2024-08-09 マックス・プランク研究所
<関連情報>
- https://www.mpg.de/22467552/0808-bich-alzheimer-s-disease-it-s-not-only-neurons-17216463-x?c=2249
- https://www.nature.com/articles/s41593-024-01730-3
オリゴデンドロサイトはアミロイドβを産生し、アルツハイマー病モデルマウスの神経細胞とともにプラーク形成に寄与する Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice
Andrew Octavian Sasmita,Constanze Depp,Taisiia Nazarenko,Ting Sun,Sophie B. Siems,Erinne Cherisse Ong,Yakum B. Nkeh,Carolin Böhler,Xuan Yu,Bastian Bues,Lisa Evangelista,Shuying Mao,Barbara Morgado,Zoe Wu,Torben Ruhwedel,Swati Subramanian,Friederike Börensen,Katharina Overhoff,Lena Spieth,Stefan A. Berghoff,Katherine Rose Sadleir,Robert Vassar,Simone Eggert,Sandra Goebbels,… Klaus-Armin Nave
Nature Neuroscience Published:05 August 2024
DOI:https://doi.org/10.1038/s41593-024-01730-3
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.
