Decoding the Cellular Trafficking of Prion-like Proteins in Neurodegenerative Diseases / 神经科学通报·英文版
Neuroscience Bulletin
; (6): 241-254, 2024.
Article
em En
| WPRIM
| ID: wpr-1010671
Biblioteca responsável:
WPRO
ABSTRACT
The accumulation and spread of prion-like proteins is a key feature of neurodegenerative diseases (NDs) such as Alzheimer's disease, Parkinson's disease, or Amyotrophic Lateral Sclerosis. In a process known as 'seeding', prion-like proteins such as amyloid beta, microtubule-associated protein tau, α-synuclein, silence superoxide dismutase 1, or transactive response DNA-binding protein 43 kDa, propagate their misfolded conformations by transforming their respective soluble monomers into fibrils. Cellular and molecular evidence of prion-like propagation in NDs, the clinical relevance of their 'seeding' capacities, and their levels of contribution towards disease progression have been intensively studied over recent years. This review unpacks the cyclic prion-like propagation in cells including factors of aggregate internalization, endo-lysosomal leaking, aggregate degradation, and secretion. Debates on the importance of the role of prion-like protein aggregates in NDs, whether causal or consequent, are also discussed. Applications lead to a greater understanding of ND pathogenesis and increased potential for therapeutic strategies.
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Texto completo:
1
Índice:
WPRIM
Assunto principal:
Doença de Parkinson
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Príons
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Peptídeos beta-Amiloides
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Proteínas tau
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Doenças Neurodegenerativas
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Alfa-Sinucleína
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Doença de Alzheimer
Limite:
Humans
Idioma:
En
Revista:
Neuroscience Bulletin
Ano de publicação:
2024
Tipo de documento:
Article