Encephalopathy of prematurity (EoP) is a major cause of morbidity in preterm neonates, causing neurodevelopmental adversities that can lead to lifelong impairments. Preterm birth-related insults, such as cerebral oxygen fluctuations and perinatal inflammation, are believed to negatively impact brain development, leading to a range of brain abnormalities. Diffuse white matter injury is a major hallmark of EoP and characterized by widespread hypomyelination, the result of disturbances in oligodendrocyte lineage development. At present, there are no treatment options available, despite the enormous burden of EoP on patients, their families, and society. Over the years, research in the field of neonatal brain injury and other white matter pathologies has led to the identification of several promising trophic factors and cytokines that contribute to the survival and maturation of oligodendrocytes, and/or dampening neuroinflammation. In this review, we discuss the current literature on selected factors and their therapeutic potential to combat EoP, covering a wide range of in vitro, preclinical and clinical studies. Furthermore, we offer a future perspective on the translatability of these factors into clinical practice.
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http://dx.doi.org/10.1002/glia.23939 | DOI Listing |
Childs Nerv Syst
January 2025
Department of Neurosurgery, Division of Pediatric Neurosurgery, University of Alabama at Birmingham, Children's of Alabama, 1600 7th Avenue South, Lowder 400, Birmingham, AL, 35233, USA.
Purpose: We hypothesize that distal shunt catheters fully impregnated with barium are more prone to failure compared to distal catheters with only a barium stripe. We sought to evaluate this distinction using a matched case-control study.
Methods: Patient records over an 8-year period were queried for distal shunt revisions for fracture or disconnection (cases).
Neuroimage Rep
December 2024
Department of Pediatrics, Division of Developmental-Behavioral Pediatrics, Stanford University, Stanford, CA, USA.
Background: Severe neonatal inflammatory conditions in very preterm infants (VPT: <32 weeks gestational age, GA) are linked to adverse neurodevelopmental outcomes. Differences in white matter (WM) microstructure of the corpus callosum (CC) have been observed at age 6 in VPT children with a history of severe neonatal inflammation. The goal of this study was to determine whether these CC differences can be detected at term-equivalent age using diffusion MRI (dMRI), and whether neonatal inflammation is associated with altered WM in additional tracts implicated in the encephalopathy of prematurity.
View Article and Find Full Text PDFPLoS One
January 2025
University Department of Life Sciences and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy.
Background: The study of women exposures and child outcomes occurring in the first 1,000 days of life since conception enhances understanding of the relationships between environmental factors, epigenetic changes, and disease development, extending beyond childhood and spanning the entire lifespan. Generation Gemelli is a recently launched case-control study that enrolls mother-newborns pairs in one of the largest university hospitals in Italy, in order to examine the association between maternal environmental exposures and intrauterine growth restriction (IUGR) and the risk of premature birth. The study will also evaluate the association of maternal exposures and the health and growth of infants and children up to 24 months of age.
View Article and Find Full Text PDFJ Neurol
January 2025
Centre de Génétique Humaine, Centre Hospitalier Universitaire de Besançon, Besançon, France.
Introduction: The MAPT gene encodes Tau, a protein mainly expressed by neurons. Tau protein plays an important role in cerebral microtubule polymerization and stabilization, in axonal transport and synaptic plasticity. Heterozygous pathogenic variation in MAPT are involved in a spectrum of autosomal dominant neurodegenerative diseases known as taupathies, including Alzheimer's disease, Pick's disease, fronto-temporal dementia, cortico-basal degeneration and progressive supranuclear palsy.
View Article and Find Full Text PDFJ Neurol
January 2025
Department of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Robinson Way, Cambridge, CB2 0PY, UK.
Ataxia-Telangiectasia (A-T) is a very rare multisystem disease of DNA repair, associated with progressive disabling neurological symptoms, respiratory failure, immunodeficiency and cancer predisposition, leading to premature death. There are no curative treatments available for A-T but clinical trials have begun. A major limiting factor in effectively evaluating therapies for A-T is the lack of suitable outcome measures and biomarkers.
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