Abstract
All cells count on precise mechanisms that regulate protein homeostasis to maintain a stable and functional proteome. Alterations in these fine-tuned mechanisms underlie the pathogenesis of severe human diseases including, among others, common neurodegenerative disorders such as Alzheimer's or Parkinson's disease. A progressive deterioration in the ability of cells to preserve the stability of their proteome occurs with age, even in the absence of disease, and it likely contributes to different aspects of "normal" aging. A group of experts in different aspects of the biology of aging met recently to discuss the implications of altered protein homeostasis in aging, the current gaps in our understanding of the mechanisms responsible for proteome maintenance, and future opportunities for discovery in this area. We summarize here some of the key topics and main outcomes of the discussions.
MeSH Terms
Adult
Age Factors
Aged
Aged, 80 and over
Aging/physiology
Alzheimer Disease/physiopathology
Cellular Senescence/physiology
Homeostasis/physiology
Humans
Longevity/physiology
Neurodegenerative Diseases/metabolism
Oxidative Stress/physiology
Parkinson Disease/physiopathology
Proteasome Endopeptidase Complex/metabolism
Protein Folding
Proteins/metabolism
Risk Factors
Chemicals
Proteins
Proteasome Endopeptidase Complex
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Morimoto Richard I
Department of Developmental and Molecular Biology, Institute for Aging Studies, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Cuervo Ana M
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