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Aβ oligomers trigger and accelerate Aβ seeding.

Natalie Katzmarski1,2,3, Stephanie Ziegler-Waldkirch1,2,3, Nina Scheffler1,3

  • 1Department of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.

Brain Pathology (Zurich, Switzerland)
|May 18, 2019
PubMed
Summary
This summary is machine-generated.

Amyloid-beta (Aβ) oligomers initiate the aggregation process in Alzheimer's disease (AD) by seeding plaque formation. Depleting these oligomers temporarily reduces Aβ deposits, highlighting their crucial role in early-stage aggregation.

Keywords:
Alzheimer's diseaseAβ oligomersAβ seedingamyloid-β plaques

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaque formation.
  • Aβ aggregation involves stepwise formation of oligomers and fibrils.
  • Prion-like seeding mechanisms accelerate Aβ aggregation in vivo.

Purpose of the Study:

  • To investigate the role of Aβ oligomers in the initiation of Aβ aggregation and seeding.
  • To determine if Aβ oligomers are essential for the early phase of Aβ seeding in vivo.

Main Methods:

  • Intracerebral injection of Aβ-containing brain homogenate into human APP transgenic mice.
  • Immunoprecipitation of brain extracts using anti-Aβ oligomer antibodies.
  • Passive immunization of recipient animals to assess seeding activity.

Main Results:

  • Aβ oligomers, along with monomers, trigger the initial phase of Aβ seeding.
  • Depletion of oligomeric Aβ delays aggregation and transiently reduces seed-induced Aβ deposits.
  • While antibody treatment abrogated seeding activity, Aβ deposition was still observed.

Conclusions:

  • Aβ oligomers play a critical role in the initiation of Aβ aggregation in vivo.
  • This study extends the understanding of Aβ oligomers beyond their cytotoxic effects.
  • Aβ oligomers are crucial for the early initiation phase of the Aβ seeding process in Alzheimer's disease.