Nerve growth factor in alzheimer’s disease: Defective retrograde transport to nucleus basalis

Elliott J. Mufson, James M. Conner, Jeffrey H. Kordower

Research output: Contribution to journalArticlepeer-review

178 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1063-1066
Number of pages4
JournalNeuroReport
Volume6
Issue number7
DOIs
StatePublished - May 1995
Externally publishedYes

Keywords

  • Aging
  • Disease
  • Human
  • Immunocytochemistry
  • Nerve growth factor
  • Receptors
  • Trophin

ASJC Scopus subject areas

  • Neuroscience(all)

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