Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury

Segovia, Kristen N.; McClure, Melissa M.; Moravec, Matthew; Luo, Ning; Wan, Yu; Gong, Xun; Riddle, Art; Craig, Andrew; Struve, Jaime; Sherman, Larry S.; Back, Stephen A.

doi:10.1002/ana.21359

Cited by 303 publications

(364 citation statements)

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“…Our findings suggest that postnatal infections are associated with a delayed development of the CST: less rapid increase in FA and less rapid decline in D av. The results of Segovia et al further suggest a potential for ongoing white matter susceptibility in regions of arrested OL development (19).…”

Section: Discussionmentioning

confidence: 88%

“…The pathogenesis of WMI is linked to a particular vulnerability of late-OL progenitors (18). Recently, hypoxia-ischemia was shown to arrest the development of OL progenitors (19). Elevated radial diffusivity and unchanged axial diffusivity values are seen with increasing white matter maturation in premature newborns with MRI abnormalities compared to those with normal MRI (12).…”

Section: Discussionmentioning

confidence: 99%

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Tractography-Based Quantitation of Corticospinal Tract Development in Premature Newborns

Adams

Chau

Poskitt

et al. 2010

The Journal of Pediatrics

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Objective-To evaluate the impact of early brain injury and neonatal illness on corticospinal tract (CST) development in premature newborns serially studied with diffusion tensor tractography (DTT).Study design-Fifty-five premature newborns (median 27.6 weeks PMA) were scanned with MRI early in life and at term-equivalent age. Moderate-severe brain abnormalities (abnormal-MRI) were characterized by moderate-severe white matter injury or ventriculomegaly. DTT was used to measure CST diffusion parameters which reflect microstructural development: fractional anisotropy (FA) and average diffusivity (D av ). The effect of abnormal-MRI and neonatal illness on FA and D av were assessed using multivariate regression for repeated measures adjusting for age at scan.Results-Twenty-one newborns (38%) had abnormal-MRI on either scan. FA increased with age significantly slower in newborns with abnormal-MRI (0.008/week) relative to newborns without these MRI abnormalities (0.011/week) (interaction term P=0.05). D av was higher in newborns with abnormal-MRI (1.5×10 −5 mm 2 /sec; P<0.001) for any given age at scan. In the 23 newborns (42%) with postnatal infection, FA increased more slowly (interaction term P=0.04), even when adjusting for the presence of abnormal-MRI.Conclusions-CST microstructural development is significantly impaired in premature newborns with abnormal-MRI or postnatal infection, with a pattern of diffusion changes suggesting impaired glial cell development.Corresponding Author: Steven P. Miller, MAS MDCM FRCPC, British Columbia Children's Hospital, Department of Pediatrics/ Division of Neurology -University of British Columbia, K3-180, 4480 Oak Street, Vancouver, British Columbia, V6H 3V4, CANADA, Telephone: 604-875-2345 ext. 5904/ Facsimile: 604-875-2285.bc.ca. The authors declare no conflicts of interest.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Diffusion tensor imaging (DTI) enables in vivo quantification of microstructural development of these white matter pathways by measuring the overall extent (average diffusivity; D av ) and directionality (fractional anisotropy; FA) of water diffusion (2, 3). Previous DTI studies suggest that early brain injury impairs white matter development, even in brain regions that are normal on conventional MRI (4). However, the region of interest (ROI)-based approach used in these studies may not be optimally sensitive to changes in an individual white matter functional pathway. Diffusion tensor tractography (DTT) is a more sophisticated DTI technique for the 3D reconstruction of specific white matter tracts (5), such as the cor...

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Tractography-Based Quantitation of Corticospinal Tract Development in Premature Newborns

Adams

Chau

Poskitt

et al. 2010

The Journal of Pediatrics

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“…The high vulnerability to oxidative stress of particularly active oligodendroglial cells because of the ongoing myelinization processes with enhanced iron metabolism, however, jeopardizes this process [61]. Thus, despite the fact that oligodendroglial precursors accumulate in brain after HI the absence of further progress to mature forms eventually results in hypomyelination [62]. In addition, despite the greater resistance of the BBB to the ischemic insult in newborn than in adult brain, the angiogenic response in immature brain is slower and weaker than in adults, which can compromise the postischemic neurorepair [63].…”

Section: Cannabinoids and Brain Damage In The Immature Brain: Neonatamentioning

confidence: 99%

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

2015

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Cannabinoids form a singular family of plantderived compounds (phytocannabinoids), endogenous signaling lipids (endocannabinoids), and synthetic derivatives with multiple biological effects and therapeutic applications in the central and peripheral nervous systems. One of these properties is the regulation of neuronal homeostasis and survival, which is the result of the combination of a myriad of effects addressed to preserve, rescue, repair, and/or replace neurons, and also glial cells against multiple insults that may potentially damage these cells. These effects are facilitated by the location of specific targets for the action of these compounds (e.g., cannabinoid type 1 and 2 receptors, endocannabinoid inactivating enzymes, and nonendocannabinoid targets) in key cellular substrates (e.g., neurons, glial cells, and neural progenitor cells). This potential is promising for acute and chronic neurodegenerative pathological conditions. In this review, we will collect all experimental evidence, mainly obtained at the preclinical level, supporting that different cannabinoid compounds may be neuroprotective in adult and neonatal ischemia, brain trauma, Alzheimer's disease, Parkinson's disease, Huntington's chorea, and amyotrophic lateral sclerosis. This increasing experimental evidence demands a prompt clinical validation of cannabinoid-based medicines for the treatment of all these disorders, which, at present, lack efficacious treatments for delaying/arresting disease progression, despite the fact that the few clinical trials conducted so far with these medicines have failed to demonstrate beneficial effects.

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“…The fetal sheep cerebrum has a predilection for relatively selective WMI under conditions of moderate cerebral ischemia [41], whereas rodents have a propensity for mixed cerebral injury such that substantial gray matter injury accompanies WMI [47][48][49][50][51][52]. This shortcoming, for example, limits the relevance of rodent hypoxia-ischemia models for the study of myelination disturbances associated with chronic human WMI.…”

Section: Advantages and Disadvantages Of The Fetal Sheep To Model Wmimentioning

confidence: 99%

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

et al. 2012

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Despite advances in neonatal intensive care, survivors of premature birth remain highly susceptible to unique patterns of developmental brain injury that manifest as cerebral palsy and cognitive-learning disabilities. The developing brain is particularly susceptible to cerebral white matter injury related to hypoxia-ischemia. Cerebral white matter development in fetal sheep shares many anatomical and physiological similarities with humans. Thus, the fetal sheep has provided unique experimental access to the complex pathophysiological processes that contribute to injury to the human brain during successive periods in development. Recent refinements have resulted in models that replicate major features of acute and chronic human cerebral injury and have provided access to complex clinically relevant studies of cerebral blood flow and neuroimaging that are not feasible in smaller laboratory animals. Here, we focus on emerging insights and methodologies from studies in fetal sheep that have begun to define cellular and vascular factors that contribute to white matter injury. Recent advances include spatially defined measurements of cerebral blood flow in utero, the definition of cellular maturational factors that define the topography of injury and the application of high-field magnetic resonance imaging to define novel neuroimaging signatures for specific types of chronic white matter injury. Despite the higher costs and technical challenges of instrumented preterm fetal sheep models, they provide powerful access to clinically relevant studies that provide a more integrated analysis of the spectrum of insults that appear to contribute to cerebral injury in human preterm infants.

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Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury

Cited by 303 publications

References 39 publications

Tractography-Based Quantitation of Corticospinal Tract Development in Premature Newborns

Tractography-Based Quantitation of Corticospinal Tract Development in Premature Newborns

Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications

The Instrumented Fetal Sheep as a Model of Cerebral White Matter Injury in the Premature Infant

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