ArticleFrontiers in cellular neuroscience2022
Seed-induced Aβ deposits in the corpus callosum disrupt white matter integrity in a mouse model of Alzheimer's disease.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- The Glial Autophagy-Lysosomal-Inflammation Axis in Alzheimer's Disease: a Unifying Mechanistic Framework.Molecular neurobiology · 2026Review
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- The Interaction between Oligodendrocytes and Aβ in Alzheimer's Disease.Current Alzheimer research · 2025Review
- White matter injury across neurodegenerative disease.Trends in neurosciences · 2024Review
- Mining Alzheimer's disease clinical data: reducing effects of natural aging for predicting progression and identifying subtypes.Frontiers in neuroscience · 2024Article
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Authors and funding
10 authors at 4 institutions in 1 country.
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Abstract
Neuropathologically, Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta peptide (Aβ) and subsequent formation of the so-called Aβ plaques. Along with neuronal loss, previous studies report white matter anomalies and corpus callosum (CC) atrophy in AD patients. Notably, perturbations in the white matter can be observed years before expected disease onset, suggesting that early stages of disease progression play a role in AD-associated loss of myelin integrity. Through seed-induced deposition of Aβ, we are able to examine alterations of central nervous system (CNS) integrity during the initial stages of plaque formation. In this study, we investigate the impact of Aβ seeding in the CC utilizing various imaging techniques as well as quantitative gene expression analysis and demonstrate that Aβ deposits result in an imbalance of glial cells in the CC. We found increased amounts of phagocytic microglia and reactive astrocytes, while oligodendrocyte progenitor cell (OPC) numbers were reduced. Moreover, white matter aberrations adjacent to the Aβ seeding were observed together with an overall decline in callosal myelination. This data indicate that the initial stages of plaque formation induce oligodendrocyte dysfunction, which might ultimately lead to myelin loss.
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