Peer-reviewed veterinary case report
Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.
- Journal:
- Nature neuroscience
- Year:
- 2024
- Authors:
- Sasmita, Andrew Octavian et al.
- Affiliation:
- Department of Neurogenetics · Germany
- Species:
- rodent
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, APP, 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.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/39103558/