Dysregulated A to I RNA editing and non-coding RNAs in neurodegeneration

Singh, Minati

doi:10.3389/fgene.2012.00326

Cited by 32 publications

(28 citation statements)

References 186 publications

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“…Common differentially expressed genes between G2019S-associated PD patients and asymptomatic G2019S carriers and between idiopathic PD patients and controls innate immune response and age-related syndromes that include dementia and amyotrophic lateral sclerosis (Singh, 2013). Several single-nucleotide polymorphisms in ADARB2 have been associated with human longevity (Sebastiani et al, 2009).…”

Section: Tablementioning

confidence: 98%

Identification of candidate genes for Parkinson's disease through blood transcriptome analysis in LRRK2-G2019S carriers, idiopathic cases, and controls

Infante

Prieto

Sierra

et al. 2015

Neurobiology of Aging

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Section: Tablementioning

confidence: 98%

Identification of candidate genes for Parkinson's disease through blood transcriptome analysis in LRRK2-G2019S carriers, idiopathic cases, and controls

Infante

Prieto

Sierra

et al. 2015

Neurobiology of Aging

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“…A further post-transcriptional mechanism that is essential for nervous system homeostasis is RNA editing, whose dysregulation has been implicated in neurodegeneration 22 . The most common form of RNA editing, adenosine (A) to inosine (I) conversion, is mediated by the adenosine deaminase acting on RNA (ADAR).…”

Section: Identification Of Post-transcriptional Changes During Prion mentioning

confidence: 99%

Genome-wide transcriptomics identifies an early preclinical signature of prion infection

Sorce

Russo

Chincisan

et al. 2020

Preprint

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2The clinical course of prion diseases is accurately predictable despite long latency periods, suggesting that prion pathogenesis is driven by precisely timed molecular events. We constructed a searchable genome-wide atlas of mRNA abundance, splicing and editing alterations during the course of disease in prion-inoculated mice. Prion infection induced transient changes in mRNA abundance and processing already at eight weeks post inoculation, well ahead of any neuropathological and clinical signs. In contrast, microglia-enriched genes displayed an increase simultaneous with the appearance of clinical symptoms, whereas neuronal-enriched transcripts remained unchanged until the very terminal stage of disease. This suggests that glial pathophysiology, rather than neuronal demise, represents the final driver of disease. The administration of young plasma attenuated the occurrence of early mRNA abundance alterations and delayed symptoms in the terminal phase of the disease. The early onset of prion-induced molecular changes might thus point to novel biomarkers and potential interventional targets. MainAfter the onset of clinical signs, prion diseases typically progress very rapidly to a terminal stage, which is characterized by micro-and astrogliosis, vacuolation and neuronal loss. Sporadic Creutzfeldt-Jakob disease (CJD), the most common human prion disease, can lead to death within months of symptom onset 1 .Conversely, prion infections are often characterized by very long incubation times: iatrogenic cases of CJD after administration of prion-contaminated growth hormone display incubation times of >20 years 2 and Kuru, an acquired form of prion disease, was reported to arise decades after consumption of contaminated materials 3 . The extraordinary duration of the latency phase has led to the presumption that CJD may be caused by a "slow virus". Although this hypothesis was dismissed 4 , prion pathogenesis is initially insidious and only acquires a rapid rate of progression in the late stages of disease.The seemingly incongruous combination of a very long latency and a rapidly progressing clinical disease can be reproduced in mouse models of prion infection 5 . After inoculation of prion-containing brain homogenate, wild-type mice experience an incubation period of several months followed by rapidly progressive neurological dysfunction. It was suggested that prion replication occurs without causing any neuronal damage until a plateau level of infectious particles is reached, whereas neurotoxicity arises because of a toxic form of PrP named "PrP L " 6-8 . However, no physical evidence for the existence of "PrP L " has ever come forth, and these experimental observations can be explained by alternative models. For example, small numbers of prion seeds may cause early molecular alterations that elicit late-onset clinical signs. This question may be addressed by File 3). Consistent with the hierarchical clustering and the PCA, 813 genes changed at 8 wpi and the number of DEGs gradually increased during the later timepoin...

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“…lncRNA have also been shown to participate in RNA editing p8artially through their role in paraspeckles, regulation of ADAR activity (see above) and complementarity of their Alu repeats to Alu repeats in coding RNA which creates preferential editing sites [reviewed in 62]…”

Section: Lncrna Biologymentioning

confidence: 99%

Basic biology and therapeutic implications of lncRNA

Khorkova

Hsiao

Wahlestedt

2015

Advanced Drug Delivery Reviews

288

195

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Long non-coding RNAs (lncRNA), a class of non-coding RNA molecules recently identified largely due to the efforts of FANTOM, and later GENCODE and ENCODE consortia, have been a subject of intense investigation in the past decade. Extensive efforts to get deeper understanding of lncRNA biology have yielded evidence of their diverse structural and regulatory roles in protecting chromosome integrity, maintaining genomic architecture, X chromosome inactivation, imprinting, transcription, translation and epigenetic regulation. Here we wil briefly review the recent studies in the field of lncRNA biology focusing mostly on mammalian species and discuss their therapeutic implications.

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Dysregulated A to I RNA editing and non-coding RNAs in neurodegeneration

Cited by 32 publications

References 186 publications

Identification of candidate genes for Parkinson's disease through blood transcriptome analysis in LRRK2-G2019S carriers, idiopathic cases, and controls

Identification of candidate genes for Parkinson's disease through blood transcriptome analysis in LRRK2-G2019S carriers, idiopathic cases, and controls

Genome-wide transcriptomics identifies an early preclinical signature of prion infection

Basic biology and therapeutic implications of lncRNA

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