Ej. Mufson et al., NERVE GROWTH-FACTOR IN ALZHEIMERS-DISEASE - DEFECTIVE RETROGRADE TRANSPORT TO NUCLEUS BASALIS, NeuroReport, 6(7), 1995, pp. 1063-1066
NGF immunohistochemistry was combined with quantitative optical densit
ometry to evaluate whether retrogradely transported NGF is altered wit
hin cholinergic basal forebrain (CBF) neurons in Alzheimer's disease (
AD). In normal aged humans, almost all CBF neurons stained for NGF. Al
though fewer in total number, remaining CBF perikarya in AD displayed
diminished (32%) or undetectable NGF immunoreactivity. Based upon thes
e data we hypothesize that there is a defect in retrograde transport o
f NGF in AD which may be due to a abnormal production and/or utilizati
on of the trk receptor. This defect may be a primary event mediating t
he degeneration of CBF neurons in AD.