Brain aging is considered the main risk factor of Alzheimer’s disease. However, the cellular mechanisms that link aging to the pathological hallmarks of AD are largely unclear. Morphological changes that can be detected in healthy brains at an advanced age could point to these age-dependent AD risk factors. Ultrastructural features of mammalian brain aging include oligodendrocyte and myelin abnormalities associated with low-grade inflammation. Myelin-forming oligodendrocytes are of specific interest because they provide metabolic support to axons and loss of myelin triggers secondary inflammation. Microglial cells themselves are subject to age-dependent changes that affect their ability to clear amyloid deposits and lead to a proinflammator phenotype. This symposium highlights novel disease models and preclinical findings that demonstrate a previously overlooked role of oligodendrocytes and microglia in driving the neuropathologic changes of AD.

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