Discovery of 4-aminoindole carboxamide derivatives to curtail alpha-synuclein and tau isoform 2N4R oligomer formation

Discovery of 4-aminoindole carboxamide derivatives to curtail alpha-synuclein and tau isoform 2N4R oligomer formation
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DOI:
10.1016/j.rechem.2023.100938
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发表时间:
2023-05-05
影响因子:
2.3
通讯作者:
Fortin, Jessica S.
Fortin, Jessica S.
中科院分区:
其他
文献类型:
--
作者:
Ramirez, Eduardo;Min, Sehong;Fortin, Jessica S.

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阿尔茨海默病(AD)是一种多因素慢性神经退行性疾病,其特征在于脑中存在细胞外β-淀粉样蛋白(A β)斑块、神经元内神经元缠结(NFT)、活化的小胶质细胞和炎症状态(涉及活性氧产生)。NFT由微管结合蛋白tau的错误折叠和过度磷酸化形式组成。有趣的是,已经发现tau的2N 4 R剪接同种型的三聚体形式比神经元前体细胞中的三聚体1 N4 R同种型更具毒性。很少有药物发现计划专注于特定的tau亚型。目前的药物发现项目集中在一系列17个4-或5-氨基吲哚甲酰胺对tau的2N 4 R亚型的抗聚集作用。使用α-突触核蛋白(α-syn)进行最佳化合物的选择。新合成的氨基吲哚甲酰胺衍生物的抗寡聚体和原纤维活性进行了评价与生物物理方法,如硫磺素T荧光测定,光诱导交联的未修饰的蛋白质,和透射电子显微镜。为了评估内含物的减少和细胞保护作用,用最好的酰胺代表物处理表达形成内含物的α-syn的M17 D神经母细胞瘤细胞。4-氨基吲哚甲酰胺衍生物表现出更好的抗纤维活性相比,其5-氨基吲哚对应物。酰胺衍生物2、8和17对tau的α-syn和2N 4 R同种型发挥抗寡聚体和抗原纤维活性。在40 μ M的浓度下,化合物8减少了表达易包涵体的α-突触核蛋白3 K::YFP的M17 D神经母细胞瘤细胞中的包涵体形成。我们的研究结果证明了4氨基吲哚甲酰胺衍生物在抑制α-syn和tau(2N 4 R亚型)的寡聚体形成方面的潜力,以便在临床前研究之前进一步优化。
Alzheimer's disease (AD) is a multifactorial, chronic neurodegenerative disease characterized by the presence of extracellular beta-amyloid (A beta) plaques, intraneuronal neurofibrillary tangles (NFTs), activated microglial cells, and an inflammatory state (involving reactive oxygen species production) in the brain. NFTs are comprised of misfolded and hyperphosphorylated forms of the microtubule-binding protein tau. Interestingly, the trimeric form of the 2N4R splice isoform of tau has been found to be more toxic than the trimeric 1N4R isoform in neuron precursor cells. Few drug discovery programs have focused on specific tau isoforms. The present drug discovery project is centered on the anti-aggregation effect of a series of seventeen 4- or 5-aminoindole carboxamides on the 2N4R isoform of tau. The selection of the best compounds was performed using alpha-synuclein (alpha-syn). The antioligomer and -fibril activities of newly synthesized aminoindole carboxamide derivatives were evaluated with biophysical methods, such as thioflavin T fluorescence assays, photo-induced cross-linking of unmodified proteins, and transmission electron microscopy. To evaluate the reduction of inclusions and cytoprotective effects, M17D neuroblastoma cells expressing inclusion-forming alpha-syn were treated with the best amide representatives. The 4-aminoindole carboxamide derivatives exhibited a better anti-fibrillar activity compared to their 5-aminoindole counterparts. The amide derivatives 2, 8, and 17 exerted anti-oligomer and anti-fibril activities on alpha-syn and the 2N4R isoform of tau. At a concentration of 40 mu M, compound 8 reduced inclusion formation in M17D neuroblastoma cells expressing inclusion-prone alpha Synuclein3K::YFP. Our results demonstrate the potential of 4aminoindole carboxamide derivatives with regard to inhibiting the oligomer formation of alpha-syn and tau (2N4R isoform) for further optimization prior to pre-clinical studies.