| First Author | Rönnbäck A | Year | 2016 |
| Journal | J Neurochem | Volume | 136 |
| Issue | 3 | Pages | 497-502 |
| PubMed ID | 26500157 | Mgi Jnum | J:229404 |
| Mgi Id | MGI:5751934 | Doi | 10.1111/jnc.13410 |
| Citation | Ronnback A, et al. (2016) Mitochondrial dysfunction in a transgenic mouse model expressing human amyloid precursor protein (APP) with the Arctic mutation. J Neurochem 136(3):497-502 |
| abstractText | Accumulation of amyloid beta-peptide (Abeta) 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 Abeta 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 Abeta deposition. More pronounced mitochondrial abnormalities were present in 24-month-old TgAPParc mice with more extensive Abeta pathology. This study demonstrates for the first time mitochondrial dysfunction in transgenic mice with a mutation within the Abeta 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. This study demonstrates mitochondrial dysfunction in transgenic mice with a mutation within the amyloid beta (Abeta) 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 Abeta 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. |
