Related Experiment Video

Updated: Jun 21, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Molecular mechanisms involved in injury to the preterm brain

Angela M Kaindl1, Géraldine Favrais, Pierre Gressens

  • 1Inserm, U676, Paris, France.

Journal of Child Neurology
|July 17, 2009
PubMed

Insights

Premature brain injury, a significant cause of infant disability, results from multiple perinatal factors. Understanding the molecular mechanisms of inflammation, excitotoxicity, and oxidative stress is key to preventing brain damage in newborns.

Area of Science:

  • Neuroscience
  • Neonatal Medicine
  • Developmental Biology

Background:

  • Premature brain injury is a leading cause of infant mortality and long-term neurological deficits.
  • The developing brain of premature infants is uniquely vulnerable to damage.
  • Perinatal factors contribute to brain injury through a multi-hit process.

Purpose of the Study:

  • To review current concepts on the molecular mechanisms underlying premature brain injury.
  • To highlight the roles of inflammation, excitotoxicity, and oxidative stress.
  • To understand how brain lesions impact subsequent development.

Main Methods:

  • Review of clinical, epidemiological, and experimental studies.
  • Analysis of molecular pathways involved in brain injury.
  • Examination of the impact of injury timing on developmental trajectories.

Main Results:

  • Inflammation, excitotoxicity, and oxidative stress are key contributors to white and gray matter injury.
  • Multiple perinatal factors interact to cause and exacerbate brain damage.
  • Lesions can alter natural developmental sequences and redirect brain development.

Conclusions:

  • Understanding the molecular underpinnings of premature brain injury is crucial.
  • Targeting inflammation, excitotoxicity, and oxidative stress may offer therapeutic avenues.
  • Early brain injury significantly impacts neurodevelopmental outcomes in preterm infants.

More Related Videos

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury07:36

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

Published on: November 19, 2019

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...