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Biomolecules
Special Issues
Molecular Advances in Mechanism and Regulation of Lifespan and Aging
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Molecular Advances in Mechanism and Regulation of Lifespan and Aging

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 4303

Special Issue Editor

Dr. Mark McCormick

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA
Interests: biology of aging; lifespan; machine learning

Special Issue Information

Dear Colleagues,

Aging is an important unsolved problem in biology. It is also by far the most significant risk factor for many major human diseases, such as cancer, heart disease, and Alzheimer’s disease. As medical advances extend the average lifespan, the already large public health significance of these aging-related diseases will only continue to grow.

Many recent studies have uncovered genes, pathways, and interventions that can have dramatic effects on aging in laboratory models, most of which suggest that their underlying biology may be conserved in humans.

This Special Issue aims to highlight recent advances that have been made in this field that deepen our understanding of genes, pathways, and interventions that alter aging in any model system. It also aims to highlight findings that shed light on aging-related biology that has the potential for translation to a human clinical setting, whether in the context of specific aging-related human diseases or of aging itself. We are also interested in new models that enhance our ability to study aging, such as biomarkers.

We encourage researchers interested in these topics to present original research articles in these areas. In addition, review articles that cover the related research and provide concluding remarks and an outlook will also be considered for inclusion in this Special Issue.

Dr. Mark McCormick
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. Biomolecules 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 2700 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

  • aging
  • lifespan
  • healthspan

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Published Papers (2 papers)

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Research

16 pages, 4530 KiB  
Article
Bcl-2 Orthologues, Buffy and Debcl, Can Suppress Drp1-Dependent Age-Related Phenotypes in Drosophila
by Azra Hasan and Brian E. Staveley
Biomolecules 2024, 14(9), 1089; https://doi.org/10.3390/biom14091089 - 30 Aug 2024
Viewed by 311
Abstract
The relationship of Amyotrophic Lateral Sclerosis, Parkinson’s disease, and other age-related neurodegenerative diseases with mitochondrial dysfunction has led to our study of the mitochondrial fission gene Drp1 in Drosophila melanogaster and aspects of aging. Previously, the Drp1 protein has been demonstrated to interact [...] Read more.
The relationship of Amyotrophic Lateral Sclerosis, Parkinson’s disease, and other age-related neurodegenerative diseases with mitochondrial dysfunction has led to our study of the mitochondrial fission gene Drp1 in Drosophila melanogaster and aspects of aging. Previously, the Drp1 protein has been demonstrated to interact with the Drosophila Bcl-2 mitochondrial proteins, and Drp1 mutations can lead to mitochondrial dysfunction and neuronal loss. In this study, the Dopa decarboxylase-Gal4 (Ddc-Gal4) transgene was exploited to direct the expression of Drp1 and Drp1-RNAi transgenes in select neurons. Here, the knockdown of Drp1 seems to compromise locomotor function throughout life but does not alter longevity. The co-expression of Buffy suppresses the poor climbing induced by the knockdown of the Drp1 function. The consequences of Drp1 overexpression, which specifically reduced median lifespan and diminished climbing abilities over time, can be suppressed through the directed co-overexpression of pro-survival Bcl-2 gene Buffy or by the co-knockdown of the pro-cell death Bcl-2 homologue Debcl. Alteration of the expression of Drp1 acts to phenocopy neurodegenerative disease phenotypes in Drosophila, while overexpression of Buffy can counteract or rescue these phenotypes to improve overall health. The diminished healthy aging due to either the overexpression of Drp1 or the RNA interference of Drp1 has produced novel Drosophila models for investigating mechanisms underlying neurodegenerative disease. Full article
(This article belongs to the Special Issue Molecular Advances in Mechanism and Regulation of Lifespan and Aging)
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11 pages, 1692 KiB  
Article
3-Hydroxyanthranilic Acid Delays Paralysis in Caenorhabditis elegans Models of Amyloid-Beta and Polyglutamine Proteotoxicity
by Bradford T. Hull, Kayla M. Miller, Caroline Corban, Grant Backer, Susan Sheehan, Ron Korstanje and George L. Sutphin
Biomolecules 2024, 14(5), 599; https://doi.org/10.3390/biom14050599 - 18 May 2024
Viewed by 3657
Abstract
Age is the primary risk factor for neurodegenerative diseases such as Alzheimer’s and Huntington’s disease. Alzheimer’s disease is the most common form of dementia and a leading cause of death in the elderly population of the United States. No effective treatments for these [...] Read more.
Age is the primary risk factor for neurodegenerative diseases such as Alzheimer’s and Huntington’s disease. Alzheimer’s disease is the most common form of dementia and a leading cause of death in the elderly population of the United States. No effective treatments for these diseases currently exist. Identifying effective treatments for Alzheimer’s, Huntington’s, and other neurodegenerative diseases is a major current focus of national scientific resources, and there is a critical need for novel therapeutic strategies. Here, we investigate the potential for targeting the kynurenine pathway metabolite 3-hydroxyanthranilic acid (3HAA) using Caenorhabditis elegans expressing amyloid-beta or a polyglutamine peptide in body wall muscle, modeling the proteotoxicity in Alzheimer’s and Huntington’s disease, respectively. We show that knocking down the enzyme that degrades 3HAA, 3HAA dioxygenase (HAAO), delays the age-associated paralysis in both models. This effect on paralysis was independent of the protein aggregation in the polyglutamine model. We also show that the mechanism of protection against proteotoxicity from HAAO knockdown is mimicked by 3HAA supplementation, supporting elevated 3HAA as the mediating event linking HAAO knockdown to delayed paralysis. This work demonstrates the potential for 3HAA as a targeted therapeutic in neurodegenerative disease, though the mechanism is yet to be explored. Full article
(This article belongs to the Special Issue Molecular Advances in Mechanism and Regulation of Lifespan and Aging)
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