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Realization of Amyloid like Aggregation as a Common Cause for the Pathogenesis in Diseases
Version 1
: Received: 22 May 2023 / Approved: 23 May 2023 / Online: 23 May 2023 (03:35:10 CEST)
A peer-reviewed article of this Preprint also exists.
Naskar, S.; Gour, N. Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases. Life 2023, 13, 1523. Naskar, S.; Gour, N. Realization of Amyloid-like Aggregation as a Common Cause for Pathogenesis in Diseases. Life 2023, 13, 1523.
Abstract
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 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 as aggregates formed by the proteins or peptides exclusively. However, since the last decade it has been discovered that other metabolites like single amino acids, nucleobases, lipids, glucose derivatives etc. have 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 which suggests amyloid-like structure formation as a common phenomenon for the disease progression and pathogenesis in multiple syndromes. The review on this topic is urgently required to create awareness about the understanding of 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.
Keywords
Amyloid; Aggregation; Self-assembly; Gene mutation; Disease Pathogenesis; Inborn errors of metabolism
Subject
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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