Pathophysiology of glia in perinatal white matter injury
Open accessAbstract
Injury to the preterm brain has a particular predilection for cerebral white matter. White matter injury (WMI) is the most common cause of brain injury in preterm infants and a major cause of chronic neurological morbidity including cerebral palsy. Factors that predispose to WMI include cerebral oxygenation disturbances and maternal–fetal infection. During the acute phase of WMI, pronounced oxidative damage occurs that targets late oligodendrocyte progenitors (pre‐OLs). The developmental predilection for WMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible pre‐OLs that are vulnerable to a variety of chemical mediators including reactive oxygen species, glutamate, cytokines, and adenosine. During the chronic phase of WMI, the white matter displays abberant regeneration and repair responses. Early OL progenitors respond to WMI with a rapid robust proliferative response that results in a several fold regeneration of pre‐OLs that fail to terminally differentiate along their normal developmental time course. Pre‐OL maturation arrest appears to be related in part to inhibitory factors that derive from reactive astrocytes in chronic lesions. Recent high field magnetic resonance imaging (MRI) data support that three distinct forms of chronic WMI exist, each of which displays unique MRI and histopathological features. These findings suggest the possibility that therapies directed at myelin regeneration and repair could be initiated early after WMI and monitored over time. These new mechanisms of acute and chronic WMI provide access to a variety of new strategies to prevent or promote repair of WMI in premature infants. GLIA 2014;62:1790–1815
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The NMDAR is regulated by redox state: GRIN1 and GRIN2A possess pairs of redox-sensitive cysteine residues whose disulfide bond formation decreases NMDAR currents, while an overlapping group of cysteine residues are subject to inhibitory S-nitrosylation which facilitates disulfide bond formation.
“The NMDAR is regulated by redox state: both GRIN1 and GRIN2A possess pairs of redox-sensitive cysteine residues whose disulfide bond formation decreases NMDAR currents 67,68 , while an overlapping group of cysteine residues are subject to inhibitory Snitrosylation which facilitates disulfide bond formation 67 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [67]
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Hypoxic-Ischemic Oligodendroglial Injury in Neonatal Rat Brain
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Oligodendrocyte maturation is inhibited by bone morphogenetic protein
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Inhibition of 12/15‐lipoxygenase as therapeutic strategy to treat stroke
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Neonatal cerebral hypoxia-ischemia: The effect of adenosine receptor antagonists
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Towards improved animal models of neonatal white matter injury associated with cerebral palsy
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Flagged first, then by citations
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Cited by
Sorted by citations
The consequences of fetal growth restriction on brain structure and neurodevelopmental outcome
Miller, S. L., Huppi, P. S., & Mallard, C. (2016) · The Journal of Physiology · doi:10.1113/jp271402 · Cited by 620 · see citing works
Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis
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Spatio-Temporal Patterns of Demyelination and Remyelination in the Cuprizone Mouse Model
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Congenital cardiac anomalies and white matter injury
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- Authors
- Back, S. A., & Rosenberg, P. A.
- Affiliations
- Oregon Health & Science University (US)
- Boston Children's Hospital (US)
- Corresponding author
- Back, Stephen A.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2014-03-31
- Volume
- 62
- Issue
- 11
- Pages
- 1790-1815
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC4163108
- OpenAlex
- W1494362497
- Cited by
- 202
- References
- 345
- Citations by year
- 2026: 14 · 2025: 12 · 2024: 13 · 2023: 4 · 2022: 16 · 2021: 8 · 2020: 11 · 2019: 22 · 2018: 19 · 2017: 37 · 2016: 19 · 2015: 18 · 2014: 8
- FWCI
- 4.12
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Neurological Diseases and Stroke (NIH) (1R01NS054044 and R37NS045737)
- National Institute of Aging (NIH) (1R01AG031892-01)
- American Heart Association (11GRNT7510072)
- March of Dimes Birth Defects Foundation (# 6-FY11-323)
- NIH (P30 HD018655 and R01 NS066019, Whitehall Foundation and Baby Alex Foundation.)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Infant Development and Preterm Care
- Keywords
- preterm brain injury, oligodendrocyte progenitors, oxidative stress, reactive oxygen species, glutamate excitotoxicity, cytokines, adenosine, reactive astrocytes, remyelination, white matter repair, cerebral palsy, cerebral hypoxia, maternal-fetal infection
- MeSH terms
- Animals, Humans, Myelin Sheath, Neuroglia, Receptors, Glutamate, Oxidative Stress, Premature Birth, Leukoencephalopathies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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