Jennifer Drake

TL;DR: Current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, are summarized, and the potential role of Abeta in this oxidative stress is discussed.

TL;DR: Results are consistent with the notion of a coupling of the oxidative environment in AD brain and increased risk of developing this disorder and strongly support a causative role of Abeta(1-42)-induced oxidative stress in AD neurodegeneration.

TL;DR: This review examines the literature of the effects of endogenous and exogenous, nutritionally-derived antioxidants in relation to AD and studies of glutathione and other SH-containing antioxidants, vitamins, and polyphenolic compounds and their use in AD and modulation of Abeta-induced oxidative stress and neurotoxicity are reviewed.

TL;DR: The increased oxidative stress in CL4176 occurred in the absence of Abeta fibril formation, consistent with the notion that the toxic species in Abeta toxicity is pre-fibrillar Abeta and not the Abetafibril.

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.