Nerve growth factor in alzheimer’s disease: Defective retrograde transport to nucleus basalis
Document Type
Article
Abstract
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. © Rapid Communications of Oxford Ltd.
Keywords
Aging, Disease, Human, Immunocytochemistry, Nerve growth factor, Receptors, Trophin
Publication Date
1-1-1995
Publication Title
NeuroReport
ISSN
09594965
E-ISSN
1473558X
Volume
6
Issue
7
First Page
1063
Last Page
1066
PubMed ID
7632896
Digital Object Identifier (DOI)
10.1097/00001756-199505090-00028
Recommended Citation
Mufson, Elliott J.; Conner, James M.; and Kordower, Jeffrey H., "Nerve growth factor in alzheimer’s disease: Defective retrograde transport to nucleus basalis" (1995). Translational Neuroscience. 1878.
https://scholar.barrowneuro.org/neurobiology/1878