Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research

Senescence-accelerated mouse (SAM) lines serve as models of aging and age-associated diseases. The SAMP8 strain has a shortened life span and early-onset manifestations of senescence with characteristic pathological features observed in elderly humans, including deficits in learning and memory. In b...

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Autores: Albasanz, José Luis, Castillo, Carlos Alberto, Barrachina Castillo, Marta, Ferrer, Isidro (Ferrer Abizanda), Martín, Mairena
Tipo de recurso: capítulo de libro
Estado:Versión publicada
Fecha de publicación:2011
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/178772
Acceso en línea:https://hdl.handle.net/2445/178772
Access Level:acceso abierto
Palabra clave:Malaltia d'Alzheimer
Envelliment cerebral
Alzheimer's disease
Aging brain
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spelling Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease ResearchAlbasanz, José LuisCastillo, Carlos AlbertoBarrachina Castillo, MartaFerrer, Isidro (Ferrer Abizanda)Martín, MairenaMalaltia d'AlzheimerEnvelliment cerebralAlzheimer's diseaseAging brainSenescence-accelerated mouse (SAM) lines serve as models of aging and age-associated diseases. The SAMP8 strain has a shortened life span and early-onset manifestations of senescence with characteristic pathological features observed in elderly humans, including deficits in learning and memory. In brains of SAMP8 mice, the processing of amyloid precursor protein (APP) is altered, resulting in excess production and accumulation of amyloid- peptide (A), tau is hyper-phosphorylated, and oxidative stress is increased. These phenotypic abnormalities are quite reminiscent of the findings in human brains with Alzheimer’s disease (AD). Mechanistically, metabolic pathways that are responsible for the generation of reactive oxygen species (ROS) are increased, while antioxidant systems are reduced in activity in the cerebral cortex of aged SAMP8 mice. Besides these structural and metabolic alterations, brains of aged SAMP8 mice exhibit neurochemical abnormalities such as altered signaling through G protein-coupled receptors for 5-hydroxytryptamine, acetylcholine, adenosine, dopamine, melatonin, glutamate and GABA, ion channel receptors, and nuclear hormone receptors (e.g. for all-trans-retinoic acid, cortisol or estradiol). Consequences include alterations in the levels of neurotransmitters, receptor numbers, receptor binding affinity, and second messengers. Of note is that in AD, G proteincoupled receptors and/or their corresponding signaling pathways are often impaired. Together, the observations in aged SAMP8 mouse brains provide convincing evidence that this model serves as an excellent research tool for studying AD pathogenesis and strategies for treatment. Additionally, many of the pathological and neurochemical abnormalities in SAMP8 mice are linked to altered expression of genes that are integrally related to processes such as neuroprotection, signal transduction, protein folding/degradation, intracellular transport and immune response. Several studies have already utilized pharmacological or dietary measures to restore cognitive function and enhance neuroprotection in aged SAMP8 mice, suggesting that these approaches may have applications in the treatment of AD. This review compiles available data concerning the signaling pathways that are altered in SAMP8 mice, and compares the effects to known abnormalities in AD brains.IntechOpen202120212011info:eu-repo/semantics/bookPartinfo:eu-repo/semantics/publishedVersion34 p.application/pdfhttps://hdl.handle.net/2445/178772Llibres / Capítols de llibre (Patologia i Terapèutica Experimental)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReprodució del document publicat a: http://doi.org/10.5772/17842Chapter 15 in: De La Monte, Suzanne. 2011. The Clinical Spectrum of Alzheimer's Disease: The Charge Toward Comprehensive Diagnostic and Therapeutic Strategies. IntechOpen. ISBN: 978-953-51-6785-3. DOI: 10.5772/722. pp: 297-330.http://doi.org/10.5772/17842cc by-nc-sa (c) Albasanz, José Luis et al., 20xxhttp://creativecommons.org/licenses/by-nc-sa/3.0/es/info:eu-repo/semantics/openAccessoai:recercat.cat:2445/1787722026-05-29T05:05:01Z
dc.title.none.fl_str_mv Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
title Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
spellingShingle Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
Albasanz, José Luis
Malaltia d'Alzheimer
Envelliment cerebral
Alzheimer's disease
Aging brain
title_short Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
title_full Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
title_fullStr Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
title_full_unstemmed Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
title_sort Modulation of Signal Transduction Pathways in Senescence-Accelerated Mice P8 Strain: A Useful Tool for Alzheimer’s Disease Research
dc.creator.none.fl_str_mv Albasanz, José Luis
Castillo, Carlos Alberto
Barrachina Castillo, Marta
Ferrer, Isidro (Ferrer Abizanda)
Martín, Mairena
author Albasanz, José Luis
author_facet Albasanz, José Luis
Castillo, Carlos Alberto
Barrachina Castillo, Marta
Ferrer, Isidro (Ferrer Abizanda)
Martín, Mairena
author_role author
author2 Castillo, Carlos Alberto
Barrachina Castillo, Marta
Ferrer, Isidro (Ferrer Abizanda)
Martín, Mairena
author2_role author
author
author
author
dc.subject.none.fl_str_mv Malaltia d'Alzheimer
Envelliment cerebral
Alzheimer's disease
Aging brain
topic Malaltia d'Alzheimer
Envelliment cerebral
Alzheimer's disease
Aging brain
description Senescence-accelerated mouse (SAM) lines serve as models of aging and age-associated diseases. The SAMP8 strain has a shortened life span and early-onset manifestations of senescence with characteristic pathological features observed in elderly humans, including deficits in learning and memory. In brains of SAMP8 mice, the processing of amyloid precursor protein (APP) is altered, resulting in excess production and accumulation of amyloid- peptide (A), tau is hyper-phosphorylated, and oxidative stress is increased. These phenotypic abnormalities are quite reminiscent of the findings in human brains with Alzheimer’s disease (AD). Mechanistically, metabolic pathways that are responsible for the generation of reactive oxygen species (ROS) are increased, while antioxidant systems are reduced in activity in the cerebral cortex of aged SAMP8 mice. Besides these structural and metabolic alterations, brains of aged SAMP8 mice exhibit neurochemical abnormalities such as altered signaling through G protein-coupled receptors for 5-hydroxytryptamine, acetylcholine, adenosine, dopamine, melatonin, glutamate and GABA, ion channel receptors, and nuclear hormone receptors (e.g. for all-trans-retinoic acid, cortisol or estradiol). Consequences include alterations in the levels of neurotransmitters, receptor numbers, receptor binding affinity, and second messengers. Of note is that in AD, G proteincoupled receptors and/or their corresponding signaling pathways are often impaired. Together, the observations in aged SAMP8 mouse brains provide convincing evidence that this model serves as an excellent research tool for studying AD pathogenesis and strategies for treatment. Additionally, many of the pathological and neurochemical abnormalities in SAMP8 mice are linked to altered expression of genes that are integrally related to processes such as neuroprotection, signal transduction, protein folding/degradation, intracellular transport and immune response. Several studies have already utilized pharmacological or dietary measures to restore cognitive function and enhance neuroprotection in aged SAMP8 mice, suggesting that these approaches may have applications in the treatment of AD. This review compiles available data concerning the signaling pathways that are altered in SAMP8 mice, and compares the effects to known abnormalities in AD brains.
publishDate 2011
dc.date.none.fl_str_mv 2011
2021
2021
dc.type.none.fl_str_mv info:eu-repo/semantics/bookPart
info:eu-repo/semantics/publishedVersion
format bookPart
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/178772
url https://hdl.handle.net/2445/178772
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reprodució del document publicat a: http://doi.org/10.5772/17842
Chapter 15 in: De La Monte, Suzanne. 2011. The Clinical Spectrum of Alzheimer's Disease: The Charge Toward Comprehensive Diagnostic and Therapeutic Strategies. IntechOpen. ISBN: 978-953-51-6785-3. DOI: 10.5772/722. pp: 297-330.
http://doi.org/10.5772/17842
dc.rights.none.fl_str_mv cc by-nc-sa (c) Albasanz, José Luis et al., 20xx
http://creativecommons.org/licenses/by-nc-sa/3.0/es/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc by-nc-sa (c) Albasanz, José Luis et al., 20xx
http://creativecommons.org/licenses/by-nc-sa/3.0/es/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 34 p.
application/pdf
dc.publisher.none.fl_str_mv IntechOpen
publisher.none.fl_str_mv IntechOpen
dc.source.none.fl_str_mv Llibres / Capítols de llibre (Patologia i Terapèutica Experimental)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,812429

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