Age-Dependent Decrease of Mitochondrial Complex II Activity in a Familial Mouse Model for Alzheimer's Disease

Tim L. Emmerzaal, Richard J. Rodenburg, Heikki Tanila, Vivienne Verweij, Amanda J. Kiliaan, Tamas Kozicz

Research output: Contribution to journalArticle

2 Scopus citations


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 languageEnglish (US)
Pages (from-to)75-82
Number of pages8
JournalJournal of Alzheimer's disease : JAD
Issue number1
StatePublished - Jan 1 2018



  • 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

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