Contribution of the oligodendrocyte lineage to CNS repair and neurodegenerative pathologies.
The concept of the oligodendrocyte lineage as simply a source of myelinating cells in the vertebrate CNS is undergoing radical revision. Elucidation of the origins of oligodendrocytes in the CNS has led to identification of important signaling pathways, the timing and mechanism of lineage commitments and overlapping as well as redundant functionality among oligodendrocytes. The realization that a significant proportion of the oligodendrocyte lineage cells remain in a proliferative and immature state suggests they have roles other than as a reservoir of myelinating cells. While early studies were focused on understanding the development of oligodendrocytes, more recent work has begun to define the role of oligodendrocyte lineage cells in CNS functionality and the identification of new avenues for neural repair. A relatively unexplored aspect of the oligodendrocyte lineage is their contribution either directly or indirectly to the pathology of neurodegenerative diseases such as ALS and Alzheimer's disease. Here we briefly consider the potential role of oligodendrocyte lineage cells as mediators of neural repair and neurodegeneration in the vertebrate CNS. This article is part of the Special Issue entitled 'Oligodendrocytes in Health and Disease'.
George Washington University, School of Medicine and Health Sciences, 2300 Eye Street NW, Ross Hall 709G, Washington, DC, 20037, USA.
Reshmi
R
Tognatta
George Washington University, School of Medicine and Health Sciences, 2300 Eye Street NW, Ross Hall 709G, Washington, DC, 20037, USA. Electronic address: Rhm3@gwu.edu.
Robert H
RH
Miller
D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D019070:Cell Lineage; D002490:Central Nervous System / Q000473:pathology*; D006801:Humans; D009186:Myelin Sheath / Q000502:physiology; D019636:Neurodegenerative Diseases / Q000503:physiopathology*; D009836:Oligodendroglia / Q000502:physiology*; D013234:Stem Cells / Q000502:physiology
ALS; Alzheimer's disease; Multiple sclerosis; Myelination; Neurodegeneration; Oligodendrocytes