Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology
Tau pathology is encountered in many neurodegenerative disorders known as tauopathies, including Alzheimer's disease. Physical activity is a lifestyle factor affecting processes crucial for memory and synaptic plasticity. Whether long-term voluntary exercise has an impact on Tau pathology and i...
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Elsevier
2011-08-01
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Series: | Neurobiology of Disease |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996111001392 |
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doaj-474624de82d042e7851d6576a260bf6a |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Karim Belarbi Sylvie Burnouf Francisco-Jose Fernandez-Gomez Cyril Laurent Sophie Lestavel Martin Figeac Audrey Sultan Laetitia Troquier Antoine Leboucher Raphaëlle Caillierez Marie-Eve Grosjean Dominique Demeyer Hélène Obriot Ingrid Brion Bérangère Barbot Marie-Christine Galas Bart Staels Sandrine Humez Nicolas Sergeant Susanna Schraen-Maschke Anne Muhr-Tailleux Malika Hamdane Luc Buée David Blum |
spellingShingle |
Karim Belarbi Sylvie Burnouf Francisco-Jose Fernandez-Gomez Cyril Laurent Sophie Lestavel Martin Figeac Audrey Sultan Laetitia Troquier Antoine Leboucher Raphaëlle Caillierez Marie-Eve Grosjean Dominique Demeyer Hélène Obriot Ingrid Brion Bérangère Barbot Marie-Christine Galas Bart Staels Sandrine Humez Nicolas Sergeant Susanna Schraen-Maschke Anne Muhr-Tailleux Malika Hamdane Luc Buée David Blum Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology Neurobiology of Disease Alzheimer's disease Exercise Tauopathies THY-Tau22 Transgenic model NPC1 |
author_facet |
Karim Belarbi Sylvie Burnouf Francisco-Jose Fernandez-Gomez Cyril Laurent Sophie Lestavel Martin Figeac Audrey Sultan Laetitia Troquier Antoine Leboucher Raphaëlle Caillierez Marie-Eve Grosjean Dominique Demeyer Hélène Obriot Ingrid Brion Bérangère Barbot Marie-Christine Galas Bart Staels Sandrine Humez Nicolas Sergeant Susanna Schraen-Maschke Anne Muhr-Tailleux Malika Hamdane Luc Buée David Blum |
author_sort |
Karim Belarbi |
title |
Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology |
title_short |
Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology |
title_full |
Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology |
title_fullStr |
Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology |
title_full_unstemmed |
Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathology |
title_sort |
beneficial effects of exercise in a transgenic mouse model of alzheimer's disease-like tau pathology |
publisher |
Elsevier |
series |
Neurobiology of Disease |
issn |
1095-953X |
publishDate |
2011-08-01 |
description |
Tau pathology is encountered in many neurodegenerative disorders known as tauopathies, including Alzheimer's disease. Physical activity is a lifestyle factor affecting processes crucial for memory and synaptic plasticity. Whether long-term voluntary exercise has an impact on Tau pathology and its pathophysiological consequences is currently unknown. To address this question, we investigated the effects of long-term voluntary exercise in the THY-Tau22 transgenic model of Alzheimer's disease-like Tau pathology, characterized by the progressive development of Tau pathology, cholinergic alterations and subsequent memory impairments. Three-month-old THY-Tau22 mice and wild-type littermates were assigned to standard housing or housing supplemented with a running wheel. After 9 months of exercise, mice were evaluated for memory performance and examined for hippocampal Tau pathology, cholinergic defects, inflammation and genes related to cholesterol metabolism. Exercise prevented memory alterations in THY-Tau22 mice. This was accompanied by a decrease in hippocampal Tau pathology and a prevention of the loss of expression of choline acetyltransferase within the medial septum. Whereas the expression of most cholesterol-related genes remained unchanged in the hippocampus of running THY-Tau22 mice, we observed a significant upregulation in mRNA levels of NPC1 and NPC2, genes involved in cholesterol trafficking from the lysosomes. Our data support the view that long-term voluntary physical exercise is an effective strategy capable of mitigating Tau pathology and its pathophysiological consequences. |
topic |
Alzheimer's disease Exercise Tauopathies THY-Tau22 Transgenic model NPC1 |
url |
http://www.sciencedirect.com/science/article/pii/S0969996111001392 |
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doaj-474624de82d042e7851d6576a260bf6a2021-03-22T12:36:56ZengElsevierNeurobiology of Disease1095-953X2011-08-01432486494Beneficial effects of exercise in a transgenic mouse model of Alzheimer's disease-like Tau pathologyKarim Belarbi0Sylvie Burnouf1Francisco-Jose Fernandez-Gomez2Cyril Laurent3Sophie Lestavel4Martin Figeac5Audrey Sultan6Laetitia Troquier7Antoine Leboucher8Raphaëlle Caillierez9Marie-Eve Grosjean10Dominique Demeyer11Hélène Obriot12Ingrid Brion13Bérangère Barbot14Marie-Christine Galas15Bart Staels16Sandrine Humez17Nicolas Sergeant18Susanna Schraen-Maschke19Anne Muhr-Tailleux20Malika Hamdane21Luc Buée22David Blum23Université Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U1011, F-59000 Lille, France; Institut Pasteur de Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U1011, F-59000 Lille, France; Institut Pasteur de Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U1011, F-59000 Lille, France; Institut Pasteur de Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, FranceUniversité Lille-Nord de France, UDSL, F-59000 Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, F-59000 Lille, France; CHRU-Lille, F-59000 Lille, France; Corresponding author at: Inserm U837, “Alzheimer & Tauopathies,” Place de Verdun, 59045 Lille Cedex, France. Fax: +33 320538562.Tau pathology is encountered in many neurodegenerative disorders known as tauopathies, including Alzheimer's disease. Physical activity is a lifestyle factor affecting processes crucial for memory and synaptic plasticity. Whether long-term voluntary exercise has an impact on Tau pathology and its pathophysiological consequences is currently unknown. To address this question, we investigated the effects of long-term voluntary exercise in the THY-Tau22 transgenic model of Alzheimer's disease-like Tau pathology, characterized by the progressive development of Tau pathology, cholinergic alterations and subsequent memory impairments. Three-month-old THY-Tau22 mice and wild-type littermates were assigned to standard housing or housing supplemented with a running wheel. After 9 months of exercise, mice were evaluated for memory performance and examined for hippocampal Tau pathology, cholinergic defects, inflammation and genes related to cholesterol metabolism. Exercise prevented memory alterations in THY-Tau22 mice. This was accompanied by a decrease in hippocampal Tau pathology and a prevention of the loss of expression of choline acetyltransferase within the medial septum. Whereas the expression of most cholesterol-related genes remained unchanged in the hippocampus of running THY-Tau22 mice, we observed a significant upregulation in mRNA levels of NPC1 and NPC2, genes involved in cholesterol trafficking from the lysosomes. Our data support the view that long-term voluntary physical exercise is an effective strategy capable of mitigating Tau pathology and its pathophysiological consequences.http://www.sciencedirect.com/science/article/pii/S0969996111001392Alzheimer's diseaseExerciseTauopathiesTHY-Tau22Transgenic modelNPC1 |