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

Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
Rabies01:28

Rabies

Rabies is a lethal zoonotic disease caused by a single-stranded, negative-sense RNA virus of the Lyssavirus genus, within the family Rhabdoviridae. Its primary mode of transmission to humans is through bites or saliva-contaminated scratches from infected mammals such as dogs, bats, raccoons, or foxes. Transmission can also occur if infectious saliva contacts abraded skin or intact mucous membranes, including the conjunctiva.Viral Entry and Early ReplicationOnce introduced at the bite or scratch...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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 l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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...

You might also read

Related Articles

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

Sort by
Same author

Neural mechanisms of time-forward predictions for naturalistic auditory tone sequences.

Nature communications·2026
Same author

Obstructive sleep apnea in people with epilepsy: Modifying risk.

Epilepsia·2026
Same author

Virtual Responsive Neurostimulation Implantation: From Intracranial Connectivity to Optimized Lead Placement.

medRxiv : the preprint server for health sciences·2026
Same author

A Probabilistic Approach to Functional Organization Based on Extraoperative Electrocortical Stimulation Mapping.

Neurology·2026
Same author

Interconnected influences of diet, gut microbiome, and metabolome on cognition across three metabolomics platforms.

Research square·2026
Same author

Frontal cortex organization supporting audiovisual processing during naturalistic viewing.

Nature communications·2026

Related Experiment Video

Updated: Jun 18, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

23.9K

Brain molecular mechanisms in Rasmussen encephalitis.

Dominique F Leitner1,2, Ziyan Lin3, Zacharia Sawaged3

  • 1Comprehensive Epilepsy Center, NYU Grossman School of Medicine, New York, New York, USA.

Epilepsia
|November 7, 2022
PubMed
Summary

Rasmussen encephalitis involves immune system activation and rare genetic variants, including Human Leukocyte Antigen (HLA) variations. Further research may target immune cell crosstalk to limit disease progression.

Keywords:
RNAseqRasmussen encephalitisexomeproteomics

More Related Videos

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

4.8K
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

7.8K

Related Experiment Videos

Last Updated: Jun 18, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

23.9K
Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

4.8K
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

7.8K

Area of Science:

  • Neuroimmunology
  • Genetics
  • Molecular Biology

Background:

  • Rasmussen encephalitis (RE) is a rare autoimmune neurological disease affecting one brain hemisphere.
  • Understanding the molecular underpinnings of RE is crucial for developing targeted therapies.

Purpose of the Study:

  • To identify molecular mechanisms in Rasmussen encephalitis (RE) brain tissue.
  • To compare molecular profiles of RE with non-RE epilepsy (PWE) and control cases.
  • To investigate the roles of genetic variants and immune signaling in RE pathogenesis.

Main Methods:

  • Whole exome sequencing (WES), RNA sequencing (RNAseq), and proteomics were performed on brain tissue samples.
  • Samples were obtained from RE cases (n=27), PWE (n=10), and controls (n=14).
  • Differential gene expression and protein abundance were analyzed, alongside WES variant analysis for RE-associated genes and Human Leukocyte Antigens (HLAs).

Main Results:

  • WES identified rare, likely deleterious variants of unknown significance (VUS) in genes like MTOR and SCN1A, and common HLA VUS in RE cases.
  • RNAseq revealed significant activation of immune signaling pathways, including crosstalk between dendritic and natural killer cells in RE.
  • Neuroinflammation signaling was activated in RE compared to controls, while phagosome formation was activated in PWE compared to controls.

Conclusions:

  • RE pathogenesis involves activated immune signaling pathways and potential contributions from rare genetic variants, including HLA variations.
  • Findings suggest a role for both innate and adaptive immune responses in RE.
  • Future studies should explore immune cell density, localization, and therapeutic modulation of immune cell crosstalk.