Related Experiment Video

Updated: Jul 28, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

35.9K

Cerebral ischemia in the developing brain

Robert M Dietz1,2,3, Andra L Dingman1,3, Paco S Herson4

  • 1Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|June 29, 2022
PubMed

Insights

Brain ischemia impacts all ages, with different developmental stages showing unique injury patterns. Understanding these differences is key to developing effective neurorestoration strategies for brain repair.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Neurology

Background:

  • Brain ischemia is a significant cause of death and disability across all age groups.
  • Preclinical rodent models are crucial for studying ischemia during brain development.
  • Existing models primarily focus on early developmental stages, potentially missing age-specific injury mechanisms.

Purpose of the Study:

  • To investigate the impact of brain ischemia timing on neuronal injury and functional outcomes.
  • To explore age-dependent differences in injury mechanisms, including excitation/inhibition balance, oxidative stress, and inflammation.
  • To review translational strategies for neurorestoration and neural repair after ischemic brain injury.

Main Methods:

  • Review of preclinical rodent models of brain ischemia at different developmental ages (neonatal, juvenile, adult).
  • Analysis of injury mechanisms: excitation/inhibition balance, oxidative stress, inflammation, blood-brain barrier integrity, and white matter injury.
  • Examination of translational strategies for delayed neurorestoration and plasticity enhancement.

Main Results:

  • Emerging evidence suggests fundamental differences in injury and outcomes between neonatal and juvenile rodent models of cerebral ischemia.
  • Timing of ischemia influences key biological processes like oxidative stress and inflammatory responses.
  • Delayed neurorestoration strategies hold promise for improving function post-ischemia.

Conclusions:

  • The age at which brain ischemia occurs significantly impacts injury patterns and functional deficits.
  • A comprehensive understanding of age-specific mechanisms is needed for targeted therapeutic interventions.
  • Future research should focus on developing and translating delayed neurorestoration strategies for diverse age groups affected by brain ischemia.

Keywords:
Juvenileglobal cerebral ischemianeonatal ischemianeurodevelopmentneurorestorationpediatric stroke

More Related Videos

Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats07:56

Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats

Published on: April 21, 2017

10.7K
Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy05:52

Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy

Published on: October 28, 2022

836

Related Concept Videos

Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...