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

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...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

You might also read

Related Articles

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

Sort by
Same author

The Financial Value of an Academic Neurologist.

Annals of neurology·2026
Same author

Uremic pancreatitis following routine initiation of losartan in advanced chronic kidney disease: A case report.

SAGE open medical case reports·2026
Same author

The Effect of Ocrelizumab on Anti-JC Virus Antibody Index.

Brain and behavior·2026
Same author

Rapidly Progressive and Relapsing Myelitis With Human T Lymphotropic Virus Type 1: A Case Report and Review of the Literature.

Neurology(R) neuroimmunology & neuroinflammation·2026
Same author

GA Depot, a long-acting glatiramer acetate, vs placebo in patients with relapsing multiple sclerosis: A randomized phase 3 clinical trial.

Multiple sclerosis (Houndmills, Basingstoke, England)·2026
Same author

Explaining the Insights Obtained from the BRANDO Database.

Arquivos de neuro-psiquiatria·2026
Same journal

Movement disorders and Parkinson's disease: collaborative and interdisciplinary research to advance understanding of neural circuit dysfunction, pathophysiology, and care: new horizons in technology, neuroimaging, neurophysiology, and genetics toward personalized medicine.

Current opinion in neurology·2026
Same journal

Editorial introduction.

Current opinion in neurology·2026
Same journal

Multimodal mapping of balance dysfunction in Parkinson's disease: a consensus roadmap for research and intervention.

Current opinion in neurology·2026
Same journal

Tourette syndrome: brain neurophysiology, circuit dysfunction, and neuromodulation across invasive and noninvasive approaches.

Current opinion in neurology·2026
Same journal

Dystonia: from phenotypes to genetics and therapeutic advances.

Current opinion in neurology·2026
Same journal

What can we learn from eye movements in movement disorders and Parkinson's disease?

Current opinion in neurology·2026
See all related articles

Related Experiment Video

Updated: Jun 2, 2026

A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice
04:55

A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice

Published on: May 11, 2022

The basis for modeling progressive multifocal leukoencephalopathy pathogenesis.

Joseph R Berger

    Current Opinion in Neurology
    |April 19, 2011
    PubMed
    Summary
    This summary is machine-generated.

    Progressive multifocal leukoencephalopathy (PML) is rare despite widespread JC virus infection, indicating significant biological barriers. Understanding these barriers is crucial for managing PML risks associated with new therapies.

    More Related Videos

    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

    Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
    05:44

    Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis

    Published on: October 13, 2023

    Related Experiment Videos

    Last Updated: Jun 2, 2026

    A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice
    04:55

    A Stably Established Two-Point Injection of Lysophosphatidylcholine-Induced Focal Demyelination Model in Mice

    Published on: May 11, 2022

    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

    Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
    05:44

    Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis

    Published on: October 13, 2023

    Area of Science:

    • Neurovirology
    • Immunology
    • Pathogenesis of demyelinating diseases

    Background:

    • Progressive multifocal leukoencephalopathy (PML) is a rare but serious demyelinating disease.
    • The increasing use of highly effective biological agents has heightened concerns regarding PML.
    • Understanding PML pathogenesis is critical for risk assessment and mitigation.

    Discussion:

    • JC virus (JCV), a common human polyomavirus, is the causative agent of PML.
    • PML development requires overcoming multiple host, viral, and immunological barriers.
    • JCV requires promoter rearrangement for oligodendrocyte infection, representing a viral barrier.

    Key Insights:

    • Cell-mediated immunity, specifically JC virus-specific cytotoxic T cells, is a primary immunological barrier against PML.
    • Despite high JCV seroprevalence, PML incidence is very low, underscoring the importance of these protective mechanisms.
    • Host factors influencing PML susceptibility remain largely uncharacterized.

    Outlook:

    • Significant knowledge gaps persist regarding JCV biology and PML pathogenesis.
    • Current understanding provides a foundation for developing predictive models and risk mitigation strategies.
    • Further research into JCV-PML mechanisms will improve patient care and therapeutic safety.