Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation
Abstract Accumulation of amyloid β‐peptide (Aβ) in the brain is an important event in the pathogenesis of Alzheimer disease. We have used a transgenic mouse model expressing human amyloid precursor protein ( APP ) with the Arctic mutation to investigate whether Aβ deposition is correlated with mitoc...
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Online Access: | http://dx.doi.org/10.1111/jnc.13410 https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fjnc.13410 https://onlinelibrary.wiley.com/doi/pdf/10.1111/jnc.13410 |
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crwiley:10.1111/jnc.13410 2024-09-09T19:20:40+00:00 Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation Rönnbäck, Annica Pavlov, Pavel. F. Mansory, Mansorah Gonze, Prisca Marlière, Nicolas Winblad, Bengt Graff, Caroline Behbahani, Homira Magnus Bergvalls Stiftelse 2015 http://dx.doi.org/10.1111/jnc.13410 https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fjnc.13410 https://onlinelibrary.wiley.com/doi/pdf/10.1111/jnc.13410 en eng Wiley http://onlinelibrary.wiley.com/termsAndConditions#vor Journal of Neurochemistry volume 136, issue 3, page 497-502 ISSN 0022-3042 1471-4159 journal-article 2015 crwiley https://doi.org/10.1111/jnc.13410 2024-08-06T04:13:34Z Abstract Accumulation of amyloid β‐peptide (Aβ) in the brain is an important event in the pathogenesis of Alzheimer disease. We have used a transgenic mouse model expressing human amyloid precursor protein ( APP ) with the Arctic mutation to investigate whether Aβ deposition is correlated with mitochondrial functions in these animals. We found evidence of mitochondrial dysfunction (i.e., decreased mitochondrial membrane potential, increased production of reactive oxygen species and oxidative DNA damage) at 6 months of age, when the mice showed very mild Aβ deposition. More pronounced mitochondrial abnormalities were present in 24‐month‐old Tg APP arc mice with more extensive Aβ pathology. This study demonstrates for the first time mitochondrial dysfunction in transgenic mice with a mutation within the Aβ peptide (the Arctic APP mutation), and confirms previous studies suggesting that mitochondrial dysfunction and oxidative stress is an early event in the pathogenesis of Alzheimer disease. image This study demonstrates mitochondrial dysfunction in transgenic mice with a mutation within the amyloid beta (Aβ) peptide (the Arctic amyloid precursor protein (APP) mutation). We found evidence of mitochondrial dysfunction (i.e. decreased mitochondrial membrane potential (MMP), increased production of reactive oxygen species (ROS) and oxidative DNA damage) at 6 months of age, when very mild Aβ deposition is present in the mice. Also, the cytochrome c (COX) activity was significantly decreased in mitochondria from transgenic mice at 24 months of age. Article in Journal/Newspaper Arctic Wiley Online Library Arctic Journal of Neurochemistry 136 3 497 502 |
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Wiley Online Library |
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English |
description |
Abstract Accumulation of amyloid β‐peptide (Aβ) in the brain is an important event in the pathogenesis of Alzheimer disease. We have used a transgenic mouse model expressing human amyloid precursor protein ( APP ) with the Arctic mutation to investigate whether Aβ deposition is correlated with mitochondrial functions in these animals. We found evidence of mitochondrial dysfunction (i.e., decreased mitochondrial membrane potential, increased production of reactive oxygen species and oxidative DNA damage) at 6 months of age, when the mice showed very mild Aβ deposition. More pronounced mitochondrial abnormalities were present in 24‐month‐old Tg APP arc mice with more extensive Aβ pathology. This study demonstrates for the first time mitochondrial dysfunction in transgenic mice with a mutation within the Aβ peptide (the Arctic APP mutation), and confirms previous studies suggesting that mitochondrial dysfunction and oxidative stress is an early event in the pathogenesis of Alzheimer disease. image This study demonstrates mitochondrial dysfunction in transgenic mice with a mutation within the amyloid beta (Aβ) peptide (the Arctic amyloid precursor protein (APP) mutation). We found evidence of mitochondrial dysfunction (i.e. decreased mitochondrial membrane potential (MMP), increased production of reactive oxygen species (ROS) and oxidative DNA damage) at 6 months of age, when very mild Aβ deposition is present in the mice. Also, the cytochrome c (COX) activity was significantly decreased in mitochondria from transgenic mice at 24 months of age. |
author2 |
Magnus Bergvalls Stiftelse |
format |
Article in Journal/Newspaper |
author |
Rönnbäck, Annica Pavlov, Pavel. F. Mansory, Mansorah Gonze, Prisca Marlière, Nicolas Winblad, Bengt Graff, Caroline Behbahani, Homira |
spellingShingle |
Rönnbäck, Annica Pavlov, Pavel. F. Mansory, Mansorah Gonze, Prisca Marlière, Nicolas Winblad, Bengt Graff, Caroline Behbahani, Homira Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
author_facet |
Rönnbäck, Annica Pavlov, Pavel. F. Mansory, Mansorah Gonze, Prisca Marlière, Nicolas Winblad, Bengt Graff, Caroline Behbahani, Homira |
author_sort |
Rönnbäck, Annica |
title |
Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
title_short |
Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
title_full |
Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
title_fullStr |
Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
title_full_unstemmed |
Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( APP) with the Arctic mutation |
title_sort |
mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein ( app) with the arctic mutation |
publisher |
Wiley |
publishDate |
2015 |
url |
http://dx.doi.org/10.1111/jnc.13410 https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fjnc.13410 https://onlinelibrary.wiley.com/doi/pdf/10.1111/jnc.13410 |
geographic |
Arctic |
geographic_facet |
Arctic |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
Journal of Neurochemistry volume 136, issue 3, page 497-502 ISSN 0022-3042 1471-4159 |
op_rights |
http://onlinelibrary.wiley.com/termsAndConditions#vor |
op_doi |
https://doi.org/10.1111/jnc.13410 |
container_title |
Journal of Neurochemistry |
container_volume |
136 |
container_issue |
3 |
container_start_page |
497 |
op_container_end_page |
502 |
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1809760833783201792 |