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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 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.
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...

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Related Experiment Video

Updated: Jul 9, 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

Nitrated alpha-synuclein-activated microglial profiling for Parkinson's disease.

Ashley D Reynolds1, Jason G Glanzer, Irena Kadiu

  • 1Center for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198-5880, USA.

Journal of Neurochemistry
|November 27, 2007
PubMed
Summary

Parkinson's disease involves neuroinflammation where modified alpha-synuclein triggers microglial activation, leading to dopaminergic neuron damage. This study reveals key inflammatory pathways and proteins involved in this process.

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Related Experiment Videos

Last Updated: Jul 9, 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

Targeting Alpha Synuclein Aggregates in Cutaneous Peripheral Nerve Fibers by Free-floating Immunofluorescence Assay
08:33

Targeting Alpha Synuclein Aggregates in Cutaneous Peripheral Nerve Fibers by Free-floating Immunofluorescence Assay

Published on: June 25, 2019

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglial neuroinflammation is central to Parkinson's disease (PD) pathogenesis.
  • Modified alpha-synuclein (alpha-syn), a key component of Lewy bodies, activates microglia.
  • Nitrated and aggregated alpha-syn induces inflammatory responses and dopaminergic neurotoxicity.

Purpose of the Study:

  • To model and investigate microglial activation by nitrated, aggregated alpha-syn in Parkinson's disease.
  • To identify molecular pathways and protein changes in activated microglia relevant to PD.
  • To correlate findings in an experimental model with human PD brain tissue.

Main Methods:

  • Stimulation of primary microglia with aggregated and nitrated alpha-syn.
  • Genomic analysis using microarrays.
  • Proteomic analysis including liquid chromatography-tandem mass spectrometry, differential gel electrophoresis, and protein arrays.
  • Examination of autopsy brain tissue from PD patients.

Main Results:

  • Activated microglia exhibited ameboid morphology and induced dopaminergic neurotoxicity.
  • Genomic studies highlighted the significant role of nuclear factor-kappa B (NF-κB) transcriptional activation.
  • Proteomic analysis revealed increased inflammatory, redox, enzyme, and cytoskeletal proteins.
  • NF-κB-related inflammatory processes were observed in human PD brain tissue.

Conclusions:

  • The study provides a comprehensive transcriptome and proteome profile of microglia activated by nitrated alpha-syn.
  • Findings suggest NF-κB activation is a key inflammatory pathway in PD pathogenesis.
  • The research offers potential new insights into the mechanisms of neurodegeneration in Parkinson's disease.