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The Butterfield laboratory studies free radical oxidative stress in aging and age-related neurodegenerative disorders, particularly Alzheimer's disease (AD). We discovered in AD brain that such oxidative stress is manifested by protein oxidation, lipid peroxidation, reactive oxygen species (ROS) production, mitochondrial dysfunction, and functional impairment of key transmembrane transport proteins, among many others. Our laboratory studies these and other aspects of oxidative stress in brain membranes using a variety of techniques, including immunochemical, metabolomic, and proteomics methods. Our group first described how oxidative stress associated with amyloid β-peptide, a 42-amino acid peptide deposited in AD brains, leads to neurotoxicity and how various antioxidants can modulate or prevent this oxidative stress and neuronal death. Insight into the molecular basis for and potential therapeutic interventions in aging and age-related neurodegenerative disorders is envisaged from our research. Recent research has emphasized the close connection between Type 2 diabetes mellitus and development of AD. We found that brain from subjects with AD and for the first time in arguably AD’s earlier form, Mild Cognitive Impairment (MCI), strong evidence of insulin resistance, which contributes to the metabolic changes in brain well known in AD.
Our laboratory pioneered the techniques of redox proteomics (see figure below) to identify oxidatively modified brain proteins in subjects with AD and MCI. Proteins identified have provided new insights into molecular processes involved in mechanisms of neuronal death in and progression of AD.
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Physiological reviewsno. 1 (2024): 103-197
Luksana Chaiswing,D. Allan Butterfield,Nicole Rummel,Daret St. Clair,Weixiong Zhong, Kristy Meyer,Mohammad Dehghan Banadaki, Spencer Backus, James Campbell,Scott Berry
Free radical biology & medicine (2022): 1-13
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