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- W2082202421 abstract "The progressive loss of functional capacity within the immune system, termed “immunosenescence,” is associated with the pathogenesis of age-related diseases including neurodegenerative, cardiovascular, and muscular/skeletal disorders, and leads to a greater susceptibility to infections, tumors and possibly cancer. Recent studies associate immunosenescence with Alzheimer's disease (AD) and propose that it may be a key contributor to AD pathogenesis. Oxidative stress, which is a pathological hallmark of AD, may also play a role in immunosenescence however, the exact mechanisms governing this phenomenon are not understood. The work presented herein employs a mouse model to investigate the molecular pathways associated with declines in the immune functions in AD. An initial survey of changes in the following oxidative stress markers has been measured in spleens isolated from AD animals and age-matched controls: protein carbonyls and 3-nitrotyrosine bound proteins, which are markers of protein oxidation, and 4-hydroxy-2-trans-nonenal bound proteins, which is a marker for lipid peroxidation. Extracted proteins were derivatized with a fluorescent hydroxylamine label prior to two-dimensional isoelectric focusing/sodium dodecyl sulfate polyacrylamide gel electrophoresis (IEF/SDS PAGE) mass spectrometry (MS) analysis in order to detect individual proteins that have been oxidized through protein carbonyls. Image analysis software was used to identify protein spots that display significant changes in expression and/or oxidative modification. These spots were excised, digested with trypsin and subjected to mass spectrometry and database searching analyses for protein identification. The measurements described above determined if significant increases in protein oxidation correlated with age-related decreases in the immune functions of these animals. In addition, specific protein pathways that are associated with premature immunosenescence in AD and immune-related oxidative stress are revealed. Overall, preliminary results obtained from these analyses will be presented as well as potential protein pathways associated with immunosenescence in AD. These studies may provide insights into the pathogenesis of premature immunosenescence in AD that may lead to potential preventative treatment of immunosenescence and/or AD. This work was supported in part by NIH (NIA) grants to D.A.B. and by the Lyman T. Johnson Postdoctoral Fellowship Program of the University of Kentucky." @default.
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- W2082202421 date "2008-07-01" @default.
- W2082202421 modified "2023-09-27" @default.
- W2082202421 title "P4-177: Assessing immune-related oxidative stress and proteomics in a mouse model of Alzheimer's disease" @default.
- W2082202421 doi "https://doi.org/10.1016/j.jalz.2008.05.2244" @default.
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