Parkinson’s disease is the second most common neurodegenerative disease characterized by the loss of dopaminergic neurons in the brain. Parkinson’s disease has both familial and sporadic cases of origin governed differentially by genetic and/or environmental factors. Different epidemiological studies have proposed an association between the pathogenesis of cancer and Parkinson’s disease; however, a precise correlation between these two illnesses could not be established yet. In this study, we examined the disease-modifying property of (a homolog of human proto-oncogene) in the paraquat-induced sporadic Parkinson’s disease model of . We report for the first time that targeted upregulation of dMyc significantly restricts paraquat-mediated neurotoxicity. We observed that paraquat feeding reduces the cellular level of dMyc. We further noted that targeted upregulation of dMyc in paraquat-exposed flies mitigates degeneration of dopaminergic neurons by reinstating the aberrantly activated JNK pathway, and this in turn improves the motor performance and survival rate of the flies. Our study provides the first evidence that improved cellular level of dMyc could efficiently minimize the neurotoxic effects of paraquat, which could be beneficial in designing novel therapeutic strategies against Parkinson’s disease.

中文翻译：

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dMyc 的靶向上调限制了百草枯诱导的果蝇帕金森病模型中 JNK 介导的多巴胺能神经元变性

帕金森病是第二常见的神经退行性疾病，其特征是大脑中多巴胺能神经元的丧失。帕金森病有家族性和散发性病例，受遗传和/或环境因素的影响不同。不同的流行病学研究提出癌症的发病机制与帕金森病之间存在关联。然而，目前还无法确定这两种疾病之间的精确关联。在这项研究中，我们在百草枯诱导的散发性帕金森病模型中检查了（人类原癌基因的同源物）的疾病缓解特性。我们首次报道 dMyc 的靶向上调可显着限制百草枯介导的神经毒性。我们观察到，喂食百草枯会降低 dMyc 的细胞水平。我们进一步注意到，在接触百草枯的果蝇中，dMyc 的定向上调通过恢复异常激活的 JNK 通路来减轻多巴胺能神经元的退化，这反过来又提高了果蝇的运动性能和存活率。我们的研究提供了第一个证据，证明提高 dMyc 的细胞水平可以有效地减少百草枯的神经毒性作用，这可能有利于设计针对帕金森病的新治疗策略。