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Rapid Generation of Amyloid from Native Proteins In vitro
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Age-Dependent Protein Aggregation Initiates Amyloid-β Aggregation.

Nicole Groh1,2, Anika Bühler3, Chaolie Huang1

  • 1Protein Aggregation and Aging, German Center for Neurodegenerative DiseasesTübingen, Germany.

Frontiers in Aging Neuroscience
|June 2, 2017
PubMed
Summary

Aging causes widespread protein aggregation, which can initiate amyloid-β aggregation in neurodegenerative diseases like Alzheimer's. Middle-age protein changes are key triggers for this pathological seeding.

Keywords:
C. elegans agingaging neuroscienceamyloid-βheterologous seedingmouse brainprotein aggregation

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Aging Research

Background:

  • Aging is the primary risk factor for neurodegenerative diseases, characterized by pathological protein aggregation.
  • Widespread protein aggregation occurs during aging, even without disease, but its role in disease initiation is unclear.
  • Some age-associated aggregation-prone proteins are found in hallmark disease aggregates, suggesting potential cross-seeding.

Purpose of the Study:

  • To investigate whether age-dependent protein aggregation can initiate amyloid-β (Aβ) aggregation.
  • To identify the specific age periods and proteins involved in initiating Aβ aggregation.

Main Methods:

  • In vitro experiments using insoluble proteins from aged and young *Caenorhabditis elegans* and mouse brains.
  • Testing the seeding potential of protein aggregates formed at different adult ages in *C. elegans*.
  • Mass spectrometry to identify proteins in age-associated aggregates.

Main Results:

  • Highly insoluble proteins from aged, but not young, individuals initiated Aβ aggregation in vitro.
  • Protein aggregates from early aging stages did not seed Aβ aggregation; middle-age aggregates did.
  • Mass spectrometry identified proteins like 14-3-3, Ubiquitin-like modifier-activating enzyme 1, and Lamin A/C as potential cross-seeders.

Conclusions:

  • Age-dependent protein aggregation, particularly from middle age, can initiate pathological protein aggregation, contributing to neurodegeneration.
  • Specific proteins accumulating with age may act as seeds for hallmark aggregates like amyloid-β plaques.
  • Targeting age-related protein misfolding and aggregation may offer therapeutic strategies for neurodegenerative diseases.