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Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases
Amyloids were conventionally referred to as extracellular and intracellular accumulation of Aβ42 peptide, which causes the formation of plaques and neurofibrillary tangles inside the brain leading to the pathogenesis in Alzheimer’s disease. Subsequently, amyloid-like deposition was found in the etio...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10381831/ https://www.ncbi.nlm.nih.gov/pubmed/37511898 http://dx.doi.org/10.3390/life13071523 |
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author | Naskar, Soumick Gour, Nidhi |
author_facet | Naskar, Soumick Gour, Nidhi |
author_sort | Naskar, Soumick |
collection | PubMed |
description | Amyloids were conventionally referred to as extracellular and intracellular accumulation of Aβ42 peptide, which causes the formation of plaques and neurofibrillary tangles inside the brain leading to the pathogenesis in Alzheimer’s disease. Subsequently, amyloid-like deposition was found in the etiology of prion diseases, Parkinson’s disease, type II diabetes, and cancer, which was attributed to the aggregation of prion protein, α-Synuclein, islet amyloid polypeptide protein, and p53 protein, respectively. Hence, traditionally amyloids were considered aggregates formed exclusively by proteins or peptides. However, since the last decade, it has been discovered that other metabolites, like single amino acids, nucleobases, lipids, glucose derivatives, etc., have a propensity to form amyloid-like toxic assemblies. Several studies suggest direct implications of these metabolite assemblies in the patho-physiology of various inborn errors of metabolisms like phenylketonuria, tyrosinemia, cystinuria, and Gaucher’s disease, to name a few. In this review, we present a comprehensive literature overview that suggests amyloid-like structure formation as a common phenomenon for disease progression and pathogenesis in multiple syndromes. The review is devoted to providing readers with a broad knowledge of the structure, mode of formation, propagation, and transmission of different extracellular amyloids and their implications in the pathogenesis of diseases. We strongly believe a review on this topic is urgently required to create awareness about the understanding of the fundamental molecular mechanism behind the origin of diseases from an amyloid perspective and possibly look for a common therapeutic strategy for the treatment of these maladies by designing generic amyloid inhibitors. |
format | Online Article Text |
id | pubmed-10381831 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-103818312023-07-29 Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases Naskar, Soumick Gour, Nidhi Life (Basel) Review Amyloids were conventionally referred to as extracellular and intracellular accumulation of Aβ42 peptide, which causes the formation of plaques and neurofibrillary tangles inside the brain leading to the pathogenesis in Alzheimer’s disease. Subsequently, amyloid-like deposition was found in the etiology of prion diseases, Parkinson’s disease, type II diabetes, and cancer, which was attributed to the aggregation of prion protein, α-Synuclein, islet amyloid polypeptide protein, and p53 protein, respectively. Hence, traditionally amyloids were considered aggregates formed exclusively by proteins or peptides. However, since the last decade, it has been discovered that other metabolites, like single amino acids, nucleobases, lipids, glucose derivatives, etc., have a propensity to form amyloid-like toxic assemblies. Several studies suggest direct implications of these metabolite assemblies in the patho-physiology of various inborn errors of metabolisms like phenylketonuria, tyrosinemia, cystinuria, and Gaucher’s disease, to name a few. In this review, we present a comprehensive literature overview that suggests amyloid-like structure formation as a common phenomenon for disease progression and pathogenesis in multiple syndromes. The review is devoted to providing readers with a broad knowledge of the structure, mode of formation, propagation, and transmission of different extracellular amyloids and their implications in the pathogenesis of diseases. We strongly believe a review on this topic is urgently required to create awareness about the understanding of the fundamental molecular mechanism behind the origin of diseases from an amyloid perspective and possibly look for a common therapeutic strategy for the treatment of these maladies by designing generic amyloid inhibitors. MDPI 2023-07-07 /pmc/articles/PMC10381831/ /pubmed/37511898 http://dx.doi.org/10.3390/life13071523 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Naskar, Soumick Gour, Nidhi Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title | Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title_full | Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title_fullStr | Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title_full_unstemmed | Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title_short | Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases |
title_sort | realization of amyloid-like aggregation as a common cause for pathogenesis in diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10381831/ https://www.ncbi.nlm.nih.gov/pubmed/37511898 http://dx.doi.org/10.3390/life13071523 |
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