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...
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...
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...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...

You might also read

Related Articles

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

Sort by
Same author

TeleROP-NI: Modernizing Retinopathy of Prematurity Screening in Northern Ireland to Enhance Decision-making and Ensure Sustainability.

Journal of pediatric ophthalmology and strabismus·2026
Same author

Efficacy and safety of intravenous prasinezumab in individuals with early-stage Parkinson's disease on stable symptomatic monotherapy (PADOVA): a phase 2b, multicentre, randomised, double-blind, placebo-controlled study.

Lancet (London, England)·2026
Same author

Neuroinflammation and neurodegeneration trigger a specific splice form of ribosomal protein S24.

Brain : a journal of neurology·2026
Same author

TIP26-315: Methods for Evaluating the Impact of a Patient Navigation System in Community Oncology Practices: A Mixed-Methods Pre/Post Implementation Study.

Journal of the National Comprehensive Cancer Network : JNCCN·2026
Same author

TIP26-315: Methods for Evaluating the Impact of a Patient Navigation System in Community Oncology Practices: A Mixed-Methods Pre/Post Implementation Study.

Journal of the National Comprehensive Cancer Network : JNCCN·2026
Same author

Genome-wide DNA methylation profiling in COVID-19 positive patients reveals alterations in pathways linked to neurological dysfunction.

Clinical epigenetics·2026
Same journal

Non-Alzheimer Aβ deposits in the human CNS: Implications with hypoxia and related conditions.

Brain pathology (Zurich, Switzerland)·2026
Same journal

Distinctly altered TRPC3 and TRPC6 expression patterns in human Alzheimer's disease cortex and hippocampus.

Brain pathology (Zurich, Switzerland)·2026
Same journal

Lewy bodies are surrounded by granulovacuolar degeneration bodies in dementia with Lewy bodies.

Brain pathology (Zurich, Switzerland)·2026
Same journal

A 3-year-old girl with a left optic nerve tumor.

Brain pathology (Zurich, Switzerland)·2026
Same journal

Chromosomal and immune dysregulation underlying granular mitosis in glioblastoma.

Brain pathology (Zurich, Switzerland)·2026
Same journal

Nearest-neighbors assisted unsupervised analysis for methylation array profiling for central nervous system tumors.

Brain pathology (Zurich, Switzerland)·2026
See all related articles

Related Experiment Video

Updated: May 12, 2026

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains
09:27

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

α-Synuclein: the long distance runner.

Sonia George1, Nolwen L Rey, Nicole Reichenbach

  • 1Neuronal Survival Unit, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.

Brain Pathology (Zurich, Switzerland)
|April 17, 2013
PubMed
Summary
This summary is machine-generated.

Parkinson's disease involves alpha-synuclein (α-synuclein) pathology spreading through the brain. This review explores if this protein spreads like a prion via cell-to-cell transfer and axonal transport.

More Related Videos

Millisecond Hydrogen/Deuterium-Exchange Mass Spectrometry for the Study of Alpha-Synuclein Structural Dynamics Under Physiological Conditions
08:40

Millisecond Hydrogen/Deuterium-Exchange Mass Spectrometry for the Study of Alpha-Synuclein Structural Dynamics Under Physiological Conditions

Published on: June 23, 2022

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
12:01

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Published on: May 30, 2015

Related Experiment Videos

Last Updated: May 12, 2026

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains
09:27

Sequential Extraction of Soluble and Insoluble Alpha-Synuclein from Parkinsonian Brains

Published on: January 5, 2016

Millisecond Hydrogen/Deuterium-Exchange Mass Spectrometry for the Study of Alpha-Synuclein Structural Dynamics Under Physiological Conditions
08:40

Millisecond Hydrogen/Deuterium-Exchange Mass Spectrometry for the Study of Alpha-Synuclein Structural Dynamics Under Physiological Conditions

Published on: June 23, 2022

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
12:01

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Published on: May 30, 2015

Area of Science:

  • Neuroscience
  • Pathology
  • Cell Biology

Background:

  • Parkinson's disease (PD) is defined by alpha-synuclein (α-synuclein) aggregation into Lewy bodies and neurites.
  • Braak's staging outlines the progressive spread of α-synuclein pathology in PD.
  • Emerging evidence suggests α-synuclein can transfer between cells.

Purpose of the Study:

  • To review the role of α-synuclein in Parkinson's disease pathology and Braak staging.
  • To discuss the potential prion-like mechanism of α-synuclein cell-to-cell spread.
  • To highlight recent research on α-synuclein cell transfer and axonal transport.

Main Methods:

  • Literature review of studies on α-synuclein pathology in Parkinson's disease.
  • Analysis of experimental data on cell-to-cell transfer of α-synuclein.
  • Focus on research concerning axonal transport of α-synuclein.

Main Results:

  • α-synuclein pathology is central to Parkinson's disease progression as described by Braak.
  • Cell-to-cell transfer of α-synuclein is experimentally supported.
  • Long-distance axonal transport is a key mechanism for α-synuclein spread.

Conclusions:

  • α-synuclein cell-to-cell transfer and axonal transport are critical mechanisms in Parkinson's disease.
  • A prion-like spread of α-synuclein may contribute to the progressive nature of PD.
  • Understanding these mechanisms is vital for developing targeted Parkinson's disease therapies.