Small molecule prevents amyloid-beta-induced neurotoxicity
2014
China Medical University, Taichung, Taiwan
Accumulation of amyloid-beta in the brain is one of the hallmarks of Alzheimer's disease and, in the amyloid hypothesis, the driving factor of the disease. To try to decrease the cytotoxicity of amyloid-beta in human neuronal cells, a peroxisome proliferator-activator receptor alpha agonist (Wy14643) is used in this study. When using Wy14643 on amyloid beta-treated neuronal cells, the researchers were able to increase cell viability after only 24 hours. In this context, the protein levels of several markers of apoptosis remained unchanged except for Endo G and AIF. Immunofluorescence assays showed that Wy14643 reduced the translocation of these two factors into the nucleus, which reduced DNA damage and apoptosis induced by amyloid-beta treatment. These results show that the activation of peroxisome proliferator-activator receptor alpha prevents amyloid beta-induced DNA damage and apoptosis of human neuronal cells and the mechanisms behind it. This study proposes a new therapeutical target in a human model that can be further translated into clinical applications to treat neurotoxicity in Alzheimer's disease.
PPARα activation attenuates amyloid-β-dependent neurodegeneration by modulating Endo G and AIF translocation
Nai Wen Chang
Added on: 08-16-2021
[1] https://link.springer.com/article/10.1007%2Fs12640-014-9485-9[2] https://data.jrc.ec.europa.eu/dataset/a8fd26ef-b113-47ab-92ba-fd2be449c7eb
