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

Stroke: Introduction and Types01:29

Stroke: Introduction and Types

A stroke is an acute neurological event caused by the sudden disruption of cerebral blood flow, leading to rapid loss of neuronal function. Neurons depend on continuous oxygen and glucose supply, so even brief interruptions can cause irreversible injury within minutes. Strokes are classified into ischemic and hemorrhagic types.Ischemic StrokeIschemic strokes are most common and occur due to arterial occlusion, depriving brain tissue of oxygen and nutrients. This leads to energy failure, ionic...
Regulation of Stroke Volume01:27

Regulation of Stroke Volume

The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
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...

You might also read

Related Articles

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

Sort by
Same author

Serum inflammatory proteomic signatures define chronic inflammatory demyelinating polyneuropathy and inform on disease activity.

EBioMedicine·2026
Same author

Infarct-associated oligoclonal T cell expansion in chronic experimental stroke across age, sex, and models.

Experimental neurology·2026
Same author

Comparative Evaluation of hiPSC-Derived Brain Organoids as Platforms for Assessing Thyroid Hormone System Disrupting Chemicals.

Cells·2026
Same author

Septin multimer autoantibodies in severe motor neuropathy mimicking lower motor neuron disease.

Brain : a journal of neurology·2026
Same author

Clinical effectiveness of efgartigimod in a broad population of patients with generalized myasthenia gravis: subgroup analyses from a randomized, double‑blind, placebo‑controlled, phase 3 trial (ADAPT).

Journal of neurology·2026
Same author

Meningococcal prophylaxis in neurological diseases treated with complement inhibitors: an expert consensus for Germany, Austria, and Switzerland.

Therapeutic advances in neurological disorders·2026
Same journal

Electrical coupling between transplanted cardiomyocytes and host myocardium to prevent arrhythmia.

Disease models & mechanisms·2026
Same journal

Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 induced pluripotent stem cell-derived neural cells.

Disease models & mechanisms·2026
Same journal

Mesoscale maladaptation in disease organoids.

Disease models & mechanisms·2026
Same journal

A modeller's guide for biomedical discovery.

Disease models & mechanisms·2026
Same journal

An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.

Disease models & mechanisms·2026
Same journal

Co-mutations of CTNNB1 and PTEN drive aggressive tumor progression in endometrial cancer.

Disease models & mechanisms·2026
See all related articles

Related Experiment Video

Updated: May 17, 2026

Modeling Stroke in Mice: Transient Middle Cerebral Artery Occlusion via the External Carotid Artery
07:26

Modeling Stroke in Mice: Transient Middle Cerebral Artery Occlusion via the External Carotid Artery

Published on: May 24, 2021

Do stroke models model stroke?

Philipp Mergenthaler1, Andreas Meisel

  • 1Department of Experimental Neurology, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10098 Berlin, Germany. philipp.mergenthaler@charite.de

Disease Models & Mechanisms
|November 2, 2012
PubMed
Summary
This summary is machine-generated.

Translational stroke research faces significant roadblocks, leading to trial failures. Improving preclinical models to better reflect patient care and implementing rigorous testing, including Phase 3 trials, is crucial for advancing stroke therapies.

More Related Videos

Modeling Stroke in Mice - Middle Cerebral Artery Occlusion with the Filament Model
06:28

Modeling Stroke in Mice - Middle Cerebral Artery Occlusion with the Filament Model

Published on: January 6, 2011

Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis
06:07

Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis

Published on: May 6, 2021

Related Experiment Videos

Last Updated: May 17, 2026

Modeling Stroke in Mice: Transient Middle Cerebral Artery Occlusion via the External Carotid Artery
07:26

Modeling Stroke in Mice: Transient Middle Cerebral Artery Occlusion via the External Carotid Artery

Published on: May 24, 2021

Modeling Stroke in Mice - Middle Cerebral Artery Occlusion with the Filament Model
06:28

Modeling Stroke in Mice - Middle Cerebral Artery Occlusion with the Filament Model

Published on: January 6, 2011

Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis
06:07

Modeling Stroke in Mice: Focal Cortical Lesions by Photothrombosis

Published on: May 6, 2021

Area of Science:

  • Neurology
  • Translational Medicine
  • Neuroscience

Background:

  • Stroke is a leading cause of death and disability globally.
  • Despite extensive basic research, many clinical trials for stroke treatments, particularly neuroprotection, have failed.
  • Key "translational roadblocks" include poor methodological standards, publication bias, and inadequate preclinical testing.

Purpose of the Study:

  • To review common preclinical stroke research models.
  • To discuss reasons for the failure of translational stroke research.
  • To propose remedies, including better modeling of patient care and advanced preclinical testing strategies.

Main Methods:

  • Introduction of commonly used preclinical stroke models.
  • Discussion of factors contributing to translational failure.
  • Review of potential solutions and remedies for improving preclinical research.

Main Results:

  • Current preclinical models often fail to adequately represent the complexity of stroke and patient care.
  • Incomplete preclinical testing and methodological weaknesses hinder the translation of basic science to clinical practice.
  • The concept of modeling "care" alongside the stroke disorder in preclinical settings is introduced.

Conclusions:

  • Preclinical stroke research requires improved modeling of the disorder and patient care.
  • Adopting methodologies similar to clinical testing, including Phase 3 randomized controlled preclinical trials, is essential.
  • Enhanced preclinical strategies are necessary before new stroke therapies advance to clinical testing.