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Neuroepigenetic: From Bench to Bedside
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Neuroepigenetic: From Bench to Bedside

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 14177

Special Issue Editors

Dr. Dragana Trifunovic

E-Mail Website
Guest Editor
University-Eye-Clinic Tübingen, Institute for Ophthalmic Research, Tübingen, Germany
Interests: retinal degeneration; cone photoreceptors; epigenetic; neuroprotection; regeneration; retinal cell biology
Dr. Livia Carvalho

E-Mail Website
Guest Editor
University of Western Australia, Lions Eye Institute, Perth, Australia
Interests: ocular gene therapy; retinal degeneration; cone photoreceptors; retinal physiology

Special Issue Information

Dear Colleagues,

The crucial role of epigenetic modifications of DNA and histones in understanding the molecular basis of complex phenotypes has been undoubtedly recognized in various diseases, ranging from imprinting disorders via autoimmune diseases to cancer. It is only reasonable to assume the same importance of epigenetic aberrations in the pathophysiology of neurological diseases. Indeed, neuroepigenetics is emerging as a hot topic in identifying the mechanisms of neurodegeneration, including in Alzheimer's and Huntington's disease, multiple sclerosis, as well as in blinding conditions such as age-related macular degeneration, glaucoma, or retinitis pigmentosa. The association of epigenome modifications with neurodegeneration has generated an exciting field of novel therapies based on epigenetic regulation with currently more than fifty ongoing clinical trials.

This Special Issue, "Neuroepigenetics: from bench to bedside," will cover a selection of recent advances in understanding the role of epigenetics in neurodegenerative disease and review current knowledge in epigenetically-driven disease mechanisms and the development of novel treatment strategies.

Dr. Dragana Trifunovic
Dr. Livia Carvalho
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  •  histones
  •  DNA methylation
  •  cell death
  •  neuroprotection
  •  neurodegeneration
  •  epigenetics
  •  transcriptional modifications
  •  epigenomics

Published Papers (3 papers)

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Review

29 pages, 5673 KiB  
Review
Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer’s Disease
by Anastasiia Ilina, Vladimir Khavinson, Natalia Linkova and Mikhael Petukhov
Int. J. Mol. Sci. 2022, 23(8), 4259; https://doi.org/10.3390/ijms23084259 - 12 Apr 2022
Cited by 8 | Viewed by 3547
Abstract
Epigenetic regulation of gene expression is necessary for maintaining higher-order cognitive functions (learning and memory). The current understanding of the role of epigenetics in the mechanism of Alzheimer’s disease (AD) is focused on DNA methylation, chromatin remodeling, histone modifications, and regulation of non-coding [...] Read more.
Epigenetic regulation of gene expression is necessary for maintaining higher-order cognitive functions (learning and memory). The current understanding of the role of epigenetics in the mechanism of Alzheimer’s disease (AD) is focused on DNA methylation, chromatin remodeling, histone modifications, and regulation of non-coding RNAs. The pathogenetic links of this disease are the misfolding and aggregation of tau protein and amyloid peptides, mitochondrial dysfunction, oxidative stress, impaired energy metabolism, destruction of the blood–brain barrier, and neuroinflammation, all of which lead to impaired synaptic plasticity and memory loss. Ultrashort peptides are promising neuroprotective compounds with a broad spectrum of activity and without reported side effects. The main aim of this review is to analyze the possible epigenetic mechanisms of the neuroprotective action of ultrashort peptides in AD. The review highlights the role of short peptides in the AD pathophysiology. We formulate the hypothesis that peptide regulation of gene expression can be mediated by the interaction of short peptides with histone proteins, cis- and transregulatory DNA elements and effector molecules (DNA/RNA-binding proteins and non-coding RNA). The development of therapeutic agents based on ultrashort peptides may offer a promising addition to the multifunctional treatment of AD. Full article
(This article belongs to the Special Issue Neuroepigenetic: From Bench to Bedside)
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22 pages, 1212 KiB  
Review
Emerging Role of HDACs in Regeneration and Ageing in the Peripheral Nervous System: Repair Schwann Cells as Pivotal Targets
by Jose A. Gomez-Sanchez, Nikiben Patel, Fernanda Martirena, Shaline V. Fazal, Clara Mutschler and Hugo Cabedo
Int. J. Mol. Sci. 2022, 23(6), 2996; https://doi.org/10.3390/ijms23062996 - 10 Mar 2022
Cited by 15 | Viewed by 3637
Abstract
The peripheral nervous system (PNS) has a remarkable regenerative capacity in comparison to the central nervous system (CNS), a phenomenon that is impaired during ageing. The ability of PNS axons to regenerate after injury is due to Schwann cells (SC) being reprogrammed into [...] Read more.
The peripheral nervous system (PNS) has a remarkable regenerative capacity in comparison to the central nervous system (CNS), a phenomenon that is impaired during ageing. The ability of PNS axons to regenerate after injury is due to Schwann cells (SC) being reprogrammed into a repair phenotype called Repair Schwann cells. These repair SCs are crucial for supporting axonal growth after injury, myelin degradation in a process known as myelinophagy, neurotropic factor secretion, and axonal growth guidance through the formation of Büngner bands. After regeneration, repair SCs can remyelinate newly regenerated axons and support nonmyelinated axons. Increasing evidence points to an epigenetic component in the regulation of repair SC gene expression changes, which is necessary for SC reprogramming and regeneration. One of these epigenetic regulations is histone acetylation by histone acetyl transferases (HATs) or histone deacetylation by histone deacetylases (HDACs). In this review, we have focused particularly on three HDAC classes (I, II, and IV) that are Zn2+-dependent deacetylases. These HDACs are important in repair SC biology and remyelination after PNS injury. Another key aspect explored in this review is HDAC genetic compensation in SCs and novel HDAC inhibitors that are being studied to improve nerve regeneration. Full article
(This article belongs to the Special Issue Neuroepigenetic: From Bench to Bedside)
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22 pages, 1731 KiB  
Review
Epigenetic Mechanisms in Memory and Cognitive Decline Associated with Aging and Alzheimer’s Disease
by Sabyasachi Maity, Kayla Farrell, Shaghayegh Navabpour, Sareesh Naduvil Narayanan and Timothy J. Jarome
Int. J. Mol. Sci. 2021, 22(22), 12280; https://doi.org/10.3390/ijms222212280 - 13 Nov 2021
Cited by 43 | Viewed by 6302
Abstract
Epigenetic mechanisms, which include DNA methylation, a variety of post-translational modifications of histone proteins (acetylation, phosphorylation, methylation, ubiquitination, sumoylation, serotonylation, dopaminylation), chromatin remodeling enzymes, and long non-coding RNAs, are robust regulators of activity-dependent changes in gene transcription. In the brain, many of these [...] Read more.
Epigenetic mechanisms, which include DNA methylation, a variety of post-translational modifications of histone proteins (acetylation, phosphorylation, methylation, ubiquitination, sumoylation, serotonylation, dopaminylation), chromatin remodeling enzymes, and long non-coding RNAs, are robust regulators of activity-dependent changes in gene transcription. In the brain, many of these epigenetic modifications have been widely implicated in synaptic plasticity and memory formation. Dysregulation of epigenetic mechanisms has been reported in the aged brain and is associated with or contributes to memory decline across the lifespan. Furthermore, alterations in the epigenome have been reported in neurodegenerative disorders, including Alzheimer’s disease. Here, we review the diverse types of epigenetic modifications and their role in activity- and learning-dependent synaptic plasticity. We then discuss how these mechanisms become dysregulated across the lifespan and contribute to memory loss with age and in Alzheimer’s disease. Collectively, the evidence reviewed here strongly supports a role for diverse epigenetic mechanisms in memory formation, aging, and neurodegeneration in the brain. Full article
(This article belongs to the Special Issue Neuroepigenetic: From Bench to Bedside)
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