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• W2014229306 abstract "The pathological hallmark of Parkinson’s disease (PD) is the loss of dopaminergic neurons and the presence of Lewy bodies and Lewy neurites in the substantia nigra pars compacta, corpus striatum and brain cortex [1]. PD is a complex disease caused by the interaction of genetic/ inherited and environmental/acquired risk factors [2]. MicroRNAs (miRNAs) are small RNAs that control gene expression by binding to the 30 UTRs of mRNAs [3]. Postmortem analysis of brain tissues and in vitro studies have identified several miRNAs implicated in PD. MiR-133b was shown to be downregulated in PD brains and to promote the survival of dopaminergic neurons [4]. MiR-433 was related with PD through targeting the FGF20, which in turn regulates the expression of a-synuclein [5]. MiR-7 targets a-synuclein and could regulate oxidative stress and cell death, while miR-184 and let-7 regulate dopaminergic neurons survival and activity [6, 7]. Recently, a miRNA profiling of PD brains identified early downregulation of miR-34b/c, modulating mitochondrial function in areas with pathological affectation [8]. Plasma (circulating) miRNAs have been proposed as biomarkers for several diseases and aging [9, 10]. Our aim was to characterize the plasma miRNA profile in PD patients and healthy controls, to determine its usefulness as a biomarker for PD. The study was approved by the Ethical Committee of Hospital Universitario Central de Asturias (HUCA) in accordance with the ethical standards of the Declaration of Helsinki and all the participants signed an informed consent. The study cohort consisted of sexand age-matched healthy controls (n = 25; mean age 67.6; 52 % males) and patients (n = 31; mean age 63.9; 55 % males) who fulfilled the PD-clinical diagnosis criteria [11]. None of the patients were receiving drugs for PD-treatment or had a diagnosis of cardiovascular or tumor disease. Full details of the experimental procedure are available as supplementary material. Briefly, blood was collected in tubes with EDTA, centrifuged and plasma was aliquoted (350 ll). A total of 2 pg of a synthetic Arabidopsis thaliana miRNA (Ath-miR-159a; 5 ll of a 0.4 pg/ll dilution) was immediately added and each aliquot stored at -80 C until use. Ath-miR-159a was used as control of the extraction process (supplementary material). Total plasma RNA was extracted (TRIzol LS Reagent, Ambion) and resuspended in 25 ll of RNAse-free water. Five ll of each sample were retrotranscribed (RT) with the Megaplex RT primers Human pool A and TaqMan microRNA Reverse transcription kit (Applied Biosystems). Three ll of the RT product were pre-amplified with the Megaplex Preamp primers Human pool A and TaqMan Universal Master Mix no AmpErase UNG (Applied Biosystems). All the preamplifications were assayed with a custom Ath-miR-159a Taqman assay in an ABI 7500 Real-Time PCR (Applied Electronic supplementary material The online version of this article (doi:10.1007/s00415-013-6900-8) contains supplementary material, which is available to authorized users." @default.
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• W2014229306 date "2013-03-30" @default.
• W2014229306 modified "2023-10-17" @default.
• W2014229306 title "Profile of microRNAs in the plasma of Parkinson’s disease patients and healthy controls" @default.
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• W2014229306 doi "https://doi.org/10.1007/s00415-013-6900-8" @default.
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