Sridhar Varadarajan

TL;DR: Significant evidence is outlined from multiidisciplinary approaches for amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity and protection against these oxidative processes and cell death by free radical scavengers and the strong evidence supporting the notion that the single methionine residue of amyloids beta- peptide is vital to the oxidative Stress and neurotoxicological properties of this peptide.

TL;DR: In vitro and in vivo models of beta-amyloid (A beta) toxicity are used to detect free radical induced oxidative stress by the measure of protein carbonyl levels, and the hypothesis that methionine is important in A beta-associated free radical oxidative stress is supported.

TL;DR: These studies reveal that two different mechanisms may be operative in the two peptides; however, the single methionine residue in the peptides appears to play a crucial role in both mechanisms.

TL;DR: It is reported that the increased protein oxidation, reactive oxygen species (ROS) formation, and neurotoxicity induced by Abeta(1-42) in primary rat embryonic hippocampal neuronal culture are prevented by the free radical scavenger and antioxidant vitamin E.

TL;DR: Investigation of damage to brain neocortical synaptosomal membrane proteins and the oxidation‐sensitive enzyme glutamine synthetase caused by exposure to ONOO shows that ONOO‐ can oxidatively modify both membranous and cytosolic proteins, affecting both their physical and chemical nature.