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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: 31 May 2025 | Viewed by 13191

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 (5 papers)

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Research

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28 pages, 3184 KiB  
Article
Possible Anti-Aging and Anti-Stress Effects of Long-Term Transcendental Meditation Practice: Differences in Gene Expression, EEG Correlates of Cognitive Function, and Hair Steroids
by Supaya Wenuganen, Kenneth G. Walton, Frederick T. Travis, Tobias Stalder, R. Keith Wallace, Meera Srivastava and John Fagan
Biomolecules 2025, 15(3), 317; https://doi.org/10.3390/biom15030317 - 20 Feb 2025
Viewed by 3387
Abstract
Background: Our previous comparison of peripheral blood mononuclear cells (PBMCs) from long-term Transcendental Meditation® (TM®) practitioners and matched non-practitioner controls found 200 differentially expressed (DE) genes. Bioinformatics analyses of these DE genes suggested a reduced risk of diseases associated [...] Read more.
Background: Our previous comparison of peripheral blood mononuclear cells (PBMCs) from long-term Transcendental Meditation® (TM®) practitioners and matched non-practitioner controls found 200 differentially expressed (DE) genes. Bioinformatics analyses of these DE genes suggested a reduced risk of diseases associated with stress and aging in the TM group. Here we assessed additional signs of reduced stress and aging. Methods: A sample of 15 of the 200 DE genes was studied using qPCR in PBMCs from 40-year TM practitioners (“Old TM”, n = 23) compared to a “Young Control” group (n = 19) and an “Old Control” group (n = 21) of non-meditators. In these three groups, plus a “Young TM”, 12-year practitioner group (n = 26), we also studied EEG-based parameters of cognitive function (the Brain Integration Scale (BIS), and latency of three components of the event-related potential (ERP)). Finally, using LC/MS/MS, we compared persistent levels of cortisol (F) and its inactive congener, cortisone (E), in hair. Results: qPCR analysis showed that 13 of the 15 genes were more highly expressed in Old Controls than in Young Controls. In the Old TM group, 7 of these 13 were lower than in Old Controls. Both TM groups had higher BIS scores than their age-matched controls. The Old TM group had shorter N2, P3a, and P3b latencies than the Old Control group, and latencies in the Old TM group were not longer than in the Young Control group. The Hair F/Hair E ratio was higher in the control subgroups than in their age-matched TM subgroups, and Hair F was higher in the Young Control and combined control groups than in the Young TM and combined TM groups. Conclusions: These results are consistent with reductions in biomarkers of chronic stress and biological age in long-term TM meditators. They are also consistent with results from the previous study suggesting that TM practice lowers energy consumption or leads to more efficient energy metabolism. Full article
(This article belongs to the Special Issue Molecular Advances in Mechanism and Regulation of Lifespan and Aging)
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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 1015
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 4634
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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Review

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33 pages, 1455 KiB  
Review
Pathological and Inflammatory Consequences of Aging
by Mario García-Domínguez
Biomolecules 2025, 15(3), 404; https://doi.org/10.3390/biom15030404 - 12 Mar 2025
Viewed by 2205
Abstract
Aging is a complex, progressive, and irreversible biological process that entails numerous structural and functional changes in the organism. These changes affect all bodily systems, reducing their ability to respond and adapt to the environment. Chronic inflammation is one of the key factors [...] Read more.
Aging is a complex, progressive, and irreversible biological process that entails numerous structural and functional changes in the organism. These changes affect all bodily systems, reducing their ability to respond and adapt to the environment. Chronic inflammation is one of the key factors driving the development of age-related diseases, ultimately causing a substantial decline in the functional abilities of older individuals. This persistent inflammatory state (commonly known as “inflammaging”) is characterized by elevated levels of pro-inflammatory cytokines, an increase in oxidative stress, and a perturbation of immune homeostasis. Several factors, including cellular senescence, contribute to this inflammatory milieu, thereby amplifying conditions such as cardiovascular disease, neurodegeneration, and metabolic disorders. Exploring the mechanisms of chronic inflammation in aging is essential for developing targeted interventions aimed at promoting healthy aging. This review explains the strong connection between aging and chronic inflammation, highlighting potential therapeutic approaches like pharmacological treatments, dietary strategies, and lifestyle changes. Full article
(This article belongs to the Special Issue Molecular Advances in Mechanism and Regulation of Lifespan and Aging)
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13 pages, 673 KiB  
Review
Perception and Longevity Control in Invertebrate Model Organisms—A Mini-Review of Recent Advances
by Nicholas Pontillo and Yang Lyu
Biomolecules 2025, 15(2), 187; https://doi.org/10.3390/biom15020187 - 28 Jan 2025
Viewed by 1206
Abstract
Perception alone can, in some cases, be sufficient to modulate aging and longevity. These influences on aging are perhaps mediated by changes in motivational states that regulate metabolism and physiology to impact health. Simple invertebrate models uniquely enable detailed dissection of integrative pathways [...] Read more.
Perception alone can, in some cases, be sufficient to modulate aging and longevity. These influences on aging are perhaps mediated by changes in motivational states that regulate metabolism and physiology to impact health. Simple invertebrate models uniquely enable detailed dissection of integrative pathways linking perceptions to aging and remain the leading systems for advancing this field. Over the past 25 years, studies using the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans have demonstrated that sensory cues, such as those related to food or mating, can influence aging independently of the physical acts associated with them. In this review, we highlight recent advancements in these invertebrate models, focusing on two key areas of progress: (i) the discovery of lifespan modulation driven by novel sensory cues across multiple modalities, including non-sexual social experience, light, and dietary choices; and (ii) the assignment of new aging-regulation functions to specific neurons downstream of sensory perception. The latter offers an exciting first glimpse at the neuronal circuits integrating sensory cues, motivational states, physiology, and aging. Full article
(This article belongs to the Special Issue Molecular Advances in Mechanism and Regulation of Lifespan and Aging)
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