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Related Concept Videos

Amyloid Fibrils03:03

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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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Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase
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Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

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Yeast models for amyloid disease.

Barry Panaretou1, Gary W Jones2

  • 1*Institute of Pharmaceutical Science, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, U.K.

Essays in Biochemistry
|August 19, 2014
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Summary
This summary is machine-generated.

Baker's yeast (Saccharomyces cerevisiae) serves as a powerful model for studying human diseases. Yeast genetic tools enable cost-effective screening for insights into neurodegenerative conditions like Alzheimer's.

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Area of Science:

  • * Molecular Biology
  • * Genetics
  • * Neuroscience

Background:

  • * Saccharomyces cerevisiae (baker's yeast) is a crucial eukaryotic model organism for understanding fundamental cellular processes.
  • * Its genetic and molecular resources facilitate genome-wide screening, aiding human disease pathobiology research.
  • * Yeast models are instrumental in studying complex mammalian diseases, particularly amyloid-related disorders.

Purpose of the Study:

  • * To provide an overview of human neurodegenerative diseases modeled in yeast.
  • * To highlight recent findings from genetic and drug screening studies in yeast.
  • * To emphasize the value of yeast as a model for conserved amyloid toxicity mechanisms.

Main Methods:

  • * Utilizing Saccharomyces cerevisiae as a model organism.
  • * Leveraging yeast's genetic and molecular resources for genome-wide screening.
  • * Analyzing conserved mechanisms of amyloid toxicity.

Main Results:

  • * Yeast models have been successfully developed for amyloid diseases like Alzheimer's, Parkinson's, and Huntington's.
  • * Genetic and drug screening studies in yeast have yielded significant recent findings.
  • * Conserved mechanisms of amyloid toxicity are evident despite the difference between yeast and mammals.

Conclusions:

  • * Saccharomyces cerevisiae is a valuable and versatile model for investigating human neurodegenerative diseases.
  • * Yeast-based research offers cost-effective and efficient methods for disease-related discoveries.
  • * The conserved nature of amyloid toxicity mechanisms validates yeast as a model for complex human conditions.