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Pathways of cellular proteostasis in aging and disease
Courtney L Klaips1, Gopal Gunanathan Jayaraj2, F Ulrich Hartl3
1Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany klaips@biochem.mpg.de.
The Journal of Cell Biology
|November 12, 2017
Summary
Cellular proteostasis (protein homeostasis) declines with age, increasing susceptibility to neurodegenerative diseases like Alzheimer's. Strategies to boost proteostasis may offer new therapies for age-related pathologies.
Area of Science:
- Cellular Biology
- Neuroscience
- Aging Research
Background:
- Cellular protein homeostasis (proteostasis) is crucial for cell function, involving synthesis, folding, and degradation.
- Molecular chaperones and regulators form a network essential for maintaining proteostasis.
- Misfolding and aggregation are hallmarks of age-associated proteinopathies, including neurodegenerative disorders.
Purpose of the Study:
- To review major proteostasis pathways in the context of aging.
- To explore the link between age-dependent proteostasis failure and disease.
- To discuss therapeutic strategies targeting proteostasis for neurodegenerative diseases.
Main Methods:
- Literature review of recent research on proteostasis pathways.
- Analysis of the role of aging in proteostasis network function.
- Discussion of therapeutic interventions for age-dependent pathologies.
Main Results:
- Proteostasis capacity declines significantly during aging.
- This decline contributes to and results from age-associated diseases.
- Dysregulation of proteostasis pathways is implicated in neurodegeneration.
Conclusions:
- Age-dependent failure of proteostasis is a key factor in developing neurodegenerative diseases.
- Modulating proteostasis offers a promising therapeutic avenue for age-related pathologies.
- Targeting proteostasis pathways may lead to urgently needed treatments for neurodegeneration.
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