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研究帕金森病患者血清外泌体 microRNA 转录组的综合数据。

Comprehensive data for studying serum exosome microRNA transcriptome in Parkinson's disease patients.

机构信息

Department of Neurology, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Department of Neurology, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.

出版信息

Sci Data. 2024 Oct 15;11(1):1128. doi: 10.1038/s41597-024-03909-6.

Abstract

Parkinson's disease (PD), the second most prevalent neurodegenerative disorder, was classically attributed to alpha-synuclein aggregation and consequent loss of dopaminergic neurons in the substantia nigra pars compacta. Recently, emerging evidence suggested a broader spectrum of contributing factors, including exosome-mediated intercellular communication, which can potentially serve as biomarkers and therapeutic targets. However, there is a remarkable lack of comprehensive studies that connect the serum exosome microRNA (miRNA) transcriptome with demographic, clinical, and neuroimaging data in PD patients. Here, we present serum exosome miRNA transcriptome data generated from four cohort studies. Two of these studies include 96 PD patients and 80 age- and gender-matched controls, with anonymised demographic, clinical, and neuroimaging data provided for PD patients. The other two studies involve 96 PD patients who were evaluated both before and after one year of treatment with rasagiline, a widely prescribed anti-parkinsonism drug. Together, the datasets provide a valuable source for understanding pathogenesis and discovering biomarkers and therapeutic targets in PD.

摘要

帕金森病(PD)是第二大常见的神经退行性疾病,传统上归因于α-突触核蛋白聚集,继而导致黑质致密部多巴胺能神经元丧失。最近,新出现的证据表明存在更广泛的致病因素,包括外泌体介导的细胞间通讯,它们可能作为生物标志物和治疗靶点。然而,目前仍缺乏将 PD 患者的血清外泌体 microRNA(miRNA)转录组与人口统计学、临床和神经影像学数据联系起来的全面研究。在这里,我们展示了来自四个队列研究的血清外泌体 miRNA 转录组数据。其中两项研究包括 96 名 PD 患者和 80 名年龄和性别匹配的对照者,为 PD 患者提供了匿名的人口统计学、临床和神经影像学数据。另外两项研究涉及 96 名 PD 患者,他们在接受广泛应用的抗帕金森病药物雷沙吉兰治疗一年前后都进行了评估。这些数据集共同为理解 PD 的发病机制以及发现生物标志物和治疗靶点提供了有价值的资源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/11480472/4b34b990e7c6/41597_2024_3909_Fig1_HTML.jpg

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