Andreu Matamoros-Angles

Postdoc fellow- Marie Skłodowska-Curie Action



Institute of Neuropathology

University Medical Center Hamburg-Eppendorf (UKE)

Campus Forschung - N27
Room 02.003
Martinistraße 52, 20246
Hamburg. Germany



Comment on "Extracellular Vesicles Slow Down Aβ(1-42) Aggregation by Interfering with the Amyloid Fibril Elongation Step".


Journal article


Mohsin Shafiq, A. Matamoros-Angles, Susanne Caroline Meister, M. Glatzel
ACS Chemical Neuroscience, 2024


Cite

Cite

APA   Click to copy
Shafiq, M., Matamoros-Angles, A., Meister, S. C., & Glatzel, M. (2024). Comment on "Extracellular Vesicles Slow Down Aβ(1-42) Aggregation by Interfering with the Amyloid Fibril Elongation Step". ACS Chemical Neuroscience. https://doi.org/10.1021/acschemneuro.4c00601


Chicago/Turabian   Click to copy
Shafiq, Mohsin, A. Matamoros-Angles, Susanne Caroline Meister, and M. Glatzel. “Comment on &Quot;Extracellular Vesicles Slow Down Aβ(1-42) Aggregation by Interfering with the Amyloid Fibril Elongation Step&Quot;.” ACS Chemical Neuroscience (2024).


MLA   Click to copy
Shafiq, Mohsin, et al. “Comment on &Quot;Extracellular Vesicles Slow Down Aβ(1-42) Aggregation by Interfering with the Amyloid Fibril Elongation Step&Quot;.” ACS Chemical Neuroscience, 2024, doi:10.1021/acschemneuro.4c00601.


BibTeX   Click to copy

@article{mohsin2024a,
  title = {Comment on "Extracellular Vesicles Slow Down Aβ(1-42) Aggregation by Interfering with the Amyloid Fibril Elongation Step".},
  year = {2024},
  journal = {ACS Chemical Neuroscience},
  doi = {10.1021/acschemneuro.4c00601},
  author = {Shafiq, Mohsin and Matamoros-Angles, A. and Meister, Susanne Caroline and Glatzel, M.}
}

Abstract

Halipi et al. explored the impact of extracellular vesicles (EVs) on amyloid-β (Aβ) aggregation. They concluded that EVs reduce Aβ aggregation, as seen by shorter and thicker fibrils. While we agree with the complex role of EVs in Alzheimer's disease, we are sceptical of the claim that EVs slow down Aβ aggregation, noting missing key references. Previous literature rather suggests that EVs (derived from neuronal cell lines) accelerate the process of Aβ fibrillation and plaque formation. Halipi et al.'s findings may be skewed due to the lack of essential neuronally expressed Aβ-binding partners, like the prion protein (PrPC) in their EV samples. The commentary, in the light of included original experiments and cited literature, suggests that membrane proteins like PrPC are crucial to fully understand the role of EVs in Aβ aggregation, and Halipi et al.'s conclusions should be reexamined in light of these factors.


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