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About the Authors:
Wayne Chadwick
Contributed equally to this work with: Wayne Chadwick, Bronwen Martin
Affiliation: Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Bronwen Martin
Contributed equally to this work with: Wayne Chadwick, Bronwen Martin
Affiliation: Metabolism Unit, Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Megan C. Chapter
Affiliation: Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Sung-Soo Park
Affiliation: Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Liyun Wang
Affiliation: Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Caitlin M. Daimon
Affiliation: Metabolism Unit, Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Randall Brenneman
Affiliation: Dodson Interdisciplinary Immunotherapy Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States of America
Stuart Maudsley
* E-mail: [email protected]
Affiliation: Receptor Pharmacology Unit, Laboratory of Neuroscience, National Institute on Aging, National Institutes of Health, Biomedical Research Center, Baltimore, Maryland, United States of America
Introduction
The aging process is associated with an accumulation of molecular perturbations and potential damage to the body's cells, tissues, and organs. These alterations affect multiple processes related to cell survival, genomic instability, altered gene expression patterns, aberrant cellular replication, oxidative damage by reactive oxygen species (ROS), and fluctuations in protein expression and coherent protein post-translational modification [1]. Therefore, with old age and a reduced ability to cope with stress, the body becomes more prone to a variety of pathophysiologies such as neurodegeneration and metabolic syndrome. These accumulated and progressive changes in complex physiological systems such as the endocrine or central nervous system (CNS) are highly likely to be mediated by entire networks of genes and proteins rather than just one single factor. Considerable evidence suggests that both neurodegenerative diseases and pathophysiological aging processes involve a functional interplay between a series of diverse biological systems...