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

Inflammation01:38

Inflammation

46.8K
Overview
46.8K
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

49
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...
49
Inflammation: Introduction01:28

Inflammation: Introduction

84
Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...
84
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

84
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
84
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

32
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...
32
Inflammatory Response01:28

Inflammatory Response

12.6K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
12.6K

You might also read

Related Articles

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

Sort by
Same author

Perioperative interventions in preventing postoperative delirium following orthopaedic surgery in the elderly: a Bayesian network meta-analysis.

Journal of orthopaedic translation·2026
Same author

Excitatory paraventricular thalamus-posterior insular cortex circuit mediates pain-anxiety comorbidity in diabetic neuropathy.

Translational psychiatry·2026
Same author

Mitochondrial flagella-like extensions (MitoFLARE) dysfunction triggers STING-mediated immune dysregulation in sepsis.

Nature communications·2026
Same author

Sleep deprivation induces anxiety-like behaviors through IL-6 driven astrocyte-GABAergic neuron crosstalk in the PAG-ACC circuit.

Journal of neuroinflammation·2026
Same author

Advancements and insights into newborn screening with tandem mass spectrometry in China: a comprehensive descriptive analysis (2017-2021).

BMJ paediatrics open·2026
Same author

Intracellular sclerostin promotes tumor progression and metastasis as a potential therapeutic target in triple-negative breast cancer.

Cell reports. Medicine·2026
Same journal

Transcriptomic and epigenetic characterization of paraventricular thalamic nucleus neurons in Polg1 mutant mice.

Neuroscience research·2026
Same journal

Modulation of the EEG alpha-band envelope during mental tasks: A task-related index based on second-order derivatives.

Neuroscience research·2026
Same journal

Enhanced calcium activity and transcriptomic alterations in iPSC-derived neurons from BAFME patients with repeat expansions.

Neuroscience research·2026
Same journal

Clustered protocadherinβs contribute to configuring functional cell populations in hippocampal-cortical regions.

Neuroscience research·2026
Same journal

ALS-associated protein TDP-43 disturbs axonal projections in the somatosensory cortex.

Neuroscience research·2026
Same journal

Microglial ontogeny and in vitro reconstruction: Bridging development and modeling.

Neuroscience research·2026
See all related articles

Related Experiment Video

Updated: May 6, 2026

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

14.7K

Neuroinflammation: the role and consequences.

Monty Lyman1, Dafydd G Lloyd1, Xunming Ji2

  • 1Section of Anaesthetics, Pain Medicine & Intensive Care, Department of Surgery and Cancer, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK.

Neuroscience Research
|October 23, 2013
PubMed
Summary
This summary is machine-generated.

Excessive neuroinflammation damages brain function and accelerates neurodegenerative diseases like dementia. Combined therapeutic approaches may be necessary for effective prevention and treatment of these conditions.

Keywords:
Alzheimer's diseaseMicrogliaMultiple sclerosisNeuroinflammationPostoperative cognitive dysfunctionSystemic inflammation

More Related Videos

Brain Ventricular Microinjections of Lipopolysaccharide into Larval Zebrafish to Assess Neuroinflammation and Neurotoxicity
07:31

Brain Ventricular Microinjections of Lipopolysaccharide into Larval Zebrafish to Assess Neuroinflammation and Neurotoxicity

Published on: August 23, 2022

3.3K
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

2.0K

Related Experiment Videos

Last Updated: May 6, 2026

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

14.7K
Brain Ventricular Microinjections of Lipopolysaccharide into Larval Zebrafish to Assess Neuroinflammation and Neurotoxicity
07:31

Brain Ventricular Microinjections of Lipopolysaccharide into Larval Zebrafish to Assess Neuroinflammation and Neurotoxicity

Published on: August 23, 2022

3.3K
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

2.0K

Area of Science:

  • Neuroscience
  • Pathology
  • Immunology

Background:

  • Neuroinflammation is a key factor in acute and chronic brain diseases.
  • Excessive and prolonged neuroinflammation has detrimental effects on brain function.

Purpose of the Study:

  • To review the consequences of excessive neuroinflammation.
  • To examine its role in disease progression and potential interventions.

Main Methods:

  • Literature review of studies on neuroinflammation and brain diseases.
  • Analysis of evidence linking neuroinflammation to cellular damage and disease.

Main Results:

  • Neuroinflammation causes and accelerates long-term neurodegenerative diseases.
  • It plays a crucial role in the early development of chronic conditions such as dementia.

Conclusions:

  • Neuroinflammation is central to the pathology of numerous brain diseases.
  • Combined preventative and therapeutic strategies are likely needed for effective management.