life, death, and replacement of oligodendrocytes in the adult CNS

• Published in: Journal of neurochemistry Vol. 107; no. 1; pp. 1 - 19
• Main Authors: McTigue, Dana M, Tripathi, Richa B
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.10.2008; Blackwell Publishing Ltd; Blackwell
• Subjects: Adult and adolescent clinical studies; Animals; apoptosis; Biochemistry; Biological and medical sciences; Cell adhesion & migration; Cell Death - physiology; Cellular biology; Central Nervous System - cytology; Central Nervous System - metabolism; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Demyelinating Diseases - etiology; Demyelinating Diseases - metabolism; Demyelinating Diseases - physiopathology; growth factors; Humans; Inflammation - etiology; Inflammation - metabolism; Inflammation - physiopathology; Injuries; Medical sciences; myelin; myelin sheath; Nerve Regeneration - physiology; Nervous System Diseases - metabolism; Nervous System Diseases - physiopathology; Neurodegenerative Diseases - metabolism; Neurodegenerative Diseases - physiopathology; Neurology; NG2; Oligodendroglia - cytology; Oligodendroglia - metabolism; Organic mental disorders. Neuropsychology; polydendrocytes; proinflammatory cytokines; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Signal transduction; Stem Cells - cytology; Stem Cells - metabolism; Spinal cord; polydendrocytes; Alzheimer disease; Neuroglia; Migration; Central nervous system; Parkinson disease; Cardiovascular disease; apoptosis; Encephalon; Signal transduction; Postnatal; Oligodendrocyte; NG2; Degenerative disease; Embryonic development; Nervous system diseases; Glial cell; Oxygen; proinflammatory cytokines; growth factors; Myelin; Precursor cell; Cell differentiation; Cerebral disorder; Central nervous system disease; Excitatory aminoacid; Neurotransmitter; Extrapyramidal syndrome
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1111/j.1471-4159.2008.05570.x

Oligodendrocytes (OLs) are mature glial cells that myelinate axons in the brain and spinal cord. As such, they are integral to functional and efficient neuronal signaling. The embryonic lineage and postnatal development of OLs have been well-studied and many features of the process have been described, including the origin, migration, proliferation, and differentiation of precursor cells. Less clear is the extent to which OLs and damaged/dysfunctional myelin are replaced following injury to the adult CNS. OLs and their precursors are very vulnerable to conditions common to CNS injury and disease sites, such as inflammation, oxidative stress, and elevated glutamate levels leading to excitotoxicity. Thus, these cells become dysfunctional or die in multiple pathologies, including Alzheimer's disease, spinal cord injury, Parkinson's disease, ischemia, and hypoxia. However, studies of certain conditions to date have detected spontaneous OL replacement. This review will summarize current information on adult OL progenitors, mechanisms that contribute to OL death, the consequences of their loss and the pathological conditions in which spontaneous oligodendrogenesis from endogenous precursors has been observed in the adult CNS.