Looking specifically at MECP2 knockout mice, male mice are studied more since their symptoms are more severe and show sooner than in female mice. Similar to humans, we have 3-6 weeks of normal development before symptoms start, followed by slowed brain development, lower brain weight, and then death by 10 weeks. There’s also a 46% decrease in the number of glutamatergic synapses, resulting in decreased LTP and impaired synaptic plasticity. Additionally, there’s a 30-40% decrease in GABA release from GABAergic neurons in the forebrain, which is due to a decrease in GABA content in synaptic vesicles. Introduction of wild-type MeCP2 in already symptomatic mice can reverse the disease phenotype. As of now, this method isn’t feasible yet in humans since the technology doesn't allow us to pick out only the defective cells and introducing MeCP2 to normal cells would cause overexpression and be detrimental rather than therapeutic.