ArticleMolecular neurodegeneration2024
Contribution of amyloid deposition from oligodendrocytes in a mouse model of Alzheimer's disease.
Article in Molecular neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Cell-specific expression of APP and GABABrain research · 2026Article
- Brain-targeted delivery of siRNA via non-viral delivery systems, the therapeutic strategy for Alzheimer's disease-Unveiling challenges and prospects.International journal of pharmaceutics: X · 2026Review
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- RNA isoform diversity, splicing variants and switching in single cells of the Alzheimer's disease brain.Communications biology · 2026Article
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
- Pre-analytical characterization of CNS-derived extracellular vesicles from human saliva: effect of room temperature and cellular origin.Frontiers in neuroscience · 2026Article
- Oligodendrocytes show enriched expression of amyloid precursor protein and GABA B receptor isoform 1a.bioRxiv : the preprint server for biology · 2025Article
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
- Targeting Oligodendrocyte Dysfunction in Alzheimer's Disease: a New Frontier for Drug Repurposing with Antihistamines and Serotonin Receptor Agonists.Journal of molecular neuroscience : MN · 2025Review
- RNA isoform diversity, splicing variants, and switching in single cells of the Alzheimer's disease brain.Research square · 2025Article
- Review
- Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Critical analysis of translational potential of rodent models of white matter pathology across a wide spectrum of human diseases.Cell death & disease · 2025Review
- Soluble β-Amyloid Oligomers Selectively Upregulate TRPC3 in Excitatory Neurons via Calcineurin-Coupled NFAT.Cells · 2025Article
- Systems pharmacology identifies ajugol-mediated NF-κB/caspase-3 inhibition and isoacteoside-driven p62/mTOR-mediated autophagy as key mechanisms of Rehmanniae Radix and its processed form in Alzheimer's treatment.Frontiers in pharmacology · 2025Article
- The Interaction between Oligodendrocytes and Aβ in Alzheimer's Disease.Current Alzheimer research · 2025Review
- Decoding neuroinflammation in Alzheimer's disease: a multi-omics and AI-driven perspective for precision medicine.Frontiers in immunology · 2025Review
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- Are oligodendrocytes the missing link in Alzheimer's disease and related dementia research?Molecular neurodegeneration · 2024Article
- The impact of amyloid beta burden on white matter dysfunction and associated transcriptomic signatures in cognitively normal elderly individuals.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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12 authors.
Funding
Abstract
backgroundThe accumulation of β-amyloid (Aβ) peptides into insoluble plaques is an early pathological feature of Alzheimer's disease (AD). BACE1 is the sole β-secretase for Aβ generation, making it an attractive therapeutic target for AD therapy. While BACE1 inhibitors have been shown to reduce Aβ levels in people with AD, clinical trials targeting BACE1 have failed due to unwanted synaptic deficits. Understanding the physiological role of BACE1 in individual cell types is essential for developing effective BACE inhibitors for the treatment of AD. Recent single-cell RNA transcriptomic assays revealed that oligodendrocytes are enriched with genes required for generating Aβ. However, the contribution of oligodendrocytes to amyloid plaque burden in AD and the side effects of oligodendrocyte-specific Bace1 deletion remain to be explored.
methodsWe generated an oligodendrocyte-specific Bace1 knockout model (Bace1
resultsBace1 deletion in oligodendrocytes caused no change in myelin thickness in the corpus callosum but a marginal reduction in myelin sheath thickness of the optic nerve. Synaptic strength measured by LTP was not different between Bace1
conclusionOur results provide compelling evidence that the amyloidogenic pathway in oligodendrocytes contributes to Aβ plaque formation in the AD brain. While specifically targeting BACE1 inhibition in oligodendrocytes for reducing Aβ pathology in AD is likely challenging, this is a potentially explorable strategy in future studies.
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