 = Juan Antonio | last8 = Leza | first8 = Juan Carlos | date = 2013-01-01 | title = Stress-induced neuroinflammation: role of the Toll-like receptor-4 pathway|url=https://www.ncbi.nlm.nih.gov/pubmed/22906518|journal=Biological Psychiatry|volume=73|issue=1|pages=32–43|doi=10.1016/j.biopsych.2012.07.005|issn=1873-2402|pmid=22906518}}</ref> One of the downstream pathways of TLRs, the oxidative and nitrosative stress pathway (O&NS) can get activated. If this pathway is overstimulated, the body will produce a larger-scale response in an effort to return to normal.<ref>{{Cite journal | last = Liu | first = JiaJun | last2 = Buisman-Pijlman | first2 = Femke | last3 = Hutchinson | first3 = Mark R.| date = 2014 | title = Toll-like receptor 4: innate immune regulator of neuroimmune and neuroendocrine interactions in stress and major depressive disorder |url =https://www.ncbi.nlm.nih.gov/pubmed/25324715|journal=Frontiers in Neuroscience|volume=8|pages=309|doi=10.3389/fnins.2014.00309|issn=1662-4548|pmc=4179746|pmid=25324715}}</ref> In this attempt, a chemical called damage-associated molecular patterns (DAMPs) triggers the release of more inflammatory molecules, some of which activate the TLRs<ref>{{Cite journal | last = Morris | first = Gerwyn | last2 = Berk | first2 = Michael | last3 = Walder | first3 = Ken | last4 = Maes | first4 = Michael | date = 2015-02-06 | title = Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses|url=https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-014-0259-2|journal=BMC Medicine|language=en|volume=13|issue=1|doi=10.1186/s12916-014-0259-2|issn=1741-7015|pmc=4320458|pmid=25856766}}</ref> (Morris et al., 2015). The process of activation from TLRs to the O&NS pathway to the production of more inflammatory molecules then becomes a cycle.<ref name=":4">{{Cite journal | last = Chaudhuri | first = A. | last2 = Condon | first2 = B.R. | last3 = Gow | first3 = J.W. | last4 = Brennan | first4 = D. | last5 = Hadley | first5 = D. M. | date = 2003-02-10 | title = Proton magnetic resonance spectroscopy of basal ganglia in chronic fatigue syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/12598734|journal=Neuroreport|volume=14|issue=2|pages=225–228|doi=10.1097/01.wnr.0000054960.21656.64|issn=0959-4965|pmid=12598734}}</ref>
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