Abstract
Alzheimer's disease (AD) is a severe neurodegenerative disorder for which the exact etiology is largely unknown. An increasingly recognized and investigated notion is the pathogenic role of mitochondrial dysfunction in AD. We assessed mitochondrial oxidative-phosphorylation (OXPHOS) enzyme activities in the APPswe/PS1ΔE9 mouse model from 4.5 to 14 months of age. We show an age-dependent decrease in mitochondrial complex-II activity starting at 9 months in APP/PS1 mice. Other enzymes of the OXPHOS do not show any alterations. Since amyloid-β (Aβ) plaques are already present from 4 months of age, mitochondrial dysfunction likely occurs downstream of Aβ pathology in this mouse model.
Original language | English (US) |
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Pages (from-to) | 75-82 |
Number of pages | 8 |
Journal | Journal of Alzheimer's disease : JAD |
Volume | 66 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2018 |
Keywords
- Alzheimer’s disease
- amyloid beta-peptides
- electron transport complex II
- electron transport complex IV
- mice
- mitochondria
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Psychology
- Geriatrics and Gerontology
- Psychiatry and Mental health