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Biomolecular Corona Dictates Aβ Fibrillation Process.

Alireza Lotfabadi, Mohammad Javad Hajipour1,2, Hossein Derakhshankhah3

  • 1Persian Gulf Marine Biotechnology Research Center, The Persian Gulf Biomedical Sciences Research Institute , Bushehr University of Medical Sciences , Bushehr 75147 , Iran.

ACS Chemical Neuroscience
|April 21, 2018
PubMed
Summary

The biomolecular corona on nanoparticles significantly impacts amyloid beta (Aβ) fibrillation. Nanoparticles coated with plasma or cerebrospinal fluid (CSF) biomolecular coronas show varied effects on Aβ1-42 and Aβ25-35 peptide aggregation.

Keywords:
Amyloid betaBiomolecular coronaCerebrospinal fluidFibrillationGold nanospheres/nanorods

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Area of Science:

  • Biomaterials Science
  • Neuroscience
  • Nanotechnology

Background:

  • Amyloid beta (Aβ) aggregation into toxic oligomers and fibrils is central to Alzheimer's disease pathology.
  • Nanoparticles (NPs) are investigated for their potential to modulate Aβ fibrillation.
  • The influence of the biomolecular corona, formed on NPs in biological fluids, on Aβ fibrillogenesis is often overlooked.

Purpose of the Study:

  • To investigate the impact of biomolecular coronas from human cerebrospinal fluid (CSF) and plasma on amyloid beta (Aβ) fibrillation.
  • To understand how corona composition affects the antifibrillation efficacy of therapeutic nanoparticles.

Main Methods:

  • Studied the fibrillation of Aβ1-42 and Aβ25-35 peptides in the presence of pristine and biomolecular corona-coated gold nanoparticles (NPs).
  • Utilized biomolecular coronas derived from human CSF and plasma.
  • Compared the fibrillation kinetics of Aβ peptides with different NP surface conditions (pristine, CSF-corona, plasma-corona).

Main Results:

  • The type of biomolecular corona dictates whether NPs inhibit or accelerate Aβ fibrillation.
  • Plasma corona-coated gold NPs exhibited less inhibition on Aβ1-42 fibrillation compared to CSF-corona and pristine NPs.
  • Pristine NPs accelerated Aβ25-35 fibrillation, while corona-coated NPs inhibited it, with CSF corona showing less inhibition than plasma corona.

Conclusions:

  • The biomolecular corona on NPs plays a crucial role in modulating Aβ fibrillation, influencing the therapeutic potential of NPs.
  • Understanding corona-NP-Aβ interactions is essential for designing effective nanoparticle-based therapies for Alzheimer's disease.
  • Different biological fluids (plasma vs. CSF) yield distinct coronas that differentially affect Aβ aggregation pathways.