ArticleBrain sciences2024
Early Postnatal Neuroinflammation Produces Key Features of Diffuse Brain White Matter Injury in Rats.
Article in Brain sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- N-Acetylcysteine protects the developing brain in neonatal sepsis-like inflammation via a redox-neurovascular pathway.Journal of neuroinflammation · 2026Article
- IMR-1 ameliorates perinatal LPS-induced brain injury by promoting the conversion of glial cells into neurons.Journal of molecular histology · 2026Article
- Sex-Dependent Behavioral and Biochemical Alterations in a Prenatal Oral Valproic Acid Rat Model of Autism.ACS chemical neuroscience · 2026Article
- Molecular Networks of Redox Dysregulation in Fetal Alcohol Spectrum Disorders: Mechanisms and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Intracranial LPS injection induces cerebral palsy-like motor and behavioral deficits in immunodeficient mice.Scientific reports · 2026Article
- The shifting landscape of the preterm brain.Neuron · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundPerinatal infection is a major risk factor for diffuse white matter injury (dWMI), which remains the most common form of neurological disability among very preterm infants. The disease primarily targets oligodendrocytes (OL) lineage cells in the white matter but also involves injury and/or dysmaturation of neurons of the gray matter. This study aimed to investigate whether neuroinflammation preferentially affects the cellular compositions of the white matter or gray matter.
methodNeuroinflammation was initiated by intracerebral administration of lipopolysaccharide (LPS) to rat pups at postnatal (P) day 5, and neurobiological and behavioral outcomes were assessed between P6 and P21.
resultsLPS challenge rapidly activates microglia and astrocytes, which is associated with the inhibition of OL and neuron differentiation leading to myelination deficits. Specifically, neuroinflammation reduces the immature OLs but not progenitors and causes acute axonal injury (β-amyloid precursor protein immunopositivity) and impaired dendritic maturation (reduced MAP2+ neural fiber density) in the cortical area at P7. Neuroinflammation also reduces the expression of doublecortin in the hippocampus, suggesting compromise in neurogenesis. Utilizing a battery of behavioral assessments, we found that LPS-exposed animals exhibited deficits in sensorimotor, neuromuscular, and cognitive domains.
conclusionOur overall results indicate that neuroinflammation alone in the early postnatal period can produce cardinal neuropathological features of dWMI.
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