Thus, the canonical rationale for the treatment of AD patients with NGF is based on reported defective retrograde transport of NGF toward BFCN (Mufson et al., 1995) and on the accumulation of proNGF, that may have neurotoxic action (Lee et al., 2001), in the brain of AD patients (Fahnestock et al., 2001). The gene discussed is NGF; the disease is Alzheimer disease.