Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease
Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. Hallmarks of AD are memory impairments and cognitive deficits, but non-cognitive impairments, especially motor dysfunctions are also associated with the disease and may even precede classic clinical sympto...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-05-01
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| Series: | Frontiers in Behavioral Neuroscience |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fnbeh.2019.00107/full |
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| author | Jannek M. Wagner Marius E. Sichler Eva M. Schleicher Timon N. Franke Caroline Irwin Maximilian Johannes Löw Nicola Beindorff Caroline Bouter Thomas A. Bayer Yvonne Bouter |
| author_facet | Jannek M. Wagner Marius E. Sichler Eva M. Schleicher Timon N. Franke Caroline Irwin Maximilian Johannes Löw Nicola Beindorff Caroline Bouter Thomas A. Bayer Yvonne Bouter |
| author_sort | Jannek M. Wagner |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. Hallmarks of AD are memory impairments and cognitive deficits, but non-cognitive impairments, especially motor dysfunctions are also associated with the disease and may even precede classic clinical symptoms. With an aging society and increasing hospitalization of the elderly, motor deficits are of major interest to improve independent activities in daily living. Consistent with clinical findings, a variety of AD mouse models develop motor deficits as well. We investigated the motor function of 3- and 7-month-old Tg4-42 mice in comparison to wild-type controls and 5XFAD mice and discuss the results in context with several other AD mouse model. Our study shows impaired balance and motor coordination in aged Tg4-42 mice in the balance beam and rotarod test, while general locomotor activity and muscle strength is not impaired at 7 months. The cerebellum is a major player in the regulation and coordination of balance and locomotion through practice. Particularly, the rotarod test is able to detect cerebellar deficits. Furthermore, supposed cerebellar impairment was verified by 18F-FDG PET/MRI. Aged Tg4-42 mice showed reduced cerebellar glucose metabolism in the 18F-FDG PET. Suggesting that, deficits in coordination and balance are most likely due to cerebellar impairment. In conclusion, Tg4-42 mice develop motor deficits before memory deficits, without confounding memory test. Thus, making the Tg4-42 mouse model a good model to study the effects on cognitive decline of therapies targeting motor impairments. |
| first_indexed | 2024-04-13T02:17:02Z |
| format | Article |
| id | doaj.art-7794290951864633a730741ade9c8016 |
| institution | Directory Open Access Journal |
| issn | 1662-5153 |
| language | English |
| last_indexed | 2024-04-13T02:17:02Z |
| publishDate | 2019-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Behavioral Neuroscience |
| spelling | doaj.art-7794290951864633a730741ade9c80162022-12-22T03:07:07ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532019-05-011310.3389/fnbeh.2019.00107457353Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s DiseaseJannek M. Wagner0Marius E. Sichler1Eva M. Schleicher2Timon N. Franke3Caroline Irwin4Maximilian Johannes Löw5Nicola Beindorff6Caroline Bouter7Thomas A. Bayer8Yvonne Bouter9Division of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyBerlin Experimental Radionuclide Imaging Center, Charité – University Medicine Berlin, Berlin, GermanyDepartment of Nuclear Medicine, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyDivision of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Georg-August-University, Göttingen, GermanyAlzheimer’s disease (AD) is a neurodegenerative disorder and the most common form of dementia. Hallmarks of AD are memory impairments and cognitive deficits, but non-cognitive impairments, especially motor dysfunctions are also associated with the disease and may even precede classic clinical symptoms. With an aging society and increasing hospitalization of the elderly, motor deficits are of major interest to improve independent activities in daily living. Consistent with clinical findings, a variety of AD mouse models develop motor deficits as well. We investigated the motor function of 3- and 7-month-old Tg4-42 mice in comparison to wild-type controls and 5XFAD mice and discuss the results in context with several other AD mouse model. Our study shows impaired balance and motor coordination in aged Tg4-42 mice in the balance beam and rotarod test, while general locomotor activity and muscle strength is not impaired at 7 months. The cerebellum is a major player in the regulation and coordination of balance and locomotion through practice. Particularly, the rotarod test is able to detect cerebellar deficits. Furthermore, supposed cerebellar impairment was verified by 18F-FDG PET/MRI. Aged Tg4-42 mice showed reduced cerebellar glucose metabolism in the 18F-FDG PET. Suggesting that, deficits in coordination and balance are most likely due to cerebellar impairment. In conclusion, Tg4-42 mice develop motor deficits before memory deficits, without confounding memory test. Thus, making the Tg4-42 mouse model a good model to study the effects on cognitive decline of therapies targeting motor impairments.https://www.frontiersin.org/article/10.3389/fnbeh.2019.00107/fullmotor functioncerebellumAlzheimertransgenic micebehaviorFDG-PET |
| spellingShingle | Jannek M. Wagner Marius E. Sichler Eva M. Schleicher Timon N. Franke Caroline Irwin Maximilian Johannes Löw Nicola Beindorff Caroline Bouter Thomas A. Bayer Yvonne Bouter Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease Frontiers in Behavioral Neuroscience motor function cerebellum Alzheimer transgenic mice behavior FDG-PET |
| title | Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease |
| title_full | Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease |
| title_fullStr | Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease |
| title_full_unstemmed | Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease |
| title_short | Analysis of Motor Function in the Tg4-42 Mouse Model of Alzheimer’s Disease |
| title_sort | analysis of motor function in the tg4 42 mouse model of alzheimer s disease |
| topic | motor function cerebellum Alzheimer transgenic mice behavior FDG-PET |
| url | https://www.frontiersin.org/article/10.3389/fnbeh.2019.00107/full |
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