Nerve growth factor in Alzheimer's disease: defective retrograde transport to nucleus basalis.
NGF immunohistochemistry was combined with quantitative optical densitometry to evaluate whether retrogradely transported NGF is altered within cholinergic basal forebrain (CBF) neurons in Alzheimer's disease (AD). In normal aged humans, almost all CBF neurons stained for NGF. Although fewer in total number, remaining CBF perikarya in AD displayed diminished (32%) or undetectable NGF immunoreactivity. Based upon these data we hypothesize that there is a defect in retrograde transport of NGF in AD which may be due to a abnormal production and/or utilization of the trk receptor. This defect may be a primary event mediating the degeneration of CBF neurons in AD.
Mufson
E J
EJ
Department of Neurological Sciences, Rush Alzheimer's Disease Center, Rush Presbyterian-St Luke's Medical Center, Chicago, IL 60612, USA.
Conner
J M
JM
Kordower
J H
JH
D000368:Aged; D000375:Aging / Q000378:metabolism; D000544:Alzheimer Disease / Q000378:metabolism*; D001479:Basal Ganglia / Q000166:cytology / Q000378:metabolism*; D003720:Densitometry; D005726:Ganglia, Parasympathetic / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D009414:Nerve Growth Factors / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism
D009414:Nerve Growth Factors; D017475:Receptors, Nerve Growth Factor