Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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 Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Real-world use of Cenobamate in pediatric drug-resistant epilepsy: A European multicenter retrospective study.

Epilepsia open·2026
Same author

Cenobamate in pediatric Dravet syndrome: two responder cases highlighting the limits of simple "sodium-channel blocker" labeling.

Frontiers in pharmacology·2026
Same author

Stress during the first 1,000 days of life in humans, when everything begins.

Frontiers in human neuroscience·2026
Same author

<i>COCH</i>-Related Hearing Loss in a French Cohort: Novel Variants and Genotype-Phenotype Correlations.

Genes·2026
Same author

Risdiplam Add-On Therapy Following Onasemnogene Abeparvovec in Children With Spinal Muscular Atrophy and 2 SMN2 Copies: A Multi-Center Case Series.

Muscle & nerve·2026
Same author

Characteristics of repeated untethering pattern in patients with myelomeningocele from infancy to adolescence.

Journal of neurosurgery. Pediatrics·2026

Related Experiment Video

Updated: Jun 13, 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

Inflammation processes in perinatal brain damage.

Vincent Degos1, Géraldine Favrais, Angela M Kaindl

  • 1Hôpital Robert Debré, Inserm, U676, 48 Blvd Serurier, 75019 Paris, France.

Journal of Neural Transmission (Vienna, Austria : 1996)
|May 18, 2010
PubMed
Summary
This summary is machine-generated.

The central nervous system is no longer considered immune-privileged. Neuroinflammation is now a key focus for understanding perinatal brain damage mechanisms.

More Related Videos

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
07:36

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

Published on: November 19, 2019

Related Experiment Videos

Last Updated: Jun 13, 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

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats
04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury
07:36

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

Published on: November 19, 2019

Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • The central nervous system (CNS) was historically viewed as isolated and immune-privileged.
  • Emerging research highlights the CNS's intricate immune interactions.
  • This paradigm shift is crucial for understanding neurological disorders.

Purpose of the Study:

  • To review current understanding of perinatal brain damage.
  • To elucidate the role of neuroinflammation in perinatal brain injury.
  • To provide an overview of the pathomechanisms involved.

Main Methods:

  • Literature review of current research on perinatal brain damage.
  • Analysis of studies investigating neuroinflammation in the developing brain.
  • Synthesis of data on inflammatory pathways in perinatal injury.

Main Results:

  • Neuroinflammation plays a significant role in the pathomechanism of perinatal brain damage.
  • Inflammatory processes are central to understanding how the perinatal brain is injured.
  • The CNS is not an immune-privileged sanctuary.

Conclusions:

  • The concept of the CNS as immune-privileged is outdated.
  • Neuroinflammation is a critical factor in perinatal brain damage.
  • Further research into neuroinflammatory pathways is essential for therapeutic development.