Amyloid-beta neurotoxicity mechanisms tested in vitro
October 2017
Tallinn University of Technology, Tallinn, Estonia
Several studies support that Alzheimer's disease onset is related to the accumulation of amyloid-beta in the brain. However, the mechanisms by which amyloid aggregates lead to neuronal degeneration are still unknown. Here, a human neuroblastoma cell line is used to study the cytotoxicity of amyloid-beta peptides. Comparing differentiated and non-differentiated cells, the researchers show that the first are more sensitive to amyloid peptides, due to having longer neurites. Soluble amyloid-beta 1-42 is shown to cover cell bodies and neurites in differentiated cells, causing neurite degeneration. When using preformed amyloid fibrils, it was not possible to reproduce the toxicity of the peptide, which was complemented with the fact that spontaneously fibrillizing amyloid-beta 1-42 was more toxic than amyloid-beta 1-40, which did not form fibrils. The results elucidate important aspects of amyloid aggregates-induced neurotoxicity that could help to better understand the pathophysiology of Alzheimer's disease.
In situ fibrillizing amyloid-beta 1-42 induces neurite degeneration and apoptosis of differentiated SH-SY5Y cells
Jekaterina Krishtal
Added on: 08-17-2021
[1] https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0186636[2] https://data.jrc.ec.europa.eu/dataset/a8fd26ef-b113-47ab-92ba-fd2be449c7eb
