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

Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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...
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.
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

You might also read

Related Articles

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

Sort by
Same author

Woven Endobridge device for ruptured vs. unruptured aneurysms: insights from the WorldWideWEB study.

Neuroradiology·2026
Same author

Meta-analysis reveals apolipoprotein ε4 confers higher susceptibility to Parkinson's disease dementia in Asian populations.

Frontiers in aging neuroscience·2026
Same author

Monosialoganglioside-Containing Nanoliposomes Protect Against Acute and Chronic Ischemic Stroke Injury.

Journal of the American Heart Association·2026
Same author

Single-layer spherical (SLS) vs single-layer (SL) Woven EndoBridge (WEB) device in the treatment of narrow-neck intracranial aneurysms: a propensity score-matched analysis.

Neurosurgical review·2026
Same author

Flow-Diversion for Complex Posterior Communicating Artery Aneurysms Associated With a Fetal Posterior Circulation.

Stroke (Hoboken, N.J.)·2026
Same author

Number Needing Review: A Novel Metric to Assess Triage Efficiency of Large Vessel Occlusion Detection Systems.

Stroke (Hoboken, N.J.)·2026

Related Experiment Video

Updated: Jun 27, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

The role of complement in stroke therapy.

Ricardo J Komotar1, Grace H Kim, Marc L Otten

  • 1Department of Neurological Surgery, Columbia University, New York, NY 10032, USA.

Advances in Experimental Medicine and Biology
|November 26, 2008
PubMed
Summary

Blocking the complement cascade may reduce brain damage after stroke. This inflammation pathway is activated during cerebral ischemia and reperfusion, offering potential therapeutic targets for neuroprotection.

More Related Videos

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Related Experiment Videos

Last Updated: Jun 27, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Cerebral ischemia and reperfusion trigger inflammation, causing secondary neuronal damage.
  • The complement cascade, a key inflammatory mediator, is activated after ischemic events.
  • Complement deposition on apoptotic neurons may harm adjacent viable cells.

Purpose of the Study:

  • To review the role of the complement cascade in neuronal injury following ischemic stroke.
  • To identify potential therapeutic targets within the complement cascade for neuroprotection.

Main Methods:

  • Review of existing literature on complement activation in cerebral ischemia.
  • Analysis of studies investigating complement inhibition as a neuroprotective strategy.

Main Results:

  • Complement activation is implicated in secondary neuronal damage post-ischemia.
  • Blocking the complement cascade early in infarct evolution may limit brain injury.
  • Specific complement components might influence neuronal cell survival.

Conclusions:

  • The complement cascade is a significant contributor to brain damage after ischemic stroke.
  • Targeting the complement cascade presents a promising therapeutic avenue for stroke treatment.
  • Further research into specific complement targets could enhance neuroprotective strategies.