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Special Issue "Physiological or Pathological Molecular Alterations in Brain Aging"

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 (30 April 2021).

Special Issue Editors

Dr. Marika Cordaro
E-Mail Website
Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
Interests: physiology; molecular pathways; oxidative stress; inflammation
Special Issues and Collections in MDPI journals
Prof. Rossana Morabito
E-Mail
Co-Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, Italy
Interests: cell phisiology, ion transport of membrane, oxidative stress

Special Issue Information

Dear Colleagues,

Aging is defined as a progressive time‐related accumulation of changes involved in the increased susceptibility to disease and death. The brain seems to be particularly sensitive to the aging process since the appearance of neurodegenerative diseases, including Alzheimer's disease, Parkinson’s Disease, Vascular Dementia and many others, are exponential with the increasing age. There has been extensive research into these common diseases with a focus on establishing the etiology and developing therapies for their treatment and, most important, their prevention.

This Special Issue on “Physiological or pathological molecular alteration in brain aging” aims to cover all aspects of brain studies and health promotion and prevention, such as studies on mitochondrial dysfunction, autophagy, oxidative stress and inflammation associated with brain disorders.

In addition, we also welcome studies on pharmacological or phytochemical or nutraceutical effects of compounds that are able to counteract the impact of the age in the brain.

Research articles collecting data from both in vitro and in vivo investigations are appreciated, as are full reviews, including news in the field of the current understanding of molecular mechanisms involved in the brain during aging.

Dr. Marika Cordaro
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 papers will be 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

  • brain
  • aging
  • oxidative stress
  • autophagy
  • mitochondrial dysfunction
  • neurological disorders
  • neurodegeneration
  • neuroinflammation

Published Papers (3 papers)

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Research

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Open AccessArticle
Selective Activation of CNS and Reference PPARGC1A Promoters Is Associated with Distinct Gene Programs Relevant for Neurodegenerative Diseases
Int. J. Mol. Sci. 2021, 22(7), 3296; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073296 - 24 Mar 2021
Viewed by 445
Abstract
The transcriptional regulator peroxisome proliferator activated receptor gamma coactivator 1A (PGC-1α), encoded by PPARGC1A, has been linked to neurodegenerative diseases. Recently discovered CNS-specific PPARGC1A transcripts are initiated far upstream of the reference promoter, spliced to exon 2 of the reference gene, and [...] Read more.
The transcriptional regulator peroxisome proliferator activated receptor gamma coactivator 1A (PGC-1α), encoded by PPARGC1A, has been linked to neurodegenerative diseases. Recently discovered CNS-specific PPARGC1A transcripts are initiated far upstream of the reference promoter, spliced to exon 2 of the reference gene, and are more abundant than reference gene transcripts in post-mortem human brain samples. The proteins translated from the CNS and reference transcripts differ only at their N-terminal regions. To dissect functional differences between CNS-specific isoforms and reference proteins, we used clustered regularly interspaced short palindromic repeats transcriptional activation (CRISPRa) for selective endogenous activation of the CNS or the reference promoters in SH-SY5Y cells. Expression and/or exon usage of the targets was ascertained by RNA sequencing. Compared to controls, more differentially expressed genes were observed after activation of the CNS than the reference gene promoter, while the magnitude of alternative exon usage was comparable between activation of the two promoters. Promoter-selective associations were observed with canonical signaling pathways, mitochondrial and nervous system functions and neurological diseases. The distinct N-terminal as well as the shared downstream regions of PGC-1α isoforms affect the exon usage of numerous genes. Furthermore, associations of risk genes of amyotrophic lateral sclerosis and Parkinson’s disease were noted with differentially expressed genes resulting from the activation of the CNS and reference gene promoter, respectively. Thus, CNS-specific isoforms markedly amplify the biological functions of PPARGC1A and CNS-specific isoforms and reference proteins have common, complementary and selective functions relevant for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)
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Review

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Open AccessReview
Senescent Microglia: The Key to the Ageing Brain?
Int. J. Mol. Sci. 2021, 22(9), 4402; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094402 - 22 Apr 2021
Viewed by 331
Abstract
Ageing represents the single biggest risk factor for development of neurodegenerative disease. Despite being such long-lived cells, microglia have been relatively understudied for their role in the ageing process. Reliably identifying aged microglia has proven challenging, not least due to the diversity of [...] Read more.
Ageing represents the single biggest risk factor for development of neurodegenerative disease. Despite being such long-lived cells, microglia have been relatively understudied for their role in the ageing process. Reliably identifying aged microglia has proven challenging, not least due to the diversity of cell populations, and the limitations of available models, further complicated by differences between human and rodent cells. Consequently, the literature contains multiple descriptions and categorisations of microglia with neurotoxic phenotypes, including senescence, without any unifying markers. The role of microglia in brain homeostasis, particularly iron storage and metabolism, may provide a key to reliable identification. Full article
(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)
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Open AccessReview
Mitophagy and the Brain
Int. J. Mol. Sci. 2020, 21(24), 9661; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249661 - 18 Dec 2020
Cited by 2 | Viewed by 638
Abstract
Stress mechanisms have long been associated with neuronal loss and neurodegenerative diseases. The origin of cell stress and neuronal loss likely stems from multiple pathways. These include (but are not limited to) bioenergetic failure, neuroinflammation, and loss of proteostasis. Cells have adapted compensatory [...] Read more.
Stress mechanisms have long been associated with neuronal loss and neurodegenerative diseases. The origin of cell stress and neuronal loss likely stems from multiple pathways. These include (but are not limited to) bioenergetic failure, neuroinflammation, and loss of proteostasis. Cells have adapted compensatory mechanisms to overcome stress and circumvent death. One mechanism is mitophagy. Mitophagy is a form of macroautophagy, were mitochondria and their contents are ubiquitinated, engulfed, and removed through lysosome degradation. Recent studies have implicated mitophagy dysregulation in several neurodegenerative diseases and clinical trials are underway which target mitophagy pathways. Here we review mitophagy pathways, the role of mitophagy in neurodegeneration, potential therapeutics, and the need for further study. Full article
(This article belongs to the Special Issue Physiological or Pathological Molecular Alterations in Brain Aging)
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