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Fig. 3 | Translational Neurodegeneration

Fig. 3

From: Oligodendrocyte progenitor cells in Alzheimer’s disease: from physiology to pathology

Fig. 3

Myelin dysfunction drives Aβ deposition. Myelin dysfunction and demyelination injury are also upstream risk factors contributing to formation of Aβ plaques in AD. Mechanistically, myelin dysfunction may exacerbate the accumulation of the Aβ-producing machinery within axonal swellings and cause the increased cleavage of cortical amyloid precursor protein. In addition, the microglia originally responsible for Aβ clearance are increasingly drawn to demyelination sites, reducing Aβ clearance

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