Current Genomics

Christian Néri
Institute of Biology Paris-Seine
CNRS UMR 8256 and UPMC
Paris, 75005
France

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The Mechanistic Links Between Proteasome Activity, Aging and Agerelated Diseases

Author(s): Isabel Saez and David Vilchez

Affiliation: Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph Stelzmann Strasse, 26 50931 Cologne, Germany.

Keywords: Aging, Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, Proteasome, Proteostasis, Stem cells.

Abstract:

Damaged and misfolded proteins accumulate during the aging process, impairing cell function and tissue homeostasis. These perturbations to protein homeostasis (proteostasis) are hallmarks of age-related neurodegenerative disorders such as Alzheimer’s, Parkinson’s or Huntington’s disease. Damaged proteins are degraded by cellular clearance mechanisms such as the proteasome, a key component of the proteostasis network. Proteasome activity declines during aging, and proteasomal dysfunction is associated with late-onset disorders. Modulation of proteasome activity extends lifespan and protects organisms from symptoms associated with proteostasis disorders. Here we review the links between proteasome activity, aging and neurodegeneration. Additionally, strategies to modulate proteasome activity and delay the onset of diseases associated to proteasomal dysfunction are discussed herein.

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Article Details

VOLUME: 15
ISSUE: 1
Page: [38 - 51]
Pages: 14
DOI: 10.2174/138920291501140306113344