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Non-coding RNAs in Alzheimer's Disease
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Non-coding RNAs in Alzheimer's Disease

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (20 November 2021) | Viewed by 15718

Special Issue Editor

Dr. Evgenia Salta

E-Mail Website
Guest Editor
Laboratory of Neurogenesis & Neurodegeneration, Netherlands Institute for Neuroscience, 1105 Amsterdam, The Netherlands
Interests: non-coding RNA; microRNA; neurodegeneration; Alzheimer’s disease; adult neurogenesis

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) was until recently perceived as a neuron-centric disorder with linearly evolving pathology. Novel molecular and genetic insights have challenged the unidirectional linearity of the pathogenic cascade in AD and underscored the significance of intertwined complex cellular pathways, gene networks, and feed-forward regulatory loops that may differentially impact distinct pathogenic endophenotypes and cellular phases of the disease. Mapping the mechanistic heterogeneity and multifactorial nature of AD is a key challenge, given the current lack of effective disease-modifying therapies.

The emerging complexity of the transcriptional landscape poses great challenges to our conventional preconceptions of how the genome regulates brain function and dysfunction. Non-protein-coding RNAs (ncRNAs) confer a high level of intricate and dynamic regulation of various molecular processes in the central nervous system and have been widely implicated in Alzheimer’s disease pathophysiology. Understanding these events may help to develop novel diagnostic and therapeutic strategies.

This Special Issue is a collection of articles reporting novel insights into the intriguing roles of ncRNAs in AD pathobiology, ranging from fundamental discoveries to therapeutic applications. Manuscripts on the following topics—but not limited to these—will be considered for publication and are encouraged: ncRNA mechanisms of function in AD/brain dysfunction, ncRNA molecular networks in AD/brain dysfunction, ncRNAs as biomarkers, ncRNAs as therapeutics, ncRNA profiling in AD, ncRNAs in animal models of AD, ncRNAs in human AD brain, ncRNAs and AD genetics.

Dr. Evgenia Salta
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Non-coding RNA
  • microRNA
  • Alzheimer’s disease
  • Neurodegeneration
  • Animal models
  • Human brain
  • Neuropathology
  • Biomarkers
  • Molecular mechanisms
  • Therapeutic targeting

Published Papers (4 papers)

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Research

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16 pages, 3433 KiB  
Article
Systematic Identification of circRNAs in Alzheimer’s Disease
by Kyle R. Cochran, Kirtana Veeraraghavan, Gautam Kundu, Krystyna Mazan-Mamczarz, Christopher Coletta, Madhav Thambisetty, Myriam Gorospe and Supriyo De
Genes 2021, 12(8), 1258; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12081258 - 18 Aug 2021
Cited by 11 | Viewed by 2716
Abstract
Mammalian circRNAs are covalently closed circular RNAs often generated through backsplicing of precursor linear RNAs. Although their functions are largely unknown, they have been found to influence gene expression at different levels and in a wide range of biological processes. Here, we investigated [...] Read more.
Mammalian circRNAs are covalently closed circular RNAs often generated through backsplicing of precursor linear RNAs. Although their functions are largely unknown, they have been found to influence gene expression at different levels and in a wide range of biological processes. Here, we investigated if some circRNAs may be differentially abundant in Alzheimer’s Disease (AD). We identified and analyzed publicly available RNA-sequencing data from the frontal lobe, temporal cortex, hippocampus, and plasma samples reported from persons with AD and persons who were cognitively normal, focusing on circRNAs shared across these datasets. We identified an overlap of significantly changed circRNAs among AD individuals in the various brain datasets, including circRNAs originating from genes strongly linked to AD pathology such as DOCK1, NTRK2, APC (implicated in synaptic plasticity and neuronal survival) and DGL1/SAP97, TRAPPC9, and KIF1B (implicated in vesicular traffic). We further predicted the presence of circRNA isoforms in AD using specialized statistical analysis packages to create approximations of entire circRNAs. We propose that the catalog of differentially abundant circRNAs can guide future investigation on the expression and splicing of the host transcripts, as well as the possible roles of these circRNAs in AD pathogenesis. Full article
(This article belongs to the Special Issue Non-coding RNAs in Alzheimer's Disease)
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Review

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16 pages, 359 KiB  
Review
Missing lnc(RNAs) in Alzheimer’s Disease?
by Rafaela Policarpo and Constantin d’Ydewalle
Genes 2022, 13(1), 39; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13010039 - 23 Dec 2021
Cited by 3 | Viewed by 3486
Abstract
With the ongoing demographic shift towards increasingly elderly populations, it is estimated that approximately 150 million people will live with Alzheimer’s disease (AD) by 2050. By then, AD will be one of the most burdensome diseases of this and potentially next centuries. Although [...] Read more.
With the ongoing demographic shift towards increasingly elderly populations, it is estimated that approximately 150 million people will live with Alzheimer’s disease (AD) by 2050. By then, AD will be one of the most burdensome diseases of this and potentially next centuries. Although its exact etiology remains elusive, both environmental and genetic factors play crucial roles in the mechanisms underlying AD neuropathology. Genome-wide association studies (GWAS) identified genetic variants associated with AD susceptibility in more than 40 different genomic loci. Most of these disease-associated variants reside in non-coding regions of the genome. In recent years, it has become clear that functionally active transcripts arise from these non-coding loci. One type of non-coding transcript, referred to as long non-coding RNAs (lncRNAs), gained significant attention due to their multiple roles in neurodevelopment, brain homeostasis, aging, and their dysregulation or dysfunction in neurological diseases including in AD. Here, we will summarize the current knowledge regarding genetic variations, expression profiles, as well as potential functions, diagnostic or therapeutic roles of lncRNAs in AD. We postulate that lncRNAs may represent the missing link in AD pathology and that unraveling their role may open avenues to better AD treatments. Full article
(This article belongs to the Special Issue Non-coding RNAs in Alzheimer's Disease)
21 pages, 1480 KiB  
Review
Small Molecule Drugs Targeting Non-Coding RNAs as Treatments for Alzheimer’s Disease and Related Dementias
by Lien D. Nguyen, Rachel K. Chau and Anna M. Krichevsky
Genes 2021, 12(12), 2005; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12122005 - 17 Dec 2021
Cited by 15 | Viewed by 4624
Abstract
Despite the enormous burden of Alzheimer’s disease and related dementias (ADRD) on patients, caregivers, and society, only a few treatments with limited efficacy are currently available. While drug development conventionally focuses on disease-associated proteins, RNA has recently been shown to be druggable for [...] Read more.
Despite the enormous burden of Alzheimer’s disease and related dementias (ADRD) on patients, caregivers, and society, only a few treatments with limited efficacy are currently available. While drug development conventionally focuses on disease-associated proteins, RNA has recently been shown to be druggable for therapeutic purposes as well. Approximately 70% of the human genome is transcribed into non-protein-coding RNAs (ncRNAs) such as microRNAs, long ncRNAs, and circular RNAs, which can adopt diverse structures and cellular functions. Many ncRNAs are specifically enriched in the central nervous system, and their dysregulation is implicated in ADRD pathogenesis, making them attractive therapeutic targets. In this review, we first detail why targeting ncRNAs with small molecules is a promising therapeutic strategy for ADRD. We then outline the process from discovery to validation of small molecules targeting ncRNAs in preclinical studies, with special emphasis on primary high-throughput screens for identifying lead compounds. Screening strategies for specific ncRNAs will also be included as examples. Key challenges—including selecting appropriate ncRNA targets, lack of specificity of small molecules, and general low success rate of neurological drugs and how they may be overcome—will be discussed throughout the review. Full article
(This article belongs to the Special Issue Non-coding RNAs in Alzheimer's Disease)
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28 pages, 1726 KiB  
Review
Advances in Genetics and Epigenetic Alterations in Alzheimer’s Disease: A Notion for Therapeutic Treatment
by Rubén Rabaneda-Bueno, Beatriz Mena-Montes, Sara Torres-Castro, Norma Torres-Carrillo and Nora Magdalena Torres-Carrillo
Genes 2021, 12(12), 1959; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12121959 - 08 Dec 2021
Cited by 9 | Viewed by 3964
Abstract
Alzheimer’s disease (AD) is a disabling neurodegenerative disorder that leads to long-term functional and cognitive impairment and greatly reduces life expectancy. Early genetic studies focused on tracking variations in genome-wide DNA sequences discovered several polymorphisms and novel susceptibility genes associated with AD. However, [...] Read more.
Alzheimer’s disease (AD) is a disabling neurodegenerative disorder that leads to long-term functional and cognitive impairment and greatly reduces life expectancy. Early genetic studies focused on tracking variations in genome-wide DNA sequences discovered several polymorphisms and novel susceptibility genes associated with AD. However, despite the numerous risk factors already identified, there is still no fully satisfactory explanation for the mechanisms underlying the onset of the disease. Also, as with other complex human diseases, the causes of low heritability are unclear. Epigenetic mechanisms, in which changes in gene expression do not depend on changes in genotype, have attracted considerable attention in recent years and are key to understanding the processes that influence age-related changes and various neurological diseases. With the recent use of massive sequencing techniques, methods for studying epigenome variations in AD have also evolved tremendously, allowing the discovery of differentially expressed disease traits under different conditions and experimental settings. This is important for understanding disease development and for unlocking new potential AD therapies. In this work, we outline the genomic and epigenomic components involved in the initiation and development of AD and identify potentially effective therapeutic targets for disease control. Full article
(This article belongs to the Special Issue Non-coding RNAs in Alzheimer's Disease)
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