Abstract
Oligodendrocytes are specialised glial cells that myelinate CNS axons. Myelinated axons are bundled together into white matter tracts that interconnect grey matter areas of the brain and are essential for rapid, integrated neuronal communication and cognitive function. Life-long generation of oligodendrocytes is required for myelination of new neuronal connections and repair of myelin lost through natural ‘wear and tear’. This is the function of a substantial population of adult oligodendrocyte progenitors (OPs). Notably, there is white matter shrinkage and decreased myelination in the ageing brain, which is accelerated in dementia. The underlying causes of myelin loss in dementia are unresolved, but it implies a decline in the regenerative capacity of OPs. A feature of OPs is that they form neuron-glial synapses and respond to glutamate released by neurons via a range of glutamate receptors. Glutamate neurotransmission onto OPs is proposed to regulate their proliferation and differentiation into myelinating oligodendrocytes. Here, we discuss evidence that deregulation of glutamate neurotransmission in dementia and compromised generation of oligodendrocytes from OPs are key features of myelin loss and associated cognitive decline.
Keywords: Alzheimer’s disease, dementia, glutamate. myelin, oligodendrocyte progenitor, oligodendrocyte, white matter.
Current Alzheimer Research
Title:Decreased Regenerative Capacity of Oligodendrocyte Progenitor Cells (NG2-Glia) in the Ageing Brain: A Vicious Cycle of Synaptic Dysfunction, Myelin Loss and Neuronal Disruption?
Volume: 13 Issue: 4
Author(s): Andrea Rivera, Ilaria Vanzuli, José Julio Rodríguez Arellano and Arthur Butt
Affiliation:
Keywords: Alzheimer’s disease, dementia, glutamate. myelin, oligodendrocyte progenitor, oligodendrocyte, white matter.
Abstract: Oligodendrocytes are specialised glial cells that myelinate CNS axons. Myelinated axons are bundled together into white matter tracts that interconnect grey matter areas of the brain and are essential for rapid, integrated neuronal communication and cognitive function. Life-long generation of oligodendrocytes is required for myelination of new neuronal connections and repair of myelin lost through natural ‘wear and tear’. This is the function of a substantial population of adult oligodendrocyte progenitors (OPs). Notably, there is white matter shrinkage and decreased myelination in the ageing brain, which is accelerated in dementia. The underlying causes of myelin loss in dementia are unresolved, but it implies a decline in the regenerative capacity of OPs. A feature of OPs is that they form neuron-glial synapses and respond to glutamate released by neurons via a range of glutamate receptors. Glutamate neurotransmission onto OPs is proposed to regulate their proliferation and differentiation into myelinating oligodendrocytes. Here, we discuss evidence that deregulation of glutamate neurotransmission in dementia and compromised generation of oligodendrocytes from OPs are key features of myelin loss and associated cognitive decline.
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Cite this article as:
Rivera Andrea, Vanzuli Ilaria, Rodríguez Arellano Julio José and Butt Arthur, Decreased Regenerative Capacity of Oligodendrocyte Progenitor Cells (NG2-Glia) in the Ageing Brain: A Vicious Cycle of Synaptic Dysfunction, Myelin Loss and Neuronal Disruption?, Current Alzheimer Research 2016; 13 (4) . https://dx.doi.org/10.2174/1567205013666151116125518
DOI https://dx.doi.org/10.2174/1567205013666151116125518 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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