Version 1
: Received: 7 December 2023 / Approved: 8 December 2023 / Online: 8 December 2023 (07:47:36 CET)
How to cite:
Johnson, A.B.; Modi, N.; Kamath, K.N.; Rajeshkumar, R.; Palanimuthu, V.R. Alpha-Synuclein Aggregation and Spread: Implications for the Pathology and Progression of Neurodegenerative Diseases. Preprints2023, 2023120569. https://doi.org/10.20944/preprints202312.0569.v1
Johnson, A.B.; Modi, N.; Kamath, K.N.; Rajeshkumar, R.; Palanimuthu, V.R. Alpha-Synuclein Aggregation and Spread: Implications for the Pathology and Progression of Neurodegenerative Diseases. Preprints 2023, 2023120569. https://doi.org/10.20944/preprints202312.0569.v1
Johnson, A.B.; Modi, N.; Kamath, K.N.; Rajeshkumar, R.; Palanimuthu, V.R. Alpha-Synuclein Aggregation and Spread: Implications for the Pathology and Progression of Neurodegenerative Diseases. Preprints2023, 2023120569. https://doi.org/10.20944/preprints202312.0569.v1
APA Style
Johnson, A.B., Modi, N., Kamath, K.N., Rajeshkumar, R., & Palanimuthu, V.R. (2023). Alpha-Synuclein Aggregation and Spread: Implications for the Pathology and Progression of Neurodegenerative Diseases. Preprints. https://doi.org/10.20944/preprints202312.0569.v1
Chicago/Turabian Style
Johnson, A.B., Raman Rajeshkumar and Vasanth Raj Palanimuthu. 2023 "Alpha-Synuclein Aggregation and Spread: Implications for the Pathology and Progression of Neurodegenerative Diseases" Preprints. https://doi.org/10.20944/preprints202312.0569.v1
Abstract
Neurodegenerative diseases, including Alzheimer's, Huntington's, Parkinson’s, and Amyotrophic Lateral Sclerosis, involve neuron degeneration linked to the misfolding of amyloidogenic proteins, resulting in β-sheet-enriched aggregates. This phenomenon disrupts the normal folding of proteins critical for cellular function. Genetic mutations, proteolytic cleavage, oxidative stress, and aging contribute to misfolding. Parkinson's disease (PD) is closely tied to alpha-synuclein (αS) misfolding, with A53T mutation and Lewy bodies (LB) in PD brains pivotal to understanding the disease mechanism. Other synuclein homologues (βS, γS) further contribute to synucleinopathies. Mutants (A30P, A53T, E46K, H50Q, and G51D) underscore αS's role in PD development. This concise review focuses on molecular and pathological aspects of neurodegenerative diseases, emphasizing αS in PD. The integration of genetic, structural, and mechanistic insights highlights the disorders. complexity, paving the way for future therapeutic strategies targeting protein misfolding and aggregation.
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.
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