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

Tim L Emmerzaal1, Richard J Rodenburg2, Heikki Tanila3

  • 1Department of Anatomy, Radboud University Medical Center, Donders Institute for Brain Cognition and Behaviour, Nijmegen, The Netherlands.

Journal of Alzheimer'S Disease : JAD
|September 25, 2018
PubMed
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Mitochondrial dysfunction, specifically decreased complex-II activity, emerges later than amyloid-beta plaques in Alzheimer's disease models. This suggests mitochondrial issues may be a consequence, not a cause, of Alzheimer's pathology.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Mitochondrial Biology

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder with unknown causes.
  • Mitochondrial dysfunction is increasingly implicated in AD pathogenesis.
  • Amyloid-beta (Aβ) plaques are a hallmark of AD, but their relationship with mitochondrial dysfunction is unclear.

Purpose of the Study:

  • To investigate the temporal relationship between amyloid-beta pathology and mitochondrial oxidative-phosphorylation (OXPHOS) dysfunction in a mouse model of Alzheimer's disease.
  • To assess age-dependent changes in OXPHOS enzyme activities in the context of Aβ plaque formation.

Main Methods:

  • Utilized the APPswe/PS1ΔE9 transgenic mouse model for Alzheimer's disease.
  • Measured mitochondrial oxidative-phosphorylation (OXPHOS) enzyme activities at various ages (4.5 to 14 months).
Keywords:
Alzheimer’s diseaseamyloid beta-peptideselectron transport complex IIelectron transport complex IVmicemitochondria

Related Experiment Videos

  • Correlated OXPHOS enzyme activity with the presence and progression of amyloid-beta plaques.

    • Main Results:

    • Observed an age-dependent decrease in mitochondrial complex-II activity in APP/PS1 mice, starting at 9 months of age.
    • No significant alterations were found in other OXPHOS enzymes.
    • Amyloid-beta plaques were present from 4 months of age, preceding the decline in complex-II activity.

    Conclusions:

    • Mitochondrial dysfunction, indicated by reduced complex-II activity, occurs downstream of amyloid-beta plaque deposition in this Alzheimer's disease mouse model.
    • These findings suggest that mitochondrial dysfunction may be a consequence rather than an initiating factor in AD pathogenesis.
    • Further research is warranted to elucidate the precise mechanisms linking Aβ pathology to mitochondrial dysfunction in Alzheimer's disease.