Estrogen and nerve growth factor-related systems in brain. Effects on basal forebrain cholinergic neurons and implications for learning and memory processes and aging

R. B. Gibbs, Kathryn Jones, B. Moorjani, V. Luine

Research output: Contribution to journalArticle

126 Citations (Scopus)

Abstract

Estrogen replacement can significantly affect the expression of ChAT and NGF receptors in specific basal forebrain cholinergic neurons. The time-course of the effects is consistent with a direct up-regulation of ChAT followed by either direct or indirect down-regulation of p75(NGFR) and trkA NGF receptors, possibly due to increased cholinergic activity in the hippocampal formation and cortex and a decrease in hippocampal levels of NGF. Current evidence suggests ChAT, p75(NGFR) trkA, and NGF all play a role in regulating cholinergic function in the hippocampal formation and cortex. In addition, all have been implicated in the maintenance of normal learning and memory processes as well as in changes in cognitive function associated with aging and with neurodegenerative disease. It is possible that estrogen may affect cognitive function via effects on NGF-related systems and basal forebrain cholinergic neurons. Effects of estrogen on cognitive function have been reported, as has some preliminary evidence for beneficial effects of estrogen in decreasing the prevalence of and reducing some cognitive deficits associated with Alzheimer's disease. Whether these effects are related to effects on NGF-related systems or basal forebrain cholinergic neurons is currently unknown. Indirect evidence suggests that estrogen interacts with NGF-related systems and that changes in circulating levels of estrogen can contribute to age-related changes in hippocampal levels of NGF. These findings have important implications for consideration of estrogen replacement therapy in pre- and post-menopausal women. Further studies examining effects of different regimens of estrogen replacement as well as estrogen combined with progesterone on NGF and basal forebrain cholinergic neurons in young and aged animals are required. Prospective studies correlating aging and estrogen replacement with numbers of basal forebrain cholinergic neurons and hippocampal and cortical levels of NGF also need to be performed to better assess the potential benefits of estrogen replacement in reducing age- and disease-related cognitive decline.

Original languageEnglish (US)
Pages (from-to)165-199
Number of pages35
JournalAnnals of the New York Academy of Sciences
Volume743
DOIs
StatePublished - 1994
Externally publishedYes

Fingerprint

Cholinergic Neurons
Nerve Growth Factor
Cholinergic Agents
Neurons
Brain
Estrogens
Aging of materials
Estrogen Replacement Therapy
Learning
Data storage equipment
Cognition
Nerve Growth Factor Receptors
Hippocampus
Basal Forebrain
Learning and Memory
Neuron
Estrogen
Nerve
Neurodegenerative diseases
Neurodegenerative Diseases

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{4a7454b27d2e4ea0ad5fb8e0b8218b1e,
title = "Estrogen and nerve growth factor-related systems in brain. Effects on basal forebrain cholinergic neurons and implications for learning and memory processes and aging",
abstract = "Estrogen replacement can significantly affect the expression of ChAT and NGF receptors in specific basal forebrain cholinergic neurons. The time-course of the effects is consistent with a direct up-regulation of ChAT followed by either direct or indirect down-regulation of p75(NGFR) and trkA NGF receptors, possibly due to increased cholinergic activity in the hippocampal formation and cortex and a decrease in hippocampal levels of NGF. Current evidence suggests ChAT, p75(NGFR) trkA, and NGF all play a role in regulating cholinergic function in the hippocampal formation and cortex. In addition, all have been implicated in the maintenance of normal learning and memory processes as well as in changes in cognitive function associated with aging and with neurodegenerative disease. It is possible that estrogen may affect cognitive function via effects on NGF-related systems and basal forebrain cholinergic neurons. Effects of estrogen on cognitive function have been reported, as has some preliminary evidence for beneficial effects of estrogen in decreasing the prevalence of and reducing some cognitive deficits associated with Alzheimer's disease. Whether these effects are related to effects on NGF-related systems or basal forebrain cholinergic neurons is currently unknown. Indirect evidence suggests that estrogen interacts with NGF-related systems and that changes in circulating levels of estrogen can contribute to age-related changes in hippocampal levels of NGF. These findings have important implications for consideration of estrogen replacement therapy in pre- and post-menopausal women. Further studies examining effects of different regimens of estrogen replacement as well as estrogen combined with progesterone on NGF and basal forebrain cholinergic neurons in young and aged animals are required. Prospective studies correlating aging and estrogen replacement with numbers of basal forebrain cholinergic neurons and hippocampal and cortical levels of NGF also need to be performed to better assess the potential benefits of estrogen replacement in reducing age- and disease-related cognitive decline.",
author = "Gibbs, {R. B.} and Kathryn Jones and B. Moorjani and V. Luine",
year = "1994",
doi = "10.1111/j.1749-6632.1994.tb55792.x",
language = "English (US)",
volume = "743",
pages = "165--199",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Estrogen and nerve growth factor-related systems in brain. Effects on basal forebrain cholinergic neurons and implications for learning and memory processes and aging

AU - Gibbs, R. B.

AU - Jones, Kathryn

AU - Moorjani, B.

AU - Luine, V.

PY - 1994

Y1 - 1994

N2 - Estrogen replacement can significantly affect the expression of ChAT and NGF receptors in specific basal forebrain cholinergic neurons. The time-course of the effects is consistent with a direct up-regulation of ChAT followed by either direct or indirect down-regulation of p75(NGFR) and trkA NGF receptors, possibly due to increased cholinergic activity in the hippocampal formation and cortex and a decrease in hippocampal levels of NGF. Current evidence suggests ChAT, p75(NGFR) trkA, and NGF all play a role in regulating cholinergic function in the hippocampal formation and cortex. In addition, all have been implicated in the maintenance of normal learning and memory processes as well as in changes in cognitive function associated with aging and with neurodegenerative disease. It is possible that estrogen may affect cognitive function via effects on NGF-related systems and basal forebrain cholinergic neurons. Effects of estrogen on cognitive function have been reported, as has some preliminary evidence for beneficial effects of estrogen in decreasing the prevalence of and reducing some cognitive deficits associated with Alzheimer's disease. Whether these effects are related to effects on NGF-related systems or basal forebrain cholinergic neurons is currently unknown. Indirect evidence suggests that estrogen interacts with NGF-related systems and that changes in circulating levels of estrogen can contribute to age-related changes in hippocampal levels of NGF. These findings have important implications for consideration of estrogen replacement therapy in pre- and post-menopausal women. Further studies examining effects of different regimens of estrogen replacement as well as estrogen combined with progesterone on NGF and basal forebrain cholinergic neurons in young and aged animals are required. Prospective studies correlating aging and estrogen replacement with numbers of basal forebrain cholinergic neurons and hippocampal and cortical levels of NGF also need to be performed to better assess the potential benefits of estrogen replacement in reducing age- and disease-related cognitive decline.

AB - Estrogen replacement can significantly affect the expression of ChAT and NGF receptors in specific basal forebrain cholinergic neurons. The time-course of the effects is consistent with a direct up-regulation of ChAT followed by either direct or indirect down-regulation of p75(NGFR) and trkA NGF receptors, possibly due to increased cholinergic activity in the hippocampal formation and cortex and a decrease in hippocampal levels of NGF. Current evidence suggests ChAT, p75(NGFR) trkA, and NGF all play a role in regulating cholinergic function in the hippocampal formation and cortex. In addition, all have been implicated in the maintenance of normal learning and memory processes as well as in changes in cognitive function associated with aging and with neurodegenerative disease. It is possible that estrogen may affect cognitive function via effects on NGF-related systems and basal forebrain cholinergic neurons. Effects of estrogen on cognitive function have been reported, as has some preliminary evidence for beneficial effects of estrogen in decreasing the prevalence of and reducing some cognitive deficits associated with Alzheimer's disease. Whether these effects are related to effects on NGF-related systems or basal forebrain cholinergic neurons is currently unknown. Indirect evidence suggests that estrogen interacts with NGF-related systems and that changes in circulating levels of estrogen can contribute to age-related changes in hippocampal levels of NGF. These findings have important implications for consideration of estrogen replacement therapy in pre- and post-menopausal women. Further studies examining effects of different regimens of estrogen replacement as well as estrogen combined with progesterone on NGF and basal forebrain cholinergic neurons in young and aged animals are required. Prospective studies correlating aging and estrogen replacement with numbers of basal forebrain cholinergic neurons and hippocampal and cortical levels of NGF also need to be performed to better assess the potential benefits of estrogen replacement in reducing age- and disease-related cognitive decline.

UR - http://www.scopus.com/inward/record.url?scp=0028607581&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028607581&partnerID=8YFLogxK

U2 - 10.1111/j.1749-6632.1994.tb55792.x

DO - 10.1111/j.1749-6632.1994.tb55792.x

M3 - Article

VL - 743

SP - 165

EP - 199

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -