The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia
Nowadays, Alzheimer's disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its incidence and, for now, there are no effective treatments since current approved medications have only shown short-term symptomatic benefits....
| Autores: | , , , , , , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2019 |
| País: | España |
| Institución: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/158019 |
| Acceso en línea: | https://hdl.handle.net/2445/158019 |
| Access Level: | acceso abierto |
| Palabra clave: | Malaltia d'Alzheimer Receptors d'insulina Alzheimer's disease Insulin receptors |
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The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's DementiaFolch, JaumeOlloquequi, JordiEttcheto Arriola, MirenBusquets Figueras, OriolSánchez-López, E. (Elena)Cano Fernández, AmandaEspinosa-Jiménez, TrianaGarcía López, María LuisaBeas Zárate, CarlosCasadesús, GemmaBulló, MònicaAuladell i Costa, M. CarmeCamins Espuny, AntoniMalaltia d'AlzheimerReceptors d'insulinaAlzheimer's diseaseInsulin receptorsNowadays, Alzheimer's disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its incidence and, for now, there are no effective treatments since current approved medications have only shown short-term symptomatic benefits. Therefore, it is imperative to increase efforts in the search for molecules and non-pharmacological strategies that are capable of slowing or stopping the progress of the disease and, ideally, to reverse it. The amyloid cascade hypothesis based on the fundamental role of amyloid has been the central hypothesis in the last 30 years. However, since amyloid-directed treatments have shown no relevant beneficial results other theories have been postulated to explain the origin of the pathology. The brain is a highly metabolically active energy-consuming tissue in the human body. It has an almost complete dependence on the metabolism of glucose and uses most of its energy for synaptic transmission. Thus, alterations on the utilization or availability of glucose may be cause for the appearance of neurodegenerative pathologies like AD. In this review article, the hypothesis known as Type 3 Diabetes (T3D) will be evaluated by summarizing some of the data that has been reported in recent years. According to published research, the adherence over time to low saturated fatty acids diets in the context of the Mediterranean diet would reduce the inflammatory levels in brain, with a decrease in the pro-inflammatory glial activation and mitochondrial oxidative stress. In this situation, the insulin receptor pathway would be able to fine tune the mitochondrial biogenesis in neuronal cells, regulation the adenosine triphosphate/adenosine diphosphate intracellular balance, and becoming a key factor involved in the preservation of the synaptic connexions and neuronal plasticity. In addition, new targets and strategies for the treatment of AD will be considered in this review for their potential as new pharmacological or non-pharmacological approaches.Frontiers Media2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/158019Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: https://doi.org/10.3389/fnagi.2019.00236Frontiers in Aging Neuroscience, 2019, vol. 6, p. 11-236https://doi.org/10.3389/fnagi.2019.00236cc-by (c) Folch, Jaume et al., 2019http://creativecommons.org/licenses/by/3.0/esinfo:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1580192026-05-27T06:46:51Z |
| dc.title.none.fl_str_mv |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| title |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| spellingShingle |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia Folch, Jaume Malaltia d'Alzheimer Receptors d'insulina Alzheimer's disease Insulin receptors |
| title_short |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| title_full |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| title_fullStr |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| title_full_unstemmed |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| title_sort |
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia |
| dc.creator.none.fl_str_mv |
Folch, Jaume Olloquequi, Jordi Ettcheto Arriola, Miren Busquets Figueras, Oriol Sánchez-López, E. (Elena) Cano Fernández, Amanda Espinosa-Jiménez, Triana García López, María Luisa Beas Zárate, Carlos Casadesús, Gemma Bulló, Mònica Auladell i Costa, M. Carme Camins Espuny, Antoni |
| author |
Folch, Jaume |
| author_facet |
Folch, Jaume Olloquequi, Jordi Ettcheto Arriola, Miren Busquets Figueras, Oriol Sánchez-López, E. (Elena) Cano Fernández, Amanda Espinosa-Jiménez, Triana García López, María Luisa Beas Zárate, Carlos Casadesús, Gemma Bulló, Mònica Auladell i Costa, M. Carme Camins Espuny, Antoni |
| author_role |
author |
| author2 |
Olloquequi, Jordi Ettcheto Arriola, Miren Busquets Figueras, Oriol Sánchez-López, E. (Elena) Cano Fernández, Amanda Espinosa-Jiménez, Triana García López, María Luisa Beas Zárate, Carlos Casadesús, Gemma Bulló, Mònica Auladell i Costa, M. Carme Camins Espuny, Antoni |
| author2_role |
author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Malaltia d'Alzheimer Receptors d'insulina Alzheimer's disease Insulin receptors |
| topic |
Malaltia d'Alzheimer Receptors d'insulina Alzheimer's disease Insulin receptors |
| description |
Nowadays, Alzheimer's disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its incidence and, for now, there are no effective treatments since current approved medications have only shown short-term symptomatic benefits. Therefore, it is imperative to increase efforts in the search for molecules and non-pharmacological strategies that are capable of slowing or stopping the progress of the disease and, ideally, to reverse it. The amyloid cascade hypothesis based on the fundamental role of amyloid has been the central hypothesis in the last 30 years. However, since amyloid-directed treatments have shown no relevant beneficial results other theories have been postulated to explain the origin of the pathology. The brain is a highly metabolically active energy-consuming tissue in the human body. It has an almost complete dependence on the metabolism of glucose and uses most of its energy for synaptic transmission. Thus, alterations on the utilization or availability of glucose may be cause for the appearance of neurodegenerative pathologies like AD. In this review article, the hypothesis known as Type 3 Diabetes (T3D) will be evaluated by summarizing some of the data that has been reported in recent years. According to published research, the adherence over time to low saturated fatty acids diets in the context of the Mediterranean diet would reduce the inflammatory levels in brain, with a decrease in the pro-inflammatory glial activation and mitochondrial oxidative stress. In this situation, the insulin receptor pathway would be able to fine tune the mitochondrial biogenesis in neuronal cells, regulation the adenosine triphosphate/adenosine diphosphate intracellular balance, and becoming a key factor involved in the preservation of the synaptic connexions and neuronal plasticity. In addition, new targets and strategies for the treatment of AD will be considered in this review for their potential as new pharmacological or non-pharmacological approaches. |
| publishDate |
2019 |
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2019 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
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article |
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publishedVersion |
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https://hdl.handle.net/2445/158019 |
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https://hdl.handle.net/2445/158019 |
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Inglés |
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Inglés |
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Reproducció del document publicat a: https://doi.org/10.3389/fnagi.2019.00236 Frontiers in Aging Neuroscience, 2019, vol. 6, p. 11-236 https://doi.org/10.3389/fnagi.2019.00236 |
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cc-by (c) Folch, Jaume et al., 2019 http://creativecommons.org/licenses/by/3.0/es info:eu-repo/semantics/openAccess |
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cc-by (c) Folch, Jaume et al., 2019 http://creativecommons.org/licenses/by/3.0/es |
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openAccess |
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application/pdf |
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Frontiers Media |
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Frontiers Media |
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Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica) reponame:Dipòsit Digital de la UB instname:Universidad de Barcelona |
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Universidad de Barcelona |
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Dipòsit Digital de la UB |
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