We and others showed some years ago that despite normal levels of NGF mRNA expression in human brain tissue from AD subjects (Jetté et al., 1994), NGF-immunoreactive protein detected by ELISA or bioassay is increased in cortex and hippocampus and decreased in basal forebrain, suggesting that NGF-immunoreactive material accumulates in AD due to failed BFCN retrograde transport (Crutcher et al., 1993; Scott et al., 1995; Fahnestock et al., 1996; Narisawa-Saito et al., 1996). Here, NGF is linked to Alzheimer disease.