Version 1
: Received: 15 August 2023 / Approved: 15 August 2023 / Online: 16 August 2023 (11:37:48 CEST)
Version 2
: Received: 17 December 2023 / Approved: 18 December 2023 / Online: 19 December 2023 (09:42:02 CET)
How to cite:
Christensen, C.S.; Li, W.; Yu, D.; Li, H.J. Structural Variations of Prions and Prion-Like Proteins Associated with Neurodegeneration. Preprints2023, 2023081162. https://doi.org/10.20944/preprints202308.1162.v2
Christensen, C.S.; Li, W.; Yu, D.; Li, H.J. Structural Variations of Prions and Prion-Like Proteins Associated with Neurodegeneration. Preprints 2023, 2023081162. https://doi.org/10.20944/preprints202308.1162.v2
Christensen, C.S.; Li, W.; Yu, D.; Li, H.J. Structural Variations of Prions and Prion-Like Proteins Associated with Neurodegeneration. Preprints2023, 2023081162. https://doi.org/10.20944/preprints202308.1162.v2
APA Style
Christensen, C.S., Li, W., Yu, D., & Li, H.J. (2023). Structural Variations of Prions and Prion-Like Proteins Associated with Neurodegeneration. Preprints. https://doi.org/10.20944/preprints202308.1162.v2
Chicago/Turabian Style
Christensen, C.S., Danyang Yu and Henry James Li. 2023 "Structural Variations of Prions and Prion-Like Proteins Associated with Neurodegeneration" Preprints. https://doi.org/10.20944/preprints202308.1162.v2
Abstract
Neurodegeneration is becoming one of the leading causes of death worldwide as the population expands and grows older. There is a growing desire to understand the mechanisms behind prion proteins as well as the prion-like proteins that make up neurodegenerative diseases (NDs) including Alzheimer’s Disease (AD). Both amyloid β (Aβ) and hyperphosphorylated tau (p-tau) proteins behave in ways similar to that of the infectious form of the prion protein, PrPSc, such as aggregating, seeding, and replicating under not yet fully understood mechanisms, thus the designation of prion-like. This review aims to highlight the shared mechanisms between prion-like proteins and prion proteins in the structural variations associated with aggregation and disease development. These mechanisms are largely focusing on the dysregulation of protein homeostasis, self-replication, and protein aggregation, and how this knowledge could contribute to diagnoses and treatments for the given NDs.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
