Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.
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ABSTRACT:
SUBMITTER: Sasmita AO
PROVIDER: S-EPMC11374705 | biostudies-literature | 2024 Sep
REPOSITORIES: biostudies-literature
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Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.
Sasmita Andrew Octavian AO Depp Constanze C Nazarenko Taisiia T Sun Ting T Siems Sophie B SB Ong Erinne Cherisse EC Nkeh Yakum B YB Böhler Carolin C Yu Xuan X Bues Bastian B Evangelista Lisa L Mao Shuying S Morgado Barbara B Wu Zoe Z Ruhwedel Torben T Subramanian Swati S Börensen Friederike F Overhoff Katharina K Spieth Lena L Berghoff Stefan A SA Sadleir Katherine Rose KR Vassar Robert R Eggert Simone S Goebbels Sandra S Saito Takashi T Saido Takaomi T Saher Gesine G Möbius Wiebke W Castelo-Branco Gonçalo G Klafki Hans-Wolfgang HW Wirths Oliver O Wiltfang Jens J Jäkel Sarah S Yan Riqiang R Nave Klaus-Armin KA
Nature neuroscience 20240805 9
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, APP<sup>NLGF</sup>, 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 relev ...[more]
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