Breaking the Balance: Cellular Stress, Proteostasis, Aggregates and Neurodegeneration
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 25 September 2026 | Viewed by 1051
Editor
Special Issue Information
Dear Colleagues,
Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease are characterized by progressive neuronal dysfunction and loss, often associated with the accumulation of misfolded proteins and intracellular aggregates. At the heart of these conditions lies a fundamental breakdown in cellular proteostasis—the ability of cells to maintain a functional proteome through finely tuned networks of protein synthesis, folding, trafficking, and degradation. Cellular stress, whether due to aging, oxidative damage, metabolic dysfunction, or environmental factors, places an increasing burden on these proteostasis mechanisms. As these systems fail, toxic aggregates form, triggering inflammation, impairing organelle function, and disrupting neural connectivity. This Special Issue will explore how various forms of cellular stress compromise proteostasis and drive the formation of protein aggregates in the nervous system. We welcome contributions investigating molecular mechanisms, stress–response pathways, protein quality control systems, and emerging therapeutic approaches for restoring proteostasis or preventing aggregate toxicity. Studies using in vitro models, in vivo systems, or human patient data are all encouraged. By bringing together diverse perspectives on the collapse of proteostasis and its link to neurodegeneration, we will highlight shared mechanisms and novel insights that could inform future interventions.
Dr. Zhaoyu Li
Guest Editor
Manuscript Submission Information
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Keywords
- proteostasis
- cellular stress
- protein aggregation
- neurodegeneration
- autophagy
- unfolded protein response
- oxidative stress
- aging
- molecular chaperones
- protein quality control
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