Long noncoding RNAs in psychiatric disorders

Zuo, Lingjun; Tan, Yunlong; Wang, Zhiren; Wang, Ke Sheng; Zhang, Xiangyang; Chen, Xiangning; Li, Chiang‐Shan R.; Wang, Tong; Luο, Xingguang

doi:10.1097/ypg.0000000000000129

Cited by 42 publications

(28 citation statements)

References 87 publications

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“…The expression level of lncRNAs is highest in brain (Derrien et al, 2012), and similar to protein-coding genes; they are regulated by neuronal activity (Barry et al, 2014) and show cell type- and brain region-specific expression patterns (Belgard et al, 2011; Mercer, Dinger, Sunkin, Mehler, & Mattick, 2008), suggesting that their expression is important in discrete CNS functions. Although the physiological roles of lncRNAs are still emerging, they appear to be involved in cis-regulation of neighboring genes (Goff et al, 2015; Zuo et al, 2016) and the regulation of gene expression involved in adaptive behavior (Bekdash & Harrison, 2015; Spadaro et al, 2015). The extent to which specific lncRNAs contribute to the development and maintenance of alcohol- or other substance-abuse disorders is currently an under-investigated area, with the potential to uncover novel regulatory gene networks involved in the addictive process.…”

Section: Long Non-coding Rnamentioning

confidence: 99%

“…According to the positional relationship between lncRNAs and their associated protein-coding genes, lncRNAs are classified as intergenic (lincRNA; located between protein-coding genes and at least 1 kb away from the nearest protein-coding genes), intronic (located within the intron of annotated protein-coding genes), anti-sense (RNA molecules that are transcribed from the opposite strand of many protein-coding genes), and sense overlapping (considered transcript isoforms of protein-coding mRNAs) (Zuo et al, 2016). …”

Section: Long Non-coding Rnamentioning

confidence: 99%

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Emerging roles for ncRNAs in alcohol use disorders

Mayfield

2017

Alcohol

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Chronic alcohol exposure produces widespread neuroadaptations and alterations in gene expression in human alcoholics and animal models. Technological advances in the past decade have increasingly highlighted the role of non-protein-coding RNAs (ncRNAs) in the regulation of gene expression and function. These recently characterized molecules were discovered to mediate diverse processes in the central nervous system, from normal development and physiology to regulation of disease, including alcoholism and other psychiatric disorders. This review will investigate the recent studies in human alcoholics and rodent models that have profiled different classes of ncRNAs and their dynamic alcohol-dependent regulation in brain.

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Section: Long Non-coding Rnamentioning

confidence: 99%

Section: Long Non-coding Rnamentioning

confidence: 99%

Emerging roles for ncRNAs in alcohol use disorders

Mayfield

2017

Alcohol

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“…On the other hand, microRNAs, small RNA molecules from non-coding RNA family, have made a remarkable impact in understanding their epigenetic role as post-transcriptional modifier in dysfunctional gene regulatory network in several central nervous systems (CNS) related psychiatric disorders (Dwivedi, 2011, 2013, 2014). Although, an in-depth discussion of these two major epigenetic modifications in relation to suicide is beyond the scope of this review, anticipating their functional relevance and future perspective of other epigenetic reagents like methylated RNA molecules and long non-coding RNAs is important (Aliperti and Donizetti, 2016; Barry et al, 2014; Satterlee et al, 2014; Zuo et al, 2016). Receiving more mechanistic insight to explore the underlying inter-molecular network, acting as a delicate interface to receive environmental inputs found to be vulnerable to the magnitude of external adversities with increasing risk of suicidal phenotype, will be more helpful to devise effective strategies for early assessment of suicidal behavior and prevention of suicide attempt.…”

Section: Discussionmentioning

confidence: 99%

Understanding epigenetic architecture of suicide neurobiology: A critical perspective

Roy

Dwivedi

2017

Neuroscience & Biobehavioral Reviews

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Current understanding of environmental cross-talk with genetic makeup is found to be mediated through an epigenetic interface which is associated with prominent reversible and heritable changes at gene expression level. Recent emergence of epigenetic modulation in shaping the genetic information has become a key regulatory factor in answering the underlying complexities associated with several mental disorders. A comprehensive understanding of the pertinent changes in the epigenetic makeup of suicide phenotype exhibits a characteristic signature with the possibility of using it as a biomarker to help predict the risk factors associated with suicide. Within the scope of this current review, the most sought after epigenetic changes of DNA methylation and histone modification are thoroughly scrutinized to understand their close functional association with the broad spectrum of suicide phenotype.

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“…BIN1 and PICALM are expressed in human brains and have widely been associated with AD by numerous studies (Wang et al 2016; Holler et al 2014). The antisense LncRNA and snRNA might use diverse transcriptional and post-transcriptional mechanisms (Faghihi and Wahlestedt 2009; Villegas and Zaphiropoulos 2015; Zuo et al 2016a) to regulate BIN1 and PICALM , respectively, to play roles in AD. PICALM and BIN1 were modifiers of Aβ toxicity and they could promote APP internalization, endocytic trafficking, and Aβ generation in neurons in vitro (Xiao et al 2012; Treusch et al 2011).…”

Section: Discussionmentioning

confidence: 99%

Genome-wide significant, replicated and functional risk variants for Alzheimer’s disease

et al. 2017

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Genome-wide association studies (GWASs) have reported numerous associations between risk variants and Alzheimer’s disease (AD). However, these associations do not necessarily indicate a causal relationship. If the risk variants can be demonstrated to be biologically functional, the possibility of a causal relationship would be increased. In this article, we reviewed all of the published GWASs to extract the genome-wide significant (p<5×10−8) and replicated associations between risk variants and AD or AD-biomarkers. The regulatory effects of these risk variants on the expression of a novel class of non-coding RNAs (piRNAs) and protein-coding RNAs (mRNAs), the alteration of proteins caused by these variants, the associations between AD and these variants in our own sample, the expression of piRNAs, mRNAs and proteins in human brains targeted by these variants, the expression correlations between the risk genes and APOE, the pathways and networks that the risk genes belonged to, and the possible long non-coding RNAs (LncRNAs) that might regulate the risk genes were analyzed, to investigate the potential biological functions of the risk variants and explore the potential mechanisms underlying the SNP-AD associations. We found replicated and significant associations for AD or AD-biomarkers, surprisingly, only at 17 SNPs located in 11 genes/snRNAs/LncRNAs in eight genomic regions. Most of these 17 SNPs enriched some AD-related pathways or networks, and were potentially functional in regulating piRNAs and mRNAs; some SNPs were associated with AD in our sample, and some SNPs altered protein structures. Most of the protein-coding genes regulated by the risk SNPs were expressed in human brain and correlated with APOE expression. We conclude that these variants were most robust risk markers for AD, and their contributions to AD risk was likely to be causal. As expected, APOE and the lipoprotein metabolism pathway possess the highest weight among these contributions.

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Long noncoding RNAs in psychiatric disorders

Cited by 42 publications

References 87 publications

Emerging roles for ncRNAs in alcohol use disorders

Emerging roles for ncRNAs in alcohol use disorders

Understanding epigenetic architecture of suicide neurobiology: A critical perspective

Genome-wide significant, replicated and functional risk variants for Alzheimer’s disease

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