Can we switch microglia's phenotype to foster neuroprotection? Focus on multiple sclerosis

摘要: Microglia cells, the resident innate immune cells in brain, are highly active, extending and retracting motile processes through which they continuously survey their microenvironment for 'danger signals' interact dynamically with surrounding cells. Upon sensing changes central nervous system microenvironment, microglia become activated, undergoing morphological functional changes. activation is not an 'all-or-none' process, but rather a continuum depending on encountered stimuli, expressed spectrum of molecular phenotypes ranging from so-called 'classically activated', pro-inflammatory profile, to 'alternatively activated' associated beneficial, less inflammatory, neuroprotective profile. has been demonstrated most neurological diseases diverse aetiology implicated as contributor neurodegeneration. The possibility promote microglia's phenotype therefore therapeutic goal. We have focused our discussion role multiple sclerosis, prototype demyelinating, neurodegenerative disease, effect currently approved or on-trial anti-inflammatory strategies that might mediate neuroprotection at least part by modifying behaviour via switch detrimental protective one. In addition pharmaceutical approaches, such treatment glatiramer acetate, interferon-β, fingolimod dimethyl fumarate, we address alternative approach mesenchymal stem potential 'calming' microglia.