Inhibition of α-synuclein aggregation and mature fibril disassembling with a minimalistic compound, ZPDm

Synucleinopathies are a group of disorders characterized by the accumulation of α-Synuclein amyloid inclusions in the brain. Preventing α-Synuclein aggregation is challenging because of the disordered nature of the protein and the stochastic nature of fibrillogenesis, but, at the same time, it is a...

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Authors: Peña Díaz, Samuel|||0000-0002-2902-823X, Pujols Pujol, Jordi|||0000-0001-9424-5866, Garcia de Carvalho Pinheiro, Francisca|||0000-0003-3778-1528, Santos Suárez, Jaime|||0000-0001-9045-7765, Pallarès i Goitiz, Irantzu|||0000-0002-8205-2060, Navarro, Susanna|||0000-0001-8160-9536, Conde Giménez, María|||0000-0003-4358-9110, García, Jesús, Salvatella, Xavier|||0000-0002-8371-4185, Dalfo, Esther|||0000-0003-4677-8515, Sancho Sanz, Javier|||0000-0002-2879-9200, Ventura, Salvador|||0000-0002-9652-6351
Format: article
Publication Date:2020
Country:España
Institution:Universitat Autònoma de Barcelona
Repository:Dipòsit Digital de Documents de la UAB
Language:English
OAI Identifier:oai:ddd.uab.cat:234673
Online Access:https://ddd.uab.cat/record/234673
https://dx.doi.org/urn:doi:10.3389/fbioe.2020.588947
Access Level:Open access
Keyword:α-synuclein
Protein aggregation
Amyloid inhibitor
Parkinson's disease
Synucleinopathies
Small molecules
Description
Summary:Synucleinopathies are a group of disorders characterized by the accumulation of α-Synuclein amyloid inclusions in the brain. Preventing α-Synuclein aggregation is challenging because of the disordered nature of the protein and the stochastic nature of fibrillogenesis, but, at the same time, it is a promising approach for therapeutic intervention in these pathologies. A high-throughput screening initiative allowed us to discover ZPDm, the smallest active molecule in a library of more than 14.000 compounds. Although the ZPDm structure is highly related to that of the previously described ZPD-2 aggregation inhibitor, we show here that their mechanisms of action are entirely different. ZPDm inhibits the aggregation of wild-type, A30P, and H50Q α-Synuclein variants in vitro and interferes with α-Synuclein seeded aggregation in protein misfolding cyclic amplification assays. However, ZPDm distinctive feature is its strong potency to dismantle preformed α-Synuclein amyloid fibrils. Studies in a Caenorhabditis elegans model of Parkinson's Disease, prove that these in vitro properties are translated into a significant reduction in the accumulation of α-Synuclein inclusions in ZPDm treated animals. Together with previous data, the present work illustrates how different chemical groups on top of a common molecular scaffold can result in divergent but complementary anti-amyloid activities.