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The challenge of understanding cerebral white matter injury in the premature infant
1Department of Neurology and the F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA; Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.
Insights
White matter injury in premature infants causes significant motor, behavioral, and cognitive issues. This review explores potential causes, including overlooked nutritional and hormonal factors, to improve infant brain development therapies.
Area of Science:
- Neuroscience
- Developmental Biology
- Pediatric Neurology
Background:
- Premature infant white matter injury (WMI) results in lifelong motor, cognitive, and behavioral deficits.
- Despite decades of research on oligodendrocyte vulnerabilities, effective therapies for WMI remain elusive.
- Current research often focuses on hypoxia-ischemia and infection/inflammation, with less attention to other contributing factors.
Observation:
- The etiology of WMI in premature infants is complex and not fully understood.
- Developing accurate animal models for WMI is challenging due to the unclear causes.
- Existing research has primarily investigated hypoxia-ischemia and infection/inflammation as primary causes.
Findings:
- This review examines the progression of WMI in premature infants.
- It critically analyzes current animal models used to study WMI.
- Evidence suggests nutritional and hormonal deprivation are significant, overlooked contributors to WMI.
Implications:
- Identifying novel etiologies like nutritional and hormonal deprivation can guide the development of new therapeutic strategies.
- Improved understanding of WMI causes may lead to more effective treatments for affected premature infants.
- Addressing these overlooked factors could reduce the societal burden of neurodevelopmental disorders stemming from WMI.
Abstract:
White matter injury in the premature infant leads to motor and more commonly behavioral and cognitive problems that are a tremendous burden to society. While there has been much progress in understanding unique vulnerabilities of developing oligodendrocytes over the past 30years, there remain no proven therapies for the premature infant beyond supportive care. The lack of translational progress may be partially explained by the challenge of developing relevant animal models when the etiology remains unclear, as is the case in this disorder. There has been an emphasis on hypoxia-ischemia and infection/inflammation as upstream etiologies, but less consideration of other contributory factors. This review highlights the evolution of white matter pathology in the premature infant, discusses the prevailing proposed etiologies, critically analyzes a sampling of common animal models and provides detailed support for our hypothesis that nutritional and hormonal deprivation may be additional factors playing critical and overlooked roles in white matter pathology in the premature infant.
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