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

Christine Grienberger, Nathalie L. Rochefort, Helmuth Adelsberger, Horst A. Henning, Daniel N. Hill, Julia Reichwald, Matthias Staufenbiel and Arthur Konnerth ()
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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

Nature Communications, 2012, vol. 3, issue 1, 1-10

Abstract: 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.

Date: 2012
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1783

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DOI: 10.1038/ncomms1783

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