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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...
Parkinson's Disease: Treatment01:24

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...
Alzheimer Disease ll: Pathophysiology01:23

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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...

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Related Experiment Video

Updated: May 24, 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 in Parkinson's disease.

Leonidas Stefanis1

  • 1Laboratory of Neurodegenerative Diseases, Biomedical Research Foundation of the Academy of Athens, and Second Department of Neurology, University of Athens Medical School, Athens 11527, Greece. Istefanis@bioacademy.gr

Cold Spring Harbor Perspectives in Medicine
|February 23, 2012
PubMed
Summary

Alpha-synuclein oligomers are toxic species implicated in Parkinson's disease (PD) pathogenesis. Targeting these toxic forms may offer new therapeutic strategies for PD and related synucleinopathies.

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

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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
  • Molecular Biology
  • Genetics

Background:

  • Alpha-synuclein is a presynaptic neuronal protein genetically and neuropathologically linked to Parkinson's disease (PD).
  • Aberrant soluble oligomeric forms of alpha-synuclein, known as protofibrils, are believed to be the toxic species driving PD pathogenesis.
  • These toxic species disrupt cellular homeostasis and neuronal function by affecting intracellular targets, including synaptic function.

Purpose of the Study:

  • To investigate the role of alpha-synuclein in Parkinson's disease pathogenesis.
  • To explore the potential of targeting toxic alpha-synuclein species for therapeutic interventions.
  • To understand the contribution of secreted alpha-synuclein to disease propagation.

Main Methods:

  • The study focuses on the known neuropathological and genetic links between alpha-synuclein and PD.
  • It examines the proposed mechanisms by which alpha-synuclein oligomers exert toxicity.
  • The research considers the role of secreted alpha-synuclein in intercellular communication and disease spread.

Main Results:

  • Aberrant soluble oligomeric conformations of alpha-synuclein (protofibrils) are identified as the likely toxic species in PD.
  • These protofibrils disrupt cellular homeostasis and neuronal death via effects on intracellular targets, notably synaptic function.
  • Secreted alpha-synuclein may promote disease propagation by seeding aggregation in neighboring cells.

Conclusions:

  • Targeting the toxic functions of dysregulated alpha-synuclein presents a promising therapeutic avenue for Parkinson's disease.
  • These strategies may also be applicable to other neurodegenerative disorders known as synucleinopathies.
  • Further research is needed to clarify the extent of alpha-synuclein involvement in all PD cases.