Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors

Autores
Bellini, María José; González Burgos, Ignacio
Año de publicación
2015
Idioma
inglés
Tipo de recurso
parte de libro
Estado
versión publicada
Descripción
There is growing evidence that documents profound effects of estrogens on learning, memory, and mood as well as neurodevelopment and neurodegenerative diseases. However, the ability of estradiol to influence synaptic plasticity, neurotransmission, neurodegeneration and cognition, could be different depending on sex dimorphisms. It emerges that estrogens have different, even opposite, effects as well as similar effects in male and female brains. The protective effects of estradiol on neural cells are mediated in part by modulation of neurotrophic factors such as insulin like growth factor (IGF-l), tyrosine kinase A (Trk A), nerve growth factors (NGF), and the like. Also, it modulates the action of neurotrophins, which in turn regulate the synaptogenesis, synaptic plasticity and synaptic functions. By these actions estrogen prevents or slows down the neurodegenerative process. Another described effect of estradiol is the capacity to modulate inflammatory response mediated by glial cells. Neuroinflammation is a feature not only of many neurological disorders but also of aging, and it is accompanied by activation of glial cells and the release of proinflammatory cytokines and chemokines. Such activation is a normal response oriented to protect neural tissue. However, excessive and chronic activation of glia may lead to neurotoxicity and may be harmful for neural tissue. Estrogenic compounds may be candidates to counteract brain inflammation under neurodegenerative conditions by targeting the production and release of proinflammatory molecules by glial cells. In this chapter we will review different mechanisms that may be implicated in the diverse actions of estradiol, the differences according to gender and we empathize in the anti-inflammatory action on glial cell. We will also explore the interaction of estradiol with others neurotrophic factors, such as IGF-I in the regulation of neurodegeneration and memory impairment. Finally, the possibility of using selective estrogen receptor modulators (SERMs) to exert estradiollike neuroprotective actions in the brain as an alternative to estrogen will be discussed.
Instituto de Investigaciones Bioquímicas de La Plata
Materia
Biología
estrogen
inflammation
cognition
sex differences
glia
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/130694

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network_name_str SEDICI (UNLP)
spelling Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factorsBellini, María JoséGonzález Burgos, IgnacioBiologíaestrogeninflammationcognitionsex differencesgliaThere is growing evidence that documents profound effects of estrogens on learning, memory, and mood as well as neurodevelopment and neurodegenerative diseases. However, the ability of estradiol to influence synaptic plasticity, neurotransmission, neurodegeneration and cognition, could be different depending on sex dimorphisms. It emerges that estrogens have different, even opposite, effects as well as similar effects in male and female brains. The protective effects of estradiol on neural cells are mediated in part by modulation of neurotrophic factors such as insulin like growth factor (IGF-l), tyrosine kinase A (Trk A), nerve growth factors (NGF), and the like. Also, it modulates the action of neurotrophins, which in turn regulate the synaptogenesis, synaptic plasticity and synaptic functions. By these actions estrogen prevents or slows down the neurodegenerative process. Another described effect of estradiol is the capacity to modulate inflammatory response mediated by glial cells. Neuroinflammation is a feature not only of many neurological disorders but also of aging, and it is accompanied by activation of glial cells and the release of proinflammatory cytokines and chemokines. Such activation is a normal response oriented to protect neural tissue. However, excessive and chronic activation of glia may lead to neurotoxicity and may be harmful for neural tissue. Estrogenic compounds may be candidates to counteract brain inflammation under neurodegenerative conditions by targeting the production and release of proinflammatory molecules by glial cells. In this chapter we will review different mechanisms that may be implicated in the diverse actions of estradiol, the differences according to gender and we empathize in the anti-inflammatory action on glial cell. We will also explore the interaction of estradiol with others neurotrophic factors, such as IGF-I in the regulation of neurodegeneration and memory impairment. Finally, the possibility of using selective estrogen receptor modulators (SERMs) to exert estradiollike neuroprotective actions in the brain as an alternative to estrogen will be discussed.Instituto de Investigaciones Bioquímicas de La PlataNova Science Publishers2015info:eu-repo/semantics/bookPartinfo:eu-repo/semantics/publishedVersionCapitulo de librohttp://purl.org/coar/resource_type/c_3248info:ar-repo/semantics/parteDeLibroapplication/pdf155-174http://sedici.unlp.edu.ar/handle/10915/130694enginfo:eu-repo/semantics/altIdentifier/isbn/978-1-63483-279-3info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:32:52Zoai:sedici.unlp.edu.ar:10915/130694Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:32:52.888SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
title Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
spellingShingle Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
Bellini, María José
Biología
estrogen
inflammation
cognition
sex differences
glia
title_short Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
title_full Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
title_fullStr Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
title_full_unstemmed Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
title_sort Estrogen actions on glial reactivity and inflammation-mediated memory impairment: sex differences and interaction with other neurotrophic factors
dc.creator.none.fl_str_mv Bellini, María José
González Burgos, Ignacio
author Bellini, María José
author_facet Bellini, María José
González Burgos, Ignacio
author_role author
author2 González Burgos, Ignacio
author2_role author
dc.subject.none.fl_str_mv Biología
estrogen
inflammation
cognition
sex differences
glia
topic Biología
estrogen
inflammation
cognition
sex differences
glia
dc.description.none.fl_txt_mv There is growing evidence that documents profound effects of estrogens on learning, memory, and mood as well as neurodevelopment and neurodegenerative diseases. However, the ability of estradiol to influence synaptic plasticity, neurotransmission, neurodegeneration and cognition, could be different depending on sex dimorphisms. It emerges that estrogens have different, even opposite, effects as well as similar effects in male and female brains. The protective effects of estradiol on neural cells are mediated in part by modulation of neurotrophic factors such as insulin like growth factor (IGF-l), tyrosine kinase A (Trk A), nerve growth factors (NGF), and the like. Also, it modulates the action of neurotrophins, which in turn regulate the synaptogenesis, synaptic plasticity and synaptic functions. By these actions estrogen prevents or slows down the neurodegenerative process. Another described effect of estradiol is the capacity to modulate inflammatory response mediated by glial cells. Neuroinflammation is a feature not only of many neurological disorders but also of aging, and it is accompanied by activation of glial cells and the release of proinflammatory cytokines and chemokines. Such activation is a normal response oriented to protect neural tissue. However, excessive and chronic activation of glia may lead to neurotoxicity and may be harmful for neural tissue. Estrogenic compounds may be candidates to counteract brain inflammation under neurodegenerative conditions by targeting the production and release of proinflammatory molecules by glial cells. In this chapter we will review different mechanisms that may be implicated in the diverse actions of estradiol, the differences according to gender and we empathize in the anti-inflammatory action on glial cell. We will also explore the interaction of estradiol with others neurotrophic factors, such as IGF-I in the regulation of neurodegeneration and memory impairment. Finally, the possibility of using selective estrogen receptor modulators (SERMs) to exert estradiollike neuroprotective actions in the brain as an alternative to estrogen will be discussed.
Instituto de Investigaciones Bioquímicas de La Plata
description There is growing evidence that documents profound effects of estrogens on learning, memory, and mood as well as neurodevelopment and neurodegenerative diseases. However, the ability of estradiol to influence synaptic plasticity, neurotransmission, neurodegeneration and cognition, could be different depending on sex dimorphisms. It emerges that estrogens have different, even opposite, effects as well as similar effects in male and female brains. The protective effects of estradiol on neural cells are mediated in part by modulation of neurotrophic factors such as insulin like growth factor (IGF-l), tyrosine kinase A (Trk A), nerve growth factors (NGF), and the like. Also, it modulates the action of neurotrophins, which in turn regulate the synaptogenesis, synaptic plasticity and synaptic functions. By these actions estrogen prevents or slows down the neurodegenerative process. Another described effect of estradiol is the capacity to modulate inflammatory response mediated by glial cells. Neuroinflammation is a feature not only of many neurological disorders but also of aging, and it is accompanied by activation of glial cells and the release of proinflammatory cytokines and chemokines. Such activation is a normal response oriented to protect neural tissue. However, excessive and chronic activation of glia may lead to neurotoxicity and may be harmful for neural tissue. Estrogenic compounds may be candidates to counteract brain inflammation under neurodegenerative conditions by targeting the production and release of proinflammatory molecules by glial cells. In this chapter we will review different mechanisms that may be implicated in the diverse actions of estradiol, the differences according to gender and we empathize in the anti-inflammatory action on glial cell. We will also explore the interaction of estradiol with others neurotrophic factors, such as IGF-I in the regulation of neurodegeneration and memory impairment. Finally, the possibility of using selective estrogen receptor modulators (SERMs) to exert estradiollike neuroprotective actions in the brain as an alternative to estrogen will be discussed.
publishDate 2015
dc.date.none.fl_str_mv 2015
dc.type.none.fl_str_mv info:eu-repo/semantics/bookPart
info:eu-repo/semantics/publishedVersion
Capitulo de libro
http://purl.org/coar/resource_type/c_3248
info:ar-repo/semantics/parteDeLibro
format bookPart
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/130694
url http://sedici.unlp.edu.ar/handle/10915/130694
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/isbn/978-1-63483-279-3
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
155-174
dc.publisher.none.fl_str_mv Nova Science Publishers
publisher.none.fl_str_mv Nova Science Publishers
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