在老化的大脑中，少突胶质细胞的母细胞再生能力下降（NG2胶质细胞）：一个恶性循环，髓磷脂损失和神经元的破坏？

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, Jose Julio Rodriguez Arellano and Arthur Butt

Affiliation:

关键词: 阿尔茨海默病；痴呆；谷氨酸；髓鞘少突胶质细胞；少突胶质细胞的母细胞；白质。

摘要: 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.

Cite this article as:

Andrea Rivera, Ilaria Vanzuli, Jose Julio Rodriguez Arellano and Arthur Butt , 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