A complex crosstalk between polymorphic microRNA target sites and AD prognosis

Mallick, Bibekanand; Ghosh, Zhumur

doi:10.4161/rna.8.4.15584

Cited by 29 publications

(10 citation statements)

References 76 publications

(103 reference statements)

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“…Finally, SNPs (single-nucleotide polymorphisms) associated with various diseases may create, modify or destroy MREs. For example, SNPs in genes related to Alzheimer’s disease may potentially dysregulate miRNA and ceRNA networks and thus contribute to aberrant gene expression in Alzheimer’s disease 90 . These observations suggest that ceRNA network interactions may have a role in determining the effectiveness of RNA-directed therapies 91 .…”

Section: Implications For Human Diseasementioning

confidence: 99%

The multilayered complexity of ceRNA crosstalk and competition

Tay

Rinn

Pandolfi

2014

Nature

3,311

2,766

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Recent reports have described an intricate interplay among diverse RNA species, including protein-coding messenger RNAs and non-coding RNAs such as long non-coding RNAs, pseudogenes and circular RNAs. These RNA transcripts act as competing endogenous RNAs (ceRNAs) or natural microRNA sponges — they communicate with and co-regulate each other by competing for binding to shared microRNAs, a family of small non-coding RNAs that are important post-transcriptional regulators of gene expression. Understanding this novel RNA crosstalk will lead to significant insight into gene regulatory networks and have implications in human development and disease.

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Section: Implications For Human Diseasementioning

confidence: 99%

The multilayered complexity of ceRNA crosstalk and competition

Tay

Rinn

Pandolfi

2014

Nature

3,311

2,766

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“…This is the first time, to our knowledge, that inhaled anesthetics induces cell death by regulating microRNAs is reported. In addition to Bax expression that may be regulated by miR-214, one single nucleotide polymophism (SNP) in presenilin-1 (PS1) (rs63750082) was shown to create a potential target site for miR-214 [45]. This may result in the downregulation of PS1 by miR-214 and thereby reduces the production of Aβ and lessens AD pathology.…”

Section: Discussionmentioning

confidence: 99%

Isoflurane Increases Neuronal Cell Death Vulnerability by Downregulating miR-214

Yan

Zhao

et al. 2013

PLoS ONE

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Since accumulating evidence suggests the application of anesthetics may increase the risk of Alzheimer’s disease (AD), we investigated the cytotoxicity of inhaled general anesthesia in neurons and its underlying mechanism. Using primary cultured rat hippocampal neurons as the study model, here we show that isoflurane increases vulnerability to intracellular or extracellular amyloid β with or without serum deprivation. This isoflurane-induced effect is mediated by the downregulation of miR-214 level that lead to an elevated expression of Bax, a prominent target for miR-214. We conclude that isoflurane increases cell death in the presence of amyloid β by increasing Bax level through downregulating miR-214. Our data provide a new insight for inhaled anesthetics toxicity and indicate a possible mechanistic link between anesthetic application and neurodegenration in AD.

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“…The significant interactions include target SNPs present in seven genes related to AD prognosis with the miRNAs miR214, 23a and 23b, 486-3p, 30e*, 143, 128, 27a &27b, 324-5p and 422a. The dys regulated miRNA network contributes to the aberrant gene expression in AD [108][109][110].…”

Section: Apoe-2/3 Apoe-3/3 Apoe-3/4 Apoe-4/4 Apoe-2/4mentioning

confidence: 99%

Pharmacogenetic Considerations in the Treatment of Alzheimer’s Disease

et al. 2016

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The practical pharmacogenetics of Alzheimer's disease (AD) is circumscribed to acetylcholinesterase inhibitors (AChEIs) and memantine. However, pharmacogenetic procedures should be applied to novel strategies in AD therapeutics including: novel AChEIs and neurotransmitter regulators, anti-Aβ treatments, anti-tau treatments, pleiotropic products, epigenetic drugs and combination therapies. Genes involved in the pharmacogenetic network are under the influence of the epigenetic machinery which regulates gene expression transcriptionally and post-transcriptionally, configuring the fundamentals of pharmacoepigenomics. Over 60% of AD patients present concomitant pathologies demanding additional treatments which increase the likelihood of drug-drug interactions. Lipid metabolism dysfunction is a pathogenic mechanism inherent to AD neurodegeneration. The therapeutic response to hypolipidemic compounds is influenced by the APOE and CYP genotypes. The development of novel compounds and the use of combination/multifactorial treatments require the implantation of pharmacogenomic procedures for the avoidance of ADRs and the optimization of therapeutics.

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A complex crosstalk between polymorphic microRNA target sites and AD prognosis

Cited by 29 publications

References 76 publications

The multilayered complexity of ceRNA crosstalk and competition

The multilayered complexity of ceRNA crosstalk and competition

Isoflurane Increases Neuronal Cell Death Vulnerability by Downregulating miR-214

Pharmacogenetic Considerations in the Treatment of Alzheimer’s Disease

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