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Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice

MPS-Authors
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Sasmita,  Andrew Octavian
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Depp,  Constanze
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Nazarenko,  Taisiia
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Sun,  Ting
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Siems,  Sophie B.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Ong,  Erinne Cherisse
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Nkeh,  Yakum B.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Böhler,  Carolin
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Yu,  Xuan
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Mao,  Shuying
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Wu,  Zoe
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Ruhwedel,  Torben
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Subramanian,  Swati
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Börensen,  Friederike
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Overhoff,  Katharina
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Spieth,  Lena
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Berghoff,  Stefan A.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Eggert,  Simone
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Goebbels,  Sandra
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Saher,  Gesine
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Möbius,  Wiebke
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Nave,  Klaus-Armin
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Citation

Sasmita, A. O., Depp, C., Nazarenko, T., Sun, T., Siems, S. B., Ong, E. C., et al. (2024). Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice. Nature Neuroscience, 27, 1668-1674. doi:10.1038/s41593-024-01730-3.


Cite as: https://hdl.handle.net/21.11116/0000-000F-CD7E-E
Abstract
Amyloid-β (Aβ) is thought to be neuronally derived in Alzheimer’s disease (AD). However, transcripts of amyloid precursor protein (APP) and amyloidogenic enzymes are equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion of Bace1 in a humanized knock-in AD model, APPNLGF, we demonstrate that OLs and neurons contribute to Aβ plaque burden. For rapid plaque seeding, excitatory projection neurons must provide a threshold level of Aβ. Ultimately, our findings are relevant for AD prevention and therapeutic strategies.