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
in English
| WPRIM
| ID: wpr-1010671
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Parkinson Disease
/
Prions
/
Amyloid beta-Peptides
/
Tau Proteins
/
Neurodegenerative Diseases
/
Alpha-Synuclein
/
Alzheimer Disease
Limits:
Humans
Language:
English
Journal:
Neuroscience Bulletin
Year:
2024
Type:
Article
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