Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Parkinson Disease ll: Pathophysiology

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 Disease l: Introduction

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...

Parkinson's Disease: Overview

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's Disease: Treatment

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of its...

Amyloid Fibrils

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 Fibrils

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...

You might also read

Related Articles

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

Sort by

Same author

Dendritic Localization and Exocytosis of NAAG in the Rat Hippocampus.

Cerebral cortex (New York, N.Y. : 1991)·2019

Same author

Vesicular glutamate transporter-3 in the rodent brain: vesicular colocalization with vesicular γ-aminobutyric acid transporter.

The Journal of comparative neurology·2013

Same author

Pre- and postsynaptic localization of NMDA receptor subunits at hippocampal mossy fibre synapses.

Neuroscience·2012

Same author

Immunogold detection of L-glutamate and D-serine in small synaptic-like microvesicles in adult hippocampal astrocytes.

Cerebral cortex (New York, N.Y. : 1991)·2011

Same author

Complementary expression of SN1 and SAT2 in the islets of Langerhans suggests concerted action of glutamine transport in the regulation of insulin secretion.

Biochemical and biophysical research communications·2009

Same author

A quantitative assessment of glutamate uptake into hippocampal synaptic terminals and astrocytes: new insights into a neuronal role for excitatory amino acid transporter 2 (EAAT2).

Neuroscience·2008

Search research articles

Related Experiment Video

Updated: Jun 11, 2026

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

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

Published on: August 16, 2020

Protein aggregation in Parkinson's disease.

¹Department of Anatomy and the CMBN, University of Oslo, Oslo, Norway. vidar.gunderson@medisin.uio.no

Acta Neurologica Scandinavica. Supplementum

|July 1, 2010

Summary

Parkinson's disease involves the loss of dopaminergic neurons and the accumulation of Lewy bodies. Protein aggregate formation in Lewy bodies is a key factor in neurodegeneration, contributing to the progression of this movement disorder.

Area of Science:

Neuroscience
Neurology
Pathology

Background:

Parkinson's disease (PD) is a primary neurodegenerative movement disorder.
It is characterized by the loss of dopaminergic neurons in the substantia nigra.
Protein aggregates, known as Lewy bodies, accumulate in neurons during the neurodegenerative process.

Purpose of the Study:

To explore the underlying pathogenic mechanisms in Parkinson's disease.
To discuss the role of protein aggregate accumulation in neuronal death.

Main Methods:

Review of existing literature on Parkinson's disease pathology.
Analysis of the contribution of Lewy body formation to neurodegeneration.

Main Results:

More Related Videos

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

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

Published on: January 5, 2016

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

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

Published on: July 29, 2022

Related Experiment Videos

Last Updated: Jun 11, 2026

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

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

Published on: August 16, 2020

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

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

Published on: January 5, 2016

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

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

Published on: July 29, 2022

Parkinson's disease involves dopaminergic neuron loss and Lewy body formation.

Non-dopaminergic neurons are also affected in Parkinson's disease.

Protein aggregation in Lewy bodies is implicated in neuronal degeneration.

Conclusions:

The exact pathogenic process leading to dopaminergic neuron death in Parkinson's disease requires further understanding.
Protein filament accumulation in Lewy bodies plays an active role in neuronal degeneration.
Further research is needed to fully elucidate the mechanisms of Parkinson's disease progression.