<b>Background:</b> Recent genome-wide association screening (GWAS) studies have linked Alzheimer's disease (AD) neuropathology to gene networks that regulate immune function.Kan et al. recently reported that <i>Arg1</i> (an anti-inflammatory gene that codes for arginase-1) is expressed in parts of the brain associated with amyloidosis prior to the onset of neuronal loss, suggesting that chronic brain arginine deprivation promotes AD-related neuropathology.
Furthermore, we found Aβ exposure increased the levels of microglial M1 markers, interleukin (IL)-1β, IL-6, and tumor necrosis factor α, and the pretreatment of TSG suppressed the increase of M1 markers and enhanced the levels of M2 markers, including IL-10, brain-derived neurotrophic factor, glial cell-derived neurotrophic factor, and arginase-1.