The delay in motor and cognitive dysfunction in Mecp2 nulls treated with ALC, therefore, may be more analogous to the later onset of motor and cognitive deficits displayed in Mecp2308 mutant mice (containing a late truncation of Mecp2), in which dendritic arbors are normal but synaptic function is disrupted [75]. The gene discussed is MECP2; the disease is Cognitive impairment.