Phosphorylation of Amyloid Beta Peptides and Alzheimer's Disease
Author Information
Author(s): Kumar Sathish, Walter Jochen
Primary Institution: University of Bonn
Hypothesis
Phosphorylation of amyloid beta (Aβ) peptides may trigger the formation of toxic aggregates in Alzheimer's disease.
Conclusion
Phosphorylation of Aβ promotes the formation of toxic aggregates that could play a significant role in the pathogenesis of Alzheimer's disease.
Supporting Evidence
- Phosphorylated Aβ was detected in the brains of transgenic mice and human AD brains.
- Phosphorylation of Aβ increased its toxicity in Drosophila models compared to non-phosphorylated Aβ.
- Phosphorylation promotes the formation of oligomeric Aβ aggregates that serve as nuclei for fibrillization.
Takeaway
When certain proteins in the brain get a chemical tag called phosphorylation, they can clump together and become harmful, which might be a big part of what causes Alzheimer's disease.
Methodology
The study involved in vitro and in vivo experiments using transgenic Drosophila models to assess the effects of Aβ phosphorylation on toxicity and aggregation.
Limitations
The study primarily focuses on the role of phosphorylation without exploring other potential factors influencing Aβ aggregation.
Digital Object Identifier (DOI)
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