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Levetiracetam antagonizes tlr4

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Lipopolysaccharides and tlr4 are implicated in disease states caused by pathogenic infection. Activation of tlr4 by lipopolysaccharides, endotoxins released by many pathogens such as lipid a, and other endotoxins such as those release by fungal infections, causes an increase in vegf and lymphangiogenesis (to promote clearance of these endotoxins via increased lymphatic function)- but also an increase in inflammatory cytokines. Tlr4 has been implicated in many disease states and neurological disorders. 

Tlr4 antagonization is a method of symptom reduction in disease states, be a pathogenic or otherwise, that act upon tlr4 positively. 

however, some lipopolysaccharides act as antagonists at tlr4 receptors. This, I would assume, benefits the pathogen as tlr4 activation is the body’s response to pathogenic infection in its attempts to clear it. 

this is interesting when looking at hppd in respects to inflammation and possibly hppd when suspected pathogenic infection is present. 

This article is intended to increase the knowledge base of levetiracetam and help elucidate why some people respond to it and some do not.  

tldr: levetiracetam antagonizes tlr4 and thus decreases lymphatic response to pathogenic infection and also decreases pathogenic or neurological states that increase inflammatory cytokines via the tlr4 receptor. 


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