Epigenetics in the Central Nervous System

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 5891

Special Issue Editor

Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA
Interests: genomics and epigenetics of tuberous sclerosis complex (TSC) and LAM disease

Special Issue Information

Dear Colleagues,

Epigenetic mechanisms act at the interface of genetic and environmental influences on human phenotype and have been implicated to be mediators of essential functions in the central nervous system. The major epigenetic mechanisms include DNA methylation, histone modification, and non-coding RNA (ncRNA)-associated gene silencing. These mechanisms play an important role in the regulation of gene expression and silencing, neuron–glial differentiation, neurogenesis, the regulation of neurobehavior, and neuroplasticity. Experiments with cellular and animal models have demonstrated that various epigenetic modifications can affect cognition in different ways, from severe dysfunction to substantial improvement. In humans, epigenetic dysregulation has been known to underlie a number of disorders that are accompanied by cognitive impairment. In this Special Issue, we will explore the epigenetic mechanisms that regulate the central nervous system and how their disruption can lead to cognitive dysfunction and neurodevelopmental and/or neurodegenerative disorders.

Dr. Krinio Giannikou
Guest Editor

Manuscript Submission Information

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Keywords

  • epigenetics
  • central nervous system
  • cognitive dysfunction
  • neurodevelopmental diseases
  • neuropsychiatric/neurodegenerative disorders
  • miRNA
  • DNA methylation
  • histone modification

Published Papers (2 papers)

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Research

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20 pages, 1836 KiB  
Article
Differentially Expressed miRNAs in Age-Related Neurodegenerative Diseases: A Meta-Analysis
by Ocana Noronha, Lucia Mesarosovo, Jasper J. Anink, Anand Iyer, Eleonora Aronica and James D. Mills
Genes 2022, 13(6), 1034; https://doi.org/10.3390/genes13061034 - 09 Jun 2022
Cited by 3 | Viewed by 2508
Abstract
To date, no neurodegenerative diseases (NDDs) have cures, and the underlying mechanism of their pathogenesis is undetermined. As miRNAs extensively regulate all biological processes and are crucial regulators of healthy brain function, miRNAs differentially expressed in NDDs may provide insight into the factors [...] Read more.
To date, no neurodegenerative diseases (NDDs) have cures, and the underlying mechanism of their pathogenesis is undetermined. As miRNAs extensively regulate all biological processes and are crucial regulators of healthy brain function, miRNAs differentially expressed in NDDs may provide insight into the factors that contribute to the emergence of protein inclusions and the propagation of deleterious cellular environments. A meta-analysis of miRNAs dysregulated in Alzheimer’s disease, Parkinson’s disease, multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies and frontotemporal lobar degeneration (TDP43 variant) was performed to determine if diseases within a proteinopathy have distinct or shared mechanisms of action leading to neuronal death, and if proteinopathies can be classified on the basis of their miRNA profiles. Our results identified both miRNAs distinct to the anatomy, disease type and pathology, and miRNAs consistently dysregulated within single proteinopathies and across neurodegeneration in general. Our results also highlight the necessity to minimize the variability between studies. These findings showcase the need for more transcriptomic research on infrequently occurring NDDs, and the need for the standardization of research techniques and platforms utilized across labs and diseases. Full article
(This article belongs to the Special Issue Epigenetics in the Central Nervous System)
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15 pages, 688 KiB  
Review
Gene Expression and Epigenetic Regulation in the Prefrontal Cortex of Schizophrenia
by Wiktor Bilecki and Marzena Maćkowiak
Genes 2023, 14(2), 243; https://doi.org/10.3390/genes14020243 - 18 Jan 2023
Cited by 4 | Viewed by 2697
Abstract
Schizophrenia pathogenesis remains challenging to define; however, there is strong evidence that the interaction of genetic and environmental factors causes the disorder. This paper focuses on transcriptional abnormalities in the prefrontal cortex (PFC), a key anatomical structure that determines functional outcomes in schizophrenia. [...] Read more.
Schizophrenia pathogenesis remains challenging to define; however, there is strong evidence that the interaction of genetic and environmental factors causes the disorder. This paper focuses on transcriptional abnormalities in the prefrontal cortex (PFC), a key anatomical structure that determines functional outcomes in schizophrenia. This review summarises genetic and epigenetic data from human studies to understand the etiological and clinical heterogeneity of schizophrenia. Gene expression studies using microarray and sequencing technologies reported the aberrant transcription of numerous genes in the PFC in patients with schizophrenia. Altered gene expression in schizophrenia is related to several biological pathways and networks (synaptic function, neurotransmission, signalling, myelination, immune/inflammatory mechanisms, energy production and response to oxidative stress). Studies investigating mechanisms driving these transcriptional abnormalities focused on alternations in transcription factors, gene promoter elements, DNA methylation, posttranslational histone modifications or posttranscriptional regulation of gene expression mediated by non-coding RNAs. Full article
(This article belongs to the Special Issue Epigenetics in the Central Nervous System)
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