In particular, the shift of GABA from the hyperpolarizing to the depolarizing direction, due to impairment of the cation-chloride KCC2 exporter, is responsible for behavioral deficits observed in the adult AD11 mouse, an animal model of AD, in which neutralization of NGF with selective anti-NGF antibodies leads to a neurodegenerative pathology similar to that observed in AD patients [153]. This evidence concerns the gene NGF and Alzheimer disease.