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Frontiers in Anti-aging Treatment Development

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 41093

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Dr. Emanuele Marzetti

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Department of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
Interests: geriatrics; sarcopenia; frailty; geriatric syndromes; geroscience; biomarkers; mitochondrial dysfunction
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Dr. Anna Picca

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Guest Editor

Department of Geriatrics, Neuroscience and Orthopedics, Fondazione Policlinico Universitario "A. Gemelli", IRCCS, 00168 Rome, Italy
Interests: aging; longevity; cognitive decline; biomarkers; inflammation; cellular bioenergetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflamm-aging is the term used to refer to the chronic low-grade inflammation that develops during aging and accompanies the development of chronic diseases (e.g., cancer, diabetes, cardiovascular disease, neurodegeneration) and functional decline in older adults. Derangements in cellular quality control systems are responsible for the accrual of intracellular “waste” (e.g., protein aggregates, damaged mitochondria, lipofuscin) and represent candidate mechanisms for the development of inflamm-aging. Indeed, many of these molecules have a pro-inflammatory nature and can be released at the systemic level unless efficiently cleared. The mechanisms that regulate the displacement of these molecules are among the processes that may be tackled for the development of anti-inflammatory strategies. Additional molecular pathways that become dysregulated during aging may actively contribute to local and systemic inflammation and thus warrant investigation.

This Special Issue aims at gathering contributions from researchers in the field of biogerontology and geroscience investigating anti-aging remedies and personalized anti-inflammatory interventions to extend one’s health- and lifespan.

We invite you to submit your latest original research or review articles to this Special Issue.

Prof. Dr. Emanuele Marzetti
Dr. Anna Picca
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

healthspan
lifespan
hallmarks of aging
cellular quality control
inflammation
gut microbiota
geroscience
intercellular signaling
geroprotective interventions
chronic conditions

Related Special Issue

Advances in Anti-aging Treatment Development 2.0 in International Journal of Molecular Sciences (1 article)

Published Papers (10 papers)

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Editorial

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2 pages, 199 KiB

Open AccessEditorial

Advancements in Anti-Aging Treatment Development

by Anna Picca and Emanuele Marzetti

Int. J. Mol. Sci. 2023, 24(10), 8515; https://doi.org/10.3390/ijms24108515 - 10 May 2023

Cited by 2 | Viewed by 1416

Abstract

Aging is a complex and multifactorial process resulting, at least partly, from the generation and accrual of damage in the setting of reduced resilience [...] Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

Research

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13 pages, 1689 KiB

Open AccessArticle

Circulating Inflammatory, Mitochondrial Dysfunction, and Senescence-Related Markers in Older Adults with Physical Frailty and Sarcopenia: A BIOSPHERE Exploratory Study

by Anna Picca, Riccardo Calvani, Hélio José Coelho-Júnior, Federico Marini, Francesco Landi and Emanuele Marzetti

Int. J. Mol. Sci. 2022, 23(22), 14006; https://doi.org/10.3390/ijms232214006 - 13 Nov 2022

Cited by 16 | Viewed by 2339

Abstract

Multisystem derangements encompassing musculoskeletal, stress, and metabolic response have been described in older adults with physical frailty and sarcopenia (PF&S). Whether PF&S is also associated with markers of cellular senescence has yet to be explored. To address this research question, we quantified the serum levels of selected inflammatory, mitochondrial, and senescence-associated secretory phenotype (SASP)-related factors in 22 older adults with PF&S (mean age 75.5 ± 4.7 years; 81.8% women) and 27 nonPF&S controls (mean age 75.0 ± 4.4 years; 62.9% women) and evaluated their association with PF&S. Markers of inflammation (interleukin (IL)1-β, IL6, and tumor necrosis factor α (TNF-α)), matrix remodeling (Serpin E1, intercellular adhesion molecule 1 (ICAM-1), and tissue inhibitor of metalloproteinases 1 (TIMP-1)), mitochondrial dysfunction (growth/differentiation factor 15 (GDF15) and fibroblast growth factor 21 (FGF21)), Activin A, and glial fibrillary acidic protein (GFAP) were assayed. Serum levels of TNF-α and those of the SASP-related factors ICAM-1 and TIMP-1 were found to be higher, while IL1-β and IL6 were lower in PF&S participants compared with controls. Partial least squares discriminant analysis allowed discrimination of PF&S from nonPF&S participants with 74.0 ± 3.4% accuracy. Markers that significantly contributed to the classification were ICAM-1, TIMP-1, TNF-α, GFAP, and IL6. Future studies are warranted to establish whether inflammatory and SASP-related pathways are causally linked to the development and progression of PF&S, and may represent new targets for interventions. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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17 pages, 2003 KiB

Open AccessArticle

Analysis of the Effects of Ninjin’yoeito on Physical Frailty in Mice

by Shotaro Otsuka, Keita Fukumaru, Akira Tani, Seiya Takada, Kiyoshi Kikuchi, Kosuke Norimatsu, Ryoma Matsuzaki, Teruki Matsuoka, Harutoshi Sakakima, Yuji Omiya, Keita Mizuno, Yosuke Matsubara and Ikuro Maruyama

Int. J. Mol. Sci. 2022, 23(19), 11183; https://doi.org/10.3390/ijms231911183 - 23 Sep 2022

Cited by 3 | Viewed by 2251

Abstract

Physical frailty is an aging-related clinical syndrome involving decreases in body weight, mobility, activity, and walking speed that occurs in individuals with sarcopenia and is accelerated by increased oxidative stress. Ninjin’yoeito, a traditional Japanese Kampo medicine, is used for treating conditions, including anemia and physical weakness. Here, we investigated whether ninjin’yoeito could improve physical frailty by controlling oxidative stress in the senescence-accelerated mouse prone 8 (SAMP8) model. First, SAMP8 mice were divided into two groups, ninjin’yoeito treated and untreated, with the former consuming a diet containing 3% ninjin’yoeito from 3 months of age. At 7 months of age, body weight, motor function, locomotor activity, and mean walking speed were measured. Subsequently, mice were euthanized and measured for muscle weight, 8-hydroxy-2′-deoxyguanosine levels in muscle and brain, and cleaved caspase-3 expression in brain. The results showed reductions in weight, locomotor function, locomotion, and average walking speed in the untreated group, which were significantly improved by ninjin’yoeito. Furthermore, 8-hydroxy-2′-deoxyguanosine levels were reduced in muscle and brain from ninjin’yoeito-treated mice, compared with the levels in untreated mice; cleaved caspase-3 expression was similarly reduced in brain from the treated mice, indicating reduced apoptosis. Our findings suggest that ninjin’yoeito inhibits sarcopenia-based physical frailty through its antioxidant effects. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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Review

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26 pages, 1241 KiB

Open AccessReview

Type 2 Diabetes Mellitus and Alzheimer’s Disease: Shared Molecular Mechanisms and Potential Common Therapeutic Targets

by Rim Hamzé, Etienne Delangre, Stefania Tolu, Manon Moreau, Nathalie Janel, Danielle Bailbé and Jamileh Movassat

Int. J. Mol. Sci. 2022, 23(23), 15287; https://doi.org/10.3390/ijms232315287 - 4 Dec 2022

Cited by 31 | Viewed by 5187

Abstract

The global prevalence of diabetes mellitus and Alzheimer’s disease is increasing alarmingly with the aging of the population. Numerous epidemiological data suggest that there is a strong association between type 2 diabetes and an increased risk of dementia. These diseases are both degenerative and progressive and share common risk factors. The amyloid cascade plays a key role in the pathophysiology of Alzheimer’s disease. The accumulation of amyloid beta peptides gradually leads to the hyperphosphorylation of tau proteins, which then form neurofibrillary tangles, resulting in neurodegeneration and cerebral atrophy. In Alzheimer’s disease, apart from these processes, the alteration of glucose metabolism and insulin signaling in the brain seems to induce early neuronal loss and the impairment of synaptic plasticity, years before the clinical manifestation of the disease. The large amount of evidence on the existence of insulin resistance in the brain during Alzheimer’s disease has led to the description of this disease as “type 3 diabetes”. Available animal models have been valuable in the understanding of the relationships between type 2 diabetes and Alzheimer’s disease, but to date, the mechanistical links are poorly understood. In this non-exhaustive review, we describe the main molecular mechanisms that may link these two diseases, with an emphasis on impaired insulin and IGF-1 signaling. We also focus on GSK3β and DYRK1A, markers of Alzheimer’s disease, which are also closely associated with pancreatic β-cell dysfunction and type 2 diabetes, and thus may represent common therapeutic targets for both diseases. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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27 pages, 2613 KiB

Open AccessReview

Rejuvenation: Turning Back Time by Enhancing CISD2

by Chi-Hsiao Yeh, Zhao-Qing Shen, Ching-Cheng Lin, Chung-Kuang Lu and Ting-Fen Tsai

Int. J. Mol. Sci. 2022, 23(22), 14014; https://doi.org/10.3390/ijms232214014 - 13 Nov 2022

Cited by 8 | Viewed by 4845

Abstract

The aging human population with age-associated diseases has become a problem worldwide. By 2050, the global population of those who are aged 65 years and older will have tripled. In this context, delaying age-associated diseases and increasing the healthy lifespan of the aged population has become an important issue for geriatric medicine. CDGSH iron-sulfur domain 2 (CISD2), the causative gene for Wolfram syndrome 2 (WFS2; MIM 604928), plays a pivotal role in mediating lifespan and healthspan by maintaining mitochondrial function, endoplasmic reticulum integrity, intracellular Ca²⁺ homeostasis, and redox status. Here, we summarize the most up-to-date publications on CISD2 and discuss the crucial role that this gene plays in aging and age-associated diseases. This review mainly focuses on the following topics: (1) CISD2 is one of the few pro-longevity genes identified in mammals. Genetic evidence from loss-of-function (knockout mice) and gain-of-function (transgenic mice) studies have demonstrated that CISD2 is essential to lifespan control. (2) CISD2 alleviates age-associated disorders. A higher level of CISD2 during natural aging, when achieved by transgenic overexpression, improves Alzheimer’s disease, ameliorates non-alcoholic fatty liver disease and steatohepatitis, and maintains corneal epithelial homeostasis. (3) CISD2, the expression of which otherwise decreases during natural aging, can be pharmaceutically activated at a late-life stage of aged mice. As a proof-of-concept, we have provided evidence that hesperetin is a promising CISD2 activator that is able to enhance CISD2 expression, thus slowing down aging and promoting longevity. (4) The anti-aging effect of hesperetin is mainly dependent on CISD2 because transcriptomic analysis of the skeletal muscle reveals that most of the differentially expressed genes linked to hesperetin are regulated by hesperetin in a CISD2-dependent manner. Furthermore, three major metabolic pathways that are affected by hesperetin have been identified in skeletal muscle, namely lipid metabolism, protein homeostasis, and nitrogen and amino acid metabolism. This review highlights the urgent need for CISD2-based pharmaceutical development to be used as a potential therapeutic strategy for aging and age-associated diseases. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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11 pages, 1102 KiB

Open AccessReview

Ellagic Acid and Its Anti-Aging Effects on Central Nervous System

by Heyu Zhu, Yuanmei Yan, Yi Jiang and Xianfang Meng

Int. J. Mol. Sci. 2022, 23(18), 10937; https://doi.org/10.3390/ijms231810937 - 19 Sep 2022

Cited by 18 | Viewed by 3779

Abstract

Aging is an unavoidable biological process that leads to the decline of human function and the reduction in people’s quality of life. Demand for anti-aging medicines has become very urgent. Many studies have shown that ellagic acid (EA), a phenolic compound widely distributed in dicotyledonous plants, has powerful anti-inflammation and antioxidant properties. Moreover, it has been demonstrated that EA can enhance neuronal viability, reduce neuronal defects, and alleviate damage in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and cerebral ischemia. This paper reviews the biochemical functions and neuroprotective effects of EA, showing the clinical value of its application. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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15 pages, 1431 KiB

Open AccessReview

Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging

by Hyun Jung Hwang, Nayeon Kim, Allison B. Herman, Myriam Gorospe and Jae-Seon Lee

Int. J. Mol. Sci. 2022, 23(17), 10135; https://doi.org/10.3390/ijms231710135 - 4 Sep 2022

Cited by 21 | Viewed by 5789

Abstract

Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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17 pages, 1884 KiB

Open AccessReview

Glucose Metabolism, Neural Cell Senescence and Alzheimer’s Disease

by Qianqian Wang, Linyan Duan, Xingfan Li, Yifu Wang, Wenna Guo, Fangxia Guan and Shanshan Ma

Int. J. Mol. Sci. 2022, 23(8), 4351; https://doi.org/10.3390/ijms23084351 - 14 Apr 2022

Cited by 34 | Viewed by 7667

Abstract

Alzheimer’s disease (AD), an elderly neurodegenerative disorder with a high incidence and progressive memory decline, is one of the most expensive, lethal, and burdening diseases. To date, the pathogenesis of AD has not been fully illustrated. Emerging studies have revealed that cellular senescence and abnormal glucose metabolism in the brain are the early hallmarks of AD. Moreover, cellular senescence and glucose metabolism disturbance in the brain of AD patients may precede amyloid-β deposition or Tau protein phosphorylation. Thus, metabolic reprogramming targeting senescent microglia and astrocytes may be a novel strategy for AD intervention and treatment. Here, we recapitulate the relationships between neural cell senescence and abnormal glucose metabolism (e.g., insulin signaling, glucose and lactate metabolism) in AD. We then discuss the potential perspective of metabolic reprogramming towards an AD intervention, providing a theoretical basis for the further exploration of the pathogenesis of and therapeutic approach toward AD. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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15 pages, 945 KiB

Open AccessReview

by Ursula Föger-Samwald, Katharina Kerschan-Schindl, Maria Butylina and Peter Pietschmann

Int. J. Mol. Sci. 2022, 23(5), 2701; https://doi.org/10.3390/ijms23052701 - 28 Feb 2022

Cited by 32 | Viewed by 4425

Abstract

Age-related chronic diseases are an enormous burden to modern societies worldwide. Among these, osteoporosis, a condition that predisposes individuals to an increased risk of fractures, substantially contributes to increased mortality and health-care costs in elderly. It is now well accepted that advanced chronical age is one of the main risk factors for chronical diseases. Hence, targeting fundamental aging mechanisms such as senescence has become a promising option in the treatment of these diseases. Moreover, for osteoporosis, the main pathophysiological concepts arise from menopause causing estrogen deficiency, and from aging. Here, we focus on recent advances in the understanding of senescence-related mechanisms contributing to age-related bone loss. Furthermore, treatment options for senile osteoporosis targeting senescent cells are reviewed. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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Other

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24 pages, 3750 KiB

Open AccessPerspective

Transcranial Electromagnetic Wave Treatment: A Fountain of Healthy Longevity?

by Gary Arendash and Chuanhai Cao

Int. J. Mol. Sci. 2023, 24(11), 9652; https://doi.org/10.3390/ijms24119652 - 2 Jun 2023

Viewed by 1846

Abstract

Most diseases of older age have as their common denominator a dysfunctional immune system, wherein a low, chronic level of inflammation is present due to an imbalance of pro-inflammatory cytokines over anti-inflammatory cytokines that develops during aging (“inflamm-aging”). A gerotherapeutic that can restore the immune balance to that shared by young/middle-aged adults and many centenarians could reduce the risk of those age-related diseases and increase healthy longevity. In this perspectives paper, we discuss potential longevity interventions that are being evaluated and compare them to a novel gerotherapeutic currently being evaluated in humans—Transcranial Electromagnetic Wave Treatment (TEMT). TEMT is provided non-invasively and safety through a novel bioengineered medical device—the MemorEM—that allows for near complete mobility during in-home treatments. Daily TEMT to mild/moderate Alzheimer’s Disease (AD) patients over a 2-month period rebalanced 11 of 12 cytokines in blood back to that of normal aged adults. A very similar TEMT-induced rebalancing of cytokines occurred in the CSF/brain for essentially all seven measurable cytokines. Overall inflammation in both blood and brain was dramatically reduced by TEMT over a 14–27 month period, as measured by C-Reactive Protein. In these same AD patients, a reversal of cognitive impairment was observed at 2 months into treatment, while cognitive decline was stopped over a 2½ year period of TEMT. Since most age-related diseases have the commonality of immune imbalance, it is reasonable to postulate that TEMT could rebalance the immune system in many age-related diseases as it appears to do in AD. We propose that TEMT has the potential to reduce the risk/severity of age-related diseases by rejuvenating the immune system to a younger age, resulting in reduced brain/body inflammation and a substantial increase in healthy longevity. Full article

(This article belongs to the Special Issue Frontiers in Anti-aging Treatment Development)

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