GFAP and Alexander disease: 2001). The gain of function of GFAP in models of Alexander's disease is suggested by the fact that mice null for GFAP develop normally (Pekny et al. 1995) and do not exhibit a phenotype that resembles Alexander's disease (Messing et al. 2012), while mice that overexpress GFAP die shortly after birth and have impaired cognition and spatial learning (Hagemann et al. 2013). Therefore, it is possible that using a pharmacological agent that dampens GFAP expression may be helpful in the treatment of Alexander's disease (Messing et al. 2010).