Skip to content

Oligodendroglial cells in Alzheimer’s disease

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Oligodendrocytes form the myelin that ensheaths CNS axons, which is essential for rapid neuronal signalling and underpins the massive computing power of the human brain. Oligodendrocytes and myelin also provide metabolic and trophic support for axons and their disruption results in axonal demise and neurodegeneration, which are key features of Alzheimer’s disease (AD). Notably, the brain has a remarkable capacity for regenerating oligodendrocytes, which is the function of adult oligodendrocyte progenitor cells (OPCs) or NG2-glia. White matter loss is often among the earliest brain changes in AD, preceding the tangles and plaques that characterize neuronal deficits. The underlying causes of myelin loss include oxidative stress, neuroinflammation and excitotoxicity, associated with accumulation of Aβ and tau hyperphosphorylation, pathological hallmarks of AD. Moreover, there is evidence that NG2-glia are disrupted in AD, which may be associated with disruption of synaptic signalling. This has led to the hypothesis that a vicious cycle of myelin loss and failure of regeneration from NG2-glia plays a key role in AD. Therapies that target NG2-glia are likely to have positive effects on myelination and neuroprotection in AD.
Original languageEnglish
Title of host publicationNeuroglia in Neurodegenerative Diseases
EditorsAlexei Verkhratsky, Margaret S. Ho, Robert Zorec, Vladimir Parpura
PublisherSpringer
Pages325-333
Number of pages9
ISBN (Electronic)978-981-13-9913-8
ISBN (Print)978-981-13-9912-1
DOIs
Publication statusEarly online - 4 Oct 2019

Publication series

NameAdvances in Experimental Medicine and Biology
PublisherSpringer
Volume1175

Related information

Relations Get citation (various referencing formats)

ID: 15929579