Comparative blood transcriptome analysis in idiopathic and LRRK2 G2019S–associated Parkinson's disease

转录组 LRRK2 生物 小桶 遗传学 基因 突变 帕金森病 发病机制 疾病 免疫学 基因表达 医学 病理
作者
Jon Infante,Carlos Prieto,María Sierra,Pascual Sánchez-Juan,Isabel González-Aramburu,Coro Sánchez-Quintana,José Berciano,Onofre Combarros,Jesus Sainz
出处
期刊:Neurobiology of Aging [Elsevier BV]
卷期号:38: 214.e1-214.e5 被引量:27
标识
DOI:10.1016/j.neurobiolaging.2015.10.026
摘要

Patients with Parkinson's disease (PD) carrying the G2019S mutation of the LRRK2 gene provide an opportunity of studying in a homogeneous setting the molecular pathways involved in the pathogenesis of common idiopathic forms of PD. However, whether common mechanisms are involved in both conditions in not known. Here, we compared genome-wide gene expression (RNA sequencing) in peripheral blood between PD patients carrying the G2019S mutation of the LRRK2 gene and idiopathic PD cases, to deepen in the understanding of this topic. In addition, we compared the blood transcriptome between 2 cohorts of carriers of the G2019S mutation (symptomatic and asymptomatic) and 2 cohorts of noncarriers (symptomatic and asymptomatic) for detecting transcriptomic changes attributable to the presence of the G2019S mutation. We searched for gene enrichment in Reactome or Kyoto Encyclopedia of Genes and Genomes pathways. We found that despite some overlap, peripheral blood transcriptome differs widely between idiopathic and LRRK2 G2019S-associated PD, with only 4 deregulated pathways shared by both conditions (complement and coagulation cascades, cell adhesion molecules, hematopoietic cell lineage, and extracellular matrix organization). Changes in the blood transcriptome observed in asymptomatic carriers of the mutation included 6 genes known to be associated with PD in genome-wide association studies and also pathways related with immunity. Our findings emphasize the notion that PD is likely a pathogenically heterogeneous condition and suggest the existence of specific mechanisms involved in LRRK2-associated PD.
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