When added in cell culture, solubilized AFA-HS lost neither its scavenging ability against ROS generation nor its protective role against Abeta, the main peptide involved in Alzheimer's disease.
Here, we use lymphoblastoid cell lines (LCLs) from AD patients and HCs to investigate the role of resveratrol (RV) and selenium (Se) in the reduction of reactive oxygen species (ROS) generated after an oxidative injury.
This review presents current knowledge about the oxidative stress-induced impairments and compromised oxidative stress defense mechanisms in AD brain and the cross-talk between various pathophysiological insults, with the focus on excessive reactive oxygen species (ROS) generation and A<i>β</i> overproduction at the early stages of the disease.
Our findings show that lysosomal ROS generation by toxic conformer of Aβ led to cell death via LMP, and suggest that these events are potential targets for AD prevention.Key words: Amyloid-beta (Aβ), Cell death, Lysosome, Lysosomal membrane permeabilization, Reactive oxygen species (ROS).
Considering its recognized major genetic risk factors in AD, apolipoprotein (APO E) has been investigated in several experimental settings regarding its role in the process of reactive oxygen species (ROS) generation.
Taken together, the results of the present study indicate that the differential toxicity of Abeta peptides containing reduced or oxidised Met-35 depends on the ability of the latter form to reduce ROS generation by enhancing MsrA gene expression and function and suggests the therapeutic potential of MsrA in Alzheimer's disease.
These results suggest that NAC fibrils increase mitochondrial ROS generation and activate NF-kappaB, thereby causing a differential change in gene expression between neurons and astrocytes in the AD brain.