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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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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,...
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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.
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Related Experiment Video

Updated: Dec 30, 2025

Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays
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Recombinant α- β- and γ-Synucleins Stimulate Protein Phosphatase 2A Catalytic Subunit Activity in Cell Free Assays

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Aβ Puts the Alpha in Synuclein.

Casey Cook1, Leonard Petrucelli1

  • 1Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.

Neuron
|January 24, 2020
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Summary
This summary is machine-generated.

Alzheimer's and Parkinson's diseases involve protein buildup. A new study shows amyloid-beta plaques worsen alpha-synuclein pathology, leading to increased neurodegeneration.

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Last Updated: Dec 30, 2025

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Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation
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Area of Science:

  • Neuroscience
  • Neuropathology

Background:

  • Neurodegenerative diseases, including Alzheimer's and Parkinson's, are defined by abnormal protein deposits.
  • Amyloid-beta (Aβ) and alpha-synuclein are key proteins implicated in these conditions.

Purpose of the Study:

  • To investigate the in vivo interaction between amyloid-beta plaques and alpha-synuclein pathology.
  • To determine if comorbid protein pathologies exacerbate neurodegeneration.

Main Methods:

  • Utilized an in vivo model to study the effects of amyloid-beta plaques on alpha-synuclein aggregation.
  • Assessed the degree of neurodegeneration in the presence of combined pathologies.

Main Results:

  • Observed a significant exacerbation of alpha-synuclein pathology when amyloid-beta plaques were present.
  • Found that comorbid pathologies were associated with a greater extent of neurodegeneration.

Conclusions:

  • Co-occurrence of amyloid-beta and alpha-synuclein pathologies intensifies disease progression.
  • This interaction highlights a potential mechanism driving increased neurodegeneration in complex cases of Alzheimer's and Parkinson's disease.