These alterations might stem from the mode of activation, as continuous administration of BDNF or its overexpression led to attenuation of microglial activation in a mouse model of HD (Lund et al., 2008; Xie et al., 2010; Giampà et al., 2013; Hixson et al., 2019), while acute administration of BDNF increased microglial activity (Jiang et al., 2010) and accelerated neurodegeneration (Colombo et al., 2012). The gene discussed is BDNF; the disease is Huntington disease.