Oligodendrogenesis after traumatic brain injury.
White matter injury is an important contributor to long term motor and cognitive dysfunction after traumatic brain injury. During brain trauma, acceleration, deceleration, torsion, and compression forces often cause direct damage to the axon tracts, and pathways that are triggered by the initial injury can trigger molecular events that result in secondary axon degeneration. White matter injury is often associated with altered mental status, memory deficits, motor or autonomic dysfunction, and contribute to the development of chronic neurodegenerative diseases. The presence and proper functioning of oligodendrocyte precursor cells offer the potential for repair and recovery of injured white matter. The process of the proliferation, maturation of oligodendrocyte precursor cells and their migration to the site of injury to replace injured or lost oligodendrocytes is know as oligodendrogenesis. The process of oligodendrogenesis, as well as the interaction of oligodendrocyte precursor cells with other elements of the neurovascular unit, will be discussed in this review.
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Hajime
H
Takase
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States; Division of Neurology, Graduate School of Medicine, Kobe University, Kobe, Japan.
Kazuo
K
Washida
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States.
Kazuhide
K
Hayakawa
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States.
Ken
K
Arai
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States.
Xiaoying
X
Wang
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Radiology, Massachusetts General Hospital, Boston, MA, United States; Department of Neurology, Massachusetts General Hospital, Boston, MA, United States.
Eng H
EH
Lo
Neuroprotection Research Laboratory, Massachusetts General Hospital, Charlestown, MA, United States; Department of Pediatrics, Massachusetts General Hospital, Boston, MA, United States. Electronic address: jlok1@mgh.harvard.edu.
Josephine
J
Lok
D000818:Animals; D000070642:Brain Injuries, Traumatic / Q000150:complications* / Q000503:physiopathology*; D005911:Gliosis / Q000209:etiology* / Q000503:physiopathology*; D006801:Humans; D009836:Oligodendroglia / Q000502:physiology*