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

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...
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...
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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...

You might also read

Related Articles

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

Sort by
Same author

Mild cognitive impairment in Parkinson's disease: current view.

Frontiers in cognition·2026
Same author

Psychosis in Huntington disease: a short update.

Journal of neural transmission (Vienna, Austria : 1996)·2026
Same author

The enigma of vascular dementia: current state and emerging perspectives.

Journal of neural transmission (Vienna, Austria : 1996)·2026
Same author

Depression and apathy in frontotemporal dementia: a short assessment of facts and outlook.

Journal of neural transmission (Vienna, Austria : 1996)·2026
Same author

Is there a link between multiple sclerosis and Alzheimer disease? A critical note.

Journal of neural transmission (Vienna, Austria : 1996)·2025
Same author

Comorbid Pathologies and Their Impact on Dementia with Lewy Bodies-Current View.

International journal of molecular sciences·2025

Related Experiment Video

Updated: May 26, 2026

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry
12:31

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Published on: December 8, 2015

Interaction between pathogenic proteins in neurodegenerative disorders.

Kurt A Jellinger1

  • 1Institute of Clinical Neurobiology, Vienna, Austria. kurt.jellinger@univie.ac.at

Journal of Cellular and Molecular Medicine
|December 20, 2011
PubMed
Summary

Protein misfolding and aggregation drive neurodegenerative diseases like Alzheimer's and Parkinson's. Understanding how these toxic proteins interact and spread is key to developing effective treatments.

More Related Videos

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
12:57

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

Published on: January 8, 2015

Monitoring Cell-to-cell Transmission of Prion-like Protein Aggregates in Drosophila Melanogaster
10:26

Monitoring Cell-to-cell Transmission of Prion-like Protein Aggregates in Drosophila Melanogaster

Published on: March 12, 2018

Related Experiment Videos

Last Updated: May 26, 2026

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry
12:31

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Published on: December 8, 2015

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans
12:57

Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

Published on: January 8, 2015

Monitoring Cell-to-cell Transmission of Prion-like Protein Aggregates in Drosophila Melanogaster
10:26

Monitoring Cell-to-cell Transmission of Prion-like Protein Aggregates in Drosophila Melanogaster

Published on: March 12, 2018

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Protein misfolding and aggregation are central to neurodegenerative disorders.
  • Significant overlap exists between synucleinopathies, tauopathies, and other protein-misfolding diseases.
  • Characteristic inclusions suggest shared downstream pathways in these conditions.

Purpose of the Study:

  • To explore the interactions between pathological proteins in neurodegeneration.
  • To understand the role of protein spreading and synergistic effects in disease pathogenesis.
  • To identify challenges and opportunities in diagnosing and treating protein-misfolding disorders.

Main Methods:

  • Review of current findings on protein interactions in Alzheimer's, Parkinson's, Huntington's, and prion diseases.
  • Analysis of evidence for prion-like mechanisms and spreading of pathogenic proteins.
  • Investigation of genetic and environmental factors influencing disease progression.

Main Results:

  • Confirmed correlations and overlaps between various neurodegenerative disorders.
  • Identified synergistic effects of proteins like tau, amyloid-β, and α-synuclein.
  • Highlighted prion-like induction and spreading as significant pathogenic mechanisms.

Conclusions:

  • Pathogenic protein interactions and spreading are critical in neurodegenerative diseases.
  • Understanding these mechanisms offers insights into pathogenesis and potential therapeutic targets.
  • Elucidating molecular mechanisms is crucial for advancing diagnosis and treatment.