| Literature DB >> 30248054 |
Tim L Emmerzaal1, Richard J Rodenburg2, Heikki Tanila3, Vivienne Verweij1, Amanda J Kiliaan1, Tamas Kozicz1,4.
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.Entities:
Keywords: Alzheimer’s disease; amyloid beta-peptides; electron transport complex II; electron transport complex IV; mice; mitochondria
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Year: 2018 PMID: 30248054 DOI: 10.3233/JAD-180337
Source DB: PubMed Journal: J Alzheimers Dis ISSN: 1387-2877 Impact factor: 4.472