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Related Concept Videos

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. 
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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...
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Updated: Jun 8, 2026

Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils
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Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils

Published on: April 13, 2017

Are synucleinopathies prion-like disorders?

Elodie Angot1, Jennifer A Steiner, Christian Hansen

  • 1Wallenberg Neuroscience Centre, Lund University, Sweden.

The Lancet. Neurology
|September 18, 2010
PubMed
Summary
This summary is machine-generated.

Misfolded alpha-synuclein (α-synuclein) aggregates may spread between brain cells, similar to prion diseases. Preventing this cell-to-cell transfer could slow the progression of Parkinson's disease and other synucleinopathies.

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Last Updated: Jun 8, 2026

Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils
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Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans

Published on: January 8, 2015

Area of Science:

  • Neuroscience
  • Neuropathology
  • Neurodegenerative Diseases

Background:

  • Idiopathic Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy share α-synuclein aggregation.
  • Pathogenesis of these synucleinopathies remains largely unknown.
  • Similarities exist between prion diseases and neurological proteinopathies.

Purpose of the Study:

  • To review experimental evidence supporting a prion-like mechanism for α-synuclein propagation.
  • To explore the potential of targeting cell-to-cell transfer for therapeutic intervention.

Main Methods:

  • Review of experimental findings on α-synuclein cell-to-cell transfer.
  • Analysis of studies investigating Lewy body formation in transplanted neurons.

Main Results:

  • Misfolded α-synuclein can transfer between cells.
  • Transferred α-synuclein seeds endogenous protein aggregation.
  • Evidence suggests a prion-like mechanism for synucleinopathy progression.

Conclusions:

  • α-synuclein propagation may occur via cell-to-cell transmission.
  • Therapeutic strategies preventing α-synuclein transfer are promising.
  • Interfering with cell-to-cell spread could mitigate Parkinson's disease symptoms.