Astrocytic proteostasis in the tale of aging and neurodegeneration.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Country of Publication: England NLM ID: 101128963 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-9649 (Electronic) Linking ISSN: 15681637 NLM ISO Abbreviation: Ageing Res Rev Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford, UK : Elsevier Science, c2002-
    • Subject Terms:
    • Abstract:
      Homeostasis of proteins (proteostasis), which governs protein processing, folding, quality control, and degradation, is a fundamental cellular process that plays a pivotal role in various neurodegenerative diseases and in the natural aging process of the mammalian brain. While the role of neuronal proteostasis in neuronal physiology is well characterized, the contribution of proteostasis of glial cells, particularly of astrocytes, has received fairly less attention in this context. Here, we summarize recent data highlighting proteostasis dysfunction in astrocytes and its putative implication to neurodegenerative diseases and aging. We discuss how distinct proteostasis nodes and pathways in astrocytes may specifically contribute to brain function and different age-associated pathologies. Finally, we argue that the understanding of astrocytic proteostasis role in neuronal physiology and functional decay may arise as a potential new avenue of intervention in neurodegenerative diseases and grant relevant data in the biology of aging.
      Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest with respect to the content of the manuscript, authorship, and/or publication of this article.
      (Copyright © 2024 Elsevier B.V. All rights reserved.)
    • Contributed Indexing:
      Keywords: Astrocyte; aging; neurodegenerative disease; protein folding; proteostasis
    • Publication Date:
      Date Created: 20241118 Date Completed: 20241211 Latest Revision: 20241217
    • Publication Date:
      20241217
    • Accession Number:
      10.1016/j.arr.2024.102580
    • Accession Number:
      39557299