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

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

doi:10.1097/00001756-199505090-00028

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 journal › Article › peer-review

188 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 language	English (US)
Pages (from-to)	1063-1066
Number of pages	4
Journal	NeuroReport
Volume	6
Issue number	7
DOIs	https://doi.org/10.1097/00001756-199505090-00028
State	Published - May 1995
Externally published	Yes

Keywords

Aging
Disease
Human
Immunocytochemistry
Nerve growth factor
Receptors
Trophin

ASJC Scopus subject areas

General Neuroscience

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10.1097/00001756-199505090-00028

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title = "Nerve growth factor in alzheimer{\textquoteright}s disease: Defective retrograde transport to nucleus basalis",

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{\textquoteright}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.",

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T1 - Nerve growth factor in alzheimer’s disease

T2 - Defective retrograde transport to nucleus basalis

AU - Mufson, Elliott J.

AU - Conner, James M.

AU - Kordower, Jeffrey H.

PY - 1995/5

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N2 - 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.

AB - 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.

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KW - Disease

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KW - Immunocytochemistry

KW - Nerve growth factor

KW - Receptors

KW - Trophin

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

Abstract

Keywords

ASJC Scopus subject areas

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