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...
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...
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...
Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...
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...

You might also read

Related Articles

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

Sort by
Same author

Dystrophic changes of nigrostriatal axons harboring a Synj1 Parkinson mutation suggest catastrophic failure of endocytic mechanisms.

bioRxiv : the preprint server for biology·2026
Same author

Altered striatal dopamine regulation in Adgrl3 knockout mice.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·2026
Same author

α-Synuclein and γ-Tubulin Cooperatively Regulate Activity-Evoked Presynaptic Microtubule Nucleation to Gate Dopamine Release.

bioRxiv : the preprint server for biology·2026
Same author

Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity.

bioRxiv : the preprint server for biology·2026
Same author

Cell- and state-specific plasticity of striatal glutamatergic synapses is critical to the expression of levodopa-induced dyskinesia.

Neuron·2026
Same author

Author Correction: Autoimmune response to C9orf72 protein in amyotrophic lateral sclerosis.

Nature·2026

Related Experiment Video

Updated: May 20, 2026

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein
14:45

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Published on: July 29, 2022

Neuronal vulnerability, pathogenesis, and Parkinson's disease.

David Sulzer1, D James Surmeier

  • 1Department of Psychiatry, Columbia University, New York, New York, USA. ds43@columbia.edu

Movement Disorders : Official Journal of the Movement Disorder Society
|July 14, 2012
PubMed
Summary

Parkinson's disease (PD) pathogenesis remains unclear, but specific neuronal traits like autonomous activity and broad action potentials may increase vulnerability. Physiological factors offer potential therapeutic targets for this neurodegenerative disease.

More Related Videos

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
10:03

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
08:09

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Related Experiment Videos

Last Updated: May 20, 2026

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein
14:45

Analyzing the Parkinson's Disease Mouse Model Induced by Adeno-associated Viral Vectors Encoding Human α-Synuclein

Published on: July 29, 2022

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
10:03

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
08:09

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease

Published on: January 7, 2014

Area of Science:

  • Neuroscience
  • Pathology
  • Neurology

Background:

  • Parkinson's disease (PD) pathogenesis is not fully understood despite advances.
  • Neuronal pathology in PD is restricted, offering clues to disease mechanisms.
  • Lewy pathology (LP), phenotypic dysregulation, and degeneration affect various neuronal populations in PD patients.

Purpose of the Study:

  • To investigate potential risk factors contributing to neuronal vulnerability in Parkinson's disease.
  • To identify specific phenotypic traits associated with increased susceptibility to PD pathology.
  • To explore therapeutic targets based on identified risk factors.

Main Methods:

  • Literature review of neuronal pathology in Parkinson's disease.
  • Analysis of phenotypic traits in affected neuronal populations.
  • Identification of common risk factors across different neuronal types.

Main Results:

  • A small set of risk factors contribute to neuronal vulnerability in PD.
  • Identified risk factors include autonomous activity, broad action potentials, and low calcium-buffering capacity.
  • Neurons utilizing monoamine neurotransmitters, particularly catecholamines, are implicated.

Conclusions:

  • Specific physiological traits of neurons may predispose them to Parkinson's disease pathology.
  • Therapeutic strategies targeting these physiological vulnerabilities are promising.
  • Further research into neuromelanin and catecholamine pathways is warranted.