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Low-dose naltrexone (LDN) has emerged as one of the most promising agents in this area, working through glial cell modulation to reduce neuroinflammation and through toll-like receptor pathways to quiet abnormal immune activation

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GLD-1 alone accounts for more than half of this repression, as LAG-1 level is elevated almost 3-fold in the gld-1 single null mutant, which is consistent with lag-1 mRNA being identified as a GLD-1 target in RNA pull-down experiments [44,45]