Artikel
Late running is not too late against Alzheimer’s pathology
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Autoren
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Arne Herring
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Yvonne Münster
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Bastian Bolczek
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Sarah Krüssel
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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David Krieter
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Ilkay Yavuz
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Fro Karim
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Constanze Roggendorf
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Anthony Stang
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Yachao Wang
- University of Duisburg-Essen, Department of Neurology, Essen, Germany
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Dirk Hermann
- University of Duisburg-Essen, Department of Neurology, Essen, Germany
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Sarah Teuber-Hanselmann
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
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Kathy Keyvani
- University of Duisburg-Essen, Institute of Neuropathology, Essen, Germany
| Veröffentlicht: | 14. September 2016 |
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Gliederung
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Introduction & Objectives: In the last decade a vast number of animal studies have produced overwhelming evidence that exercise not only compensates for memory loss by increasing brain plasticity and cognitive reserve but also directly counteracts Alzheimer-like pathology when provided before disease onset or in early disease stages. But so far, there is little knowledge about therapeutic effects of training when started in advanced disease stages. Accordingly, we asked whether late and prolonged exercise solely experienced in an advanced disease stage might still have the potential to counteract Alzheimer’s disease (AD).
Materials & Methods: TgCRND8 mice (characterized by disease onset at three months of age) and their wildtype littermates were housed without access to physical stimulation until seven months of age to model a sedentary life style before experiencing five months of wheel running in an advanced disease stage. Afterwards, exercised in comparison to physically inactive TgCRND8 and wildtype mice were tested for cognitive performance and their brains were investigated for structural plasticity, beta-amyloid (Aβ) plaque burden, amyloid precursor protein (APP) metabolism, neurovascular dysfunction, microgliosis, inflammation, oxidative stress, autophagy, and tau pathology.
Results: In the present study we show that five months of wheel running in an advanced disease stage was still able to mitigate at least some aspects of the full-blown Alzheimer’s pathology in TgCRND8 mice. Late running had mild but significant effects on structural plasticity by increasing the dendritic complexity. It further reduced Aβ plaque burden and enhanced Aβ clearance across the blood-brain barrier, along with attenuating microgliosis, inflammation, oxidative stress, and autophagy deficits, resulting in better memory performance and less agitation. However, unlike early exercise, late running did not affect abnormal APP metabolism, tau pathology, or angiogenesis.
Conclusions: These results allow concluding that it is never too late to counteract AD with physical training but the earlier the intervention starts, the more pronounced is the therapeutic potential.
