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

3.3K
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...
3.3K
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

9.9K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
9.9K
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

1.0K
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...
1.0K
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

64
Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
64
Coagulation01:09

Coagulation

7.9K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
7.9K
Disorders of Hemostasis01:24

Disorders of Hemostasis

1.3K
Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
1.3K

You might also read

Related Articles

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

Sort by
Same author

Hexokinase controls platelet activation and hemostasis.

Platelets·2026
Same author

Fibrinogen wags its disordered tail: α chain and thrombosis.

Blood·2026
Same author

Potential Role of Polyphenols in Platelet Aggregation and Blood Coagulation.

Journal of cardiovascular development and disease·2026
Same author

Modulatory Effects of Polyphenols on Altered Leukocyte Functions in Thromboinflammation and Diabetes Mellitus.

International journal of molecular sciences·2026
Same author

International Society on Thrombosis and Haemostasis conflict of interest management and tools: presentation of a case study.

Journal of thrombosis and haemostasis : JTH·2026
Same author

A Neutrophil-like Cell Model as Substitute for Human Neutrophils in NETs and Thrombosis Research.

Cells·2026

Related Experiment Video

Updated: Oct 7, 2025

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

12.0K

Vascular Dementia and Crosstalk Between the Complement and Coagulation Systems.

Milad Mossanen Parsi1, Cédric Duval1, Robert A S Ariëns1

  • 1Discovery and Translational Science Department, School of Medicine, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom.

Frontiers in Cardiovascular Medicine
|January 10, 2022
PubMed
Summary

Vascular dementia (VaD) involves brain damage from reduced blood flow. This review explores how complement and coagulation systems contribute to VaD, potentially revealing new therapeutic targets.

Keywords:
coagulationcomplementcrosstalksmall vessel diseasevascular dementia (VaD)

More Related Videos

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

7.9K
In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

9.2K

Related Experiment Videos

Last Updated: Oct 7, 2025

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

12.0K
Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

7.9K
In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
09:19

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

Published on: May 24, 2020

9.2K

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Vascular Dementia (VaD) is a major neurocognitive disorder caused by impaired blood flow to the brain.
  • The complement and coagulation systems are crucial for host defense but their overactivation is implicated in neurological diseases.
  • While their role in Alzheimer's and multiple sclerosis is known, their specific involvement in VaD pathogenesis remains underexplored.

Purpose of the Study:

  • To review and synthesize current knowledge on the role of complement and coagulation systems in Vascular Dementia.
  • To identify specific components within these systems that contribute to VaD pathogenesis.
  • To explore the potential impact of crosstalk between these systems on VaD development.

Main Methods:

  • Literature review and synthesis of existing research on Vascular Dementia.
  • Analysis of studies investigating the complement system in neurological disorders.
  • Examination of research on the coagulation system and its link to brain injury.

Main Results:

  • The complement and coagulation systems are activated by tissue injury, leading to inflammation and clot formation.
  • Interactions and crosstalk between these systems can influence disease progression.
  • Evidence suggests these interconnected systems play a significant role in the pathological mechanisms of VaD.

Conclusions:

  • Understanding the interplay between complement and coagulation systems is crucial for comprehending VaD.
  • Identifying specific molecular players and their interactions may lead to novel therapeutic strategies for VaD.
  • Further research into these pathways could uncover new biomarkers for VaD diagnosis and treatment.