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Staged decline of neuronal function in vivo in an animal model of Alzheimer's disease

Author

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  • Christine Grienberger

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

  • Nathalie L. Rochefort

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

  • Helmuth Adelsberger

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

  • Horst A. Henning

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

  • Daniel N. Hill

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

  • Julia Reichwald

    (Novartis Institutes for Biomedical Research)

  • Matthias Staufenbiel

    (Novartis Institutes for Biomedical Research)

  • Arthur Konnerth

    (Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich)

Abstract

The accumulation of amyloid-β in the brain is an essential feature of Alzheimer's disease. However, the impact of amyloid-β-accumulation on neuronal dysfunction on the single cell level in vivo is poorly understood. Here we investigate the progression of amyloid-β load in relation to neuronal dysfunction in the visual system of the APP23×PS45 mouse model of Alzheimer's disease. Using in vivo two-photon calcium imaging in the visual cortex, we demonstrate that a progressive deterioration of neuronal tuning for the orientation of visual stimuli occurs in parallel with the age-dependent increase of the amyloid-β load. Importantly, we find this deterioration only in neurons that are hyperactive during spontaneous activity. This impairment of visual cortical circuit function also correlates with pronounced deficits in visual-pattern discrimination. Together, our results identify distinct stages of decline in sensory cortical performance in vivo as a function of the increased amyloid-β-load.

Suggested Citation

  • Christine Grienberger & Nathalie L. Rochefort & Helmuth Adelsberger & Horst A. Henning & Daniel N. Hill & Julia Reichwald & Matthias Staufenbiel & Arthur Konnerth, 2012. "Staged decline of neuronal function in vivo in an animal model of Alzheimer's disease," Nature Communications, Nature, vol. 3(1), pages 1-10, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1783
    DOI: 10.1038/ncomms1783
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    Cited by:

    1. Annie Lee & Chandana Kondapalli & Daniel M. Virga & Tommy L. Lewis & So Yeon Koo & Archana Ashok & Georges Mairet-Coello & Sebastien Herzig & Marc Foretz & Benoit Viollet & Reuben Shaw & Andrew Sproul, 2022. "Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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