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Abeta42 oligomers impair the bioenergetic activity in hippocampal synaptosomes derived from APP-KO mice

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Acker-Palmer,  Amparo
Neurovascular interface Group, Max Planck Institute for Brain Research, Max Planck Society;

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Citation

Beckert, B., Acker-Palmer, A., & Volknandt, W. (2018). Abeta42 oligomers impair the bioenergetic activity in hippocampal synaptosomes derived from APP-KO mice. Biological Chemistry, 399(5), 453-465. doi:10.1515/hsz-2017-0238.


Cite as: https://hdl.handle.net/21.11116/0000-0008-0BFA-3
Abstract
Employing hippocampal synaptosomes from amyloid precursor protein (APP)-deleted mice we analyzed the immediate effects of amyloid beta peptide 42 (Abeta42) peptide in its oligomeric or fibrillar assembly or of soluble amyloid precursor protein alpha (sAPPalpha) protein on their bioenergetic activity. Upon administration of oligomeric Abeta42 peptide for 30 min we observed a robust decrease both in mitochondrial activity and in mitochondrial membrane potential (MMP). In contrast the respective fibrillary or scrambled peptides showed no effect, indicating that inhibition strictly depends on the oligomerization status of the peptide. Hippocampal synaptosomes from old APP-KO mice revealed a further reduction of their already impaired bioenergetic activity upon incubation with 10 mum Abeta42 peptide. In addition we evaluated the influence of the sAPPalpha protein on mitochondrial activity of hippocampal synaptosomes derived from young or old APP-KO animals. In neither case 20 nm nor 200 nm sAPPalpha protein had an effect on mitochondrial metabolic activity. Our findings demonstrate that hippocampal synaptosomes derived from APP-KO mice are a most suitable model system to evaluate the impact of Abeta42 peptide on its bioenergetic activity and to further elucidate the molecular mechanisms underlying the impairments by oligomeric Abeta42 on mitochondrial function. Our data demonstrate that extracellular Abeta42 peptide is taken up into synaptosomes where it immediately attenuates mitochondrial activity.