Protein quality control pathways at the crossroad of synucleinopathies
The pathophysiology of Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and many others converge at alpha-synuclein (alpha-Syn) aggregation. Although it is still not entirely clear what precise biophysical processes act as triggers, cumulative evidence points towards a c...
Gespeichert in:
| Hauptverfasser: | , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2 January 2020
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| In: |
Journal of Parkinson's Disease
Year: 2020, Jahrgang: 10, Heft: 2, Pages: 369-382 |
| ISSN: | 1877-718X |
| DOI: | 10.3233/JPD-191790 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.3233/JPD-191790
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| Verfasserangaben: | Eduardo P. De Mattos, Anne Wentink, Carmen Nussbaum-Krammer, Christian Hansen, Steven Bergink, Ronald Melki, Harm H. Kampinga |
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| 520 | |a The pathophysiology of Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and many others converge at alpha-synuclein (alpha-Syn) aggregation. Although it is still not entirely clear what precise biophysical processes act as triggers, cumulative evidence points towards a crucial role for protein quality control (PQC) systems in modulating alpha-Syn aggregation and toxicity. These encompass distinct cellular strategies that tightly balance protein production, stability, and degradation, ultimately regulating alpha-Syn levels. Here, we review the main aspects of alpha-Syn biology, focusing on the cellular PQC components that are at the heart of recognizing and disposing toxic, aggregate-prone alpha-Syn assemblies: molecular chaperones and the ubiquitin-proteasome system and autophagy-lysosome pathway, respectively. A deeper understanding of these basic protein homeostasis mechanisms might contribute to the development of new therapeutic strategies envisioning the prevention and/or enhanced degradation of alpha-Syn aggregates. | ||
| 650 | 4 | |a Alpha-synuclein | |
| 650 | 4 | |a autophagy | |
| 650 | 4 | |a chaperone-mediated autophagy | |
| 650 | 4 | |a fibril formation | |
| 650 | 4 | |a glial cytoplasmic inclusions | |
| 650 | 4 | |a heat-shock proteins | |
| 650 | 4 | |a impairs macroautophagy | |
| 650 | 4 | |a lysosomal degradation | |
| 650 | 4 | |a molecular chaperones | |
| 650 | 4 | |a multiple system atrophy | |
| 650 | 4 | |a mutant alpha-synuclein | |
| 650 | 4 | |a parkinsons-disease | |
| 650 | 4 | |a protein aggregation | |
| 650 | 4 | |a protein homeostasis | |
| 650 | 4 | |a synucleinopathies | |
| 650 | 4 | |a ubiquitin-proteasome system | |
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| 700 | 1 | |a Melki, Ronald |e VerfasserIn |4 aut | |
| 700 | 1 | |a Kampinga, Harm H. |e VerfasserIn |4 aut | |
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