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Molecular Research in Gerontology and Geriatrics
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Molecular Research in Gerontology and Geriatrics

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 (31 July 2020) | Viewed by 40627

Special Issue Editor

Prof. Gaetano Serviddio

E-Mail Website
Guest Editor
Universita degli Studi di Foggia, Department of Medical and Surgical Sciences, Foggia, Italy
Interests: liver metabolism; aging; mitochondria and redox balance

Special Issue Information

Dear Colleagues,

Though “aging is the only way to live longer”, a new era in geriatric sciences is incoming. The increased life expectancy is provoking a progressive aging of the population worldwide. Sustaining healthcare and quality of life in elderly people is a political and social burden. Moreover, recent advances in the understanding of molecular mechanisms responsible for aging and geriatric diseases may accelerate this process. Full pathogenetic comprehension and especially treatment options of aging-related disorders remained scarce for decades, although today, the rise of new important discoveries in this field is in a boost phase. We know that many geriatric diseases are driven by a variety of conditions, such as inflammation, dysmetabolism, microbiota alterations, oxidative stress, mitochondria, endoplasmic dysfunction, etc. Accordingly, DNA methylation, autophagy, and cell senescence are emerging as driving forces in the aging process. Along these lines, a number of new therapeutic strategies are under investigation, and more attention is being given to drugs for chronic diseases in elderly people. In this scenario, aging is only the phenotype, and it is extremely important to clarify the molecular mechanisms accounting for aging and age-related diseases. The aim of this Special Issue is to review recent advances in molecular mechanisms involved in aging, dementia, cell senescence, metabolism of age-related neurodegenerative disorders, frailty, geriatric multimorbidity, and new molecular therapeutic strategies.

Prof. Gaetano Serviddio
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. 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

  • aging
  • neurodegenerative disorders
  • molecular strategy
  • senescence metabolism

Published Papers (6 papers)

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Review

28 pages, 1757 KiB  
Review
The Dual Role of Glutamatergic Neurotransmission in Alzheimer’s Disease: From Pathophysiology to Pharmacotherapy
by Vidyasagar Naik Bukke, Moola Archana, Rosanna Villani, Antonino Davide Romano, Agata Wawrzyniak, Krzysztof Balawender, Stanislaw Orkisz, Sarah Beggiato, Gaetano Serviddio and Tommaso Cassano
Int. J. Mol. Sci. 2020, 21(20), 7452; https://doi.org/10.3390/ijms21207452 - 9 Oct 2020
Cited by 60 | Viewed by 11553
Abstract
Alzheimer’s disease (AD) is an age-related dementia and neurodegenerative disorder, characterized by Aβ and tau protein deposition impairing learning, memory and suppressing synaptic plasticity of neurons. Increasing evidence suggests that there is a link between the glucose and glutamate alterations with age that [...] Read more.
Alzheimer’s disease (AD) is an age-related dementia and neurodegenerative disorder, characterized by Aβ and tau protein deposition impairing learning, memory and suppressing synaptic plasticity of neurons. Increasing evidence suggests that there is a link between the glucose and glutamate alterations with age that down-regulates glucose utilization reducing glutamate levels in AD patients. Deviations in brain energy metabolism reinforce the development of AD by hampering glutamate levels in the brain. Glutamate is a nonessential amino acid and the major excitatory neurotransmitter synthesized from glucose. Alterations in cerebral glucose and glutamate levels precede the deposition of Aβ plaques. In the brain, over 40% of neuronal synapses are glutamatergic and disturbances in glutamatergic function have been implicated in pathophysiology of AD. Nevertheless, targeting the glutamatergic system seems to be a promising strategy to develop novel, improved therapeutics for AD. Here, we review data supporting the involvement of the glutamatergic system in AD pathophysiology as well as the efficacy of glutamatergic agents in this neurodegenerative disorder. We also discuss exciting new prospects for the development of improved therapeutics for this devastating disorder. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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12 pages, 504 KiB  
Review
Interaction between Cognitive Reserve and Biomarkers in Alzheimer Disease
by Elena Carapelle, Ciro Mundi, Tommaso Cassano and Carlo Avolio
Int. J. Mol. Sci. 2020, 21(17), 6279; https://doi.org/10.3390/ijms21176279 - 30 Aug 2020
Cited by 11 | Viewed by 2805
Abstract
Patients with comparable degree of neuropathology could show different cognitive impairments. This could be explained with the concept of cognitive reserve (CR), which includes a passive and an active component. In particular, CR is used to explain the gap between tissue damage and [...] Read more.
Patients with comparable degree of neuropathology could show different cognitive impairments. This could be explained with the concept of cognitive reserve (CR), which includes a passive and an active component. In particular, CR is used to explain the gap between tissue damage and clinical symptoms that has been observed in dementia and, in particular, in patients affected by Alzheimer disease (AD). Different studies confirm brain neuroplasticity. Our preliminary study demonstrated that AD patients with high education showed a CR inversely associated with glucose uptake measured in fluorodeoxyglucose positron emission tomography (FDG-PET), whereas the inverse correlation was observed in AD patients with low education. In other words, our findings suggest that CR compensates the neurodegeneration and allows the maintenance of patients’ cognitive performance. Best understanding of the concept of CR could lead to interventions to slow cognitive aging or reduce the risk of dementia. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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14 pages, 808 KiB  
Review
Sclerostin and Vascular Pathophysiology
by Antonino Catalano, Federica Bellone, Nunziata Morabito and Francesco Corica
Int. J. Mol. Sci. 2020, 21(13), 4779; https://doi.org/10.3390/ijms21134779 - 6 Jul 2020
Cited by 35 | Viewed by 4535
Abstract
There is cumulating evidence for a contribution of Wnt signaling pathways in multiple processes involved in atherosclerosis and vascular aging. Wnt signaling plays a role in endothelial dysfunction, in the proliferation and migration of vascular smooth muscle cells (VSMCs) and intimal thickening. Moreover, [...] Read more.
There is cumulating evidence for a contribution of Wnt signaling pathways in multiple processes involved in atherosclerosis and vascular aging. Wnt signaling plays a role in endothelial dysfunction, in the proliferation and migration of vascular smooth muscle cells (VSMCs) and intimal thickening. Moreover, it interferes with inflammation processes, monocyte adhesion and migration, as well as with foam cell formation and vascular calcification progression. Sclerostin is a negative regulator of the canonical Wnt signaling pathway and, accordingly, the consequence of increased sclerostin availability can be disruption of the Wnt signalling cascade. Sclerostin is becoming a marker for clinical and subclinical vascular diseases and several lines of evidence illustrate its role in the pathophysiology of the vascular system. Sclerostin levels increase with aging and persist higher in some diseases (e.g., diabetes, chronic kidney disease) that are known to precipitate atherosclerosis and enhance cardiovascular risk. Current knowledge on the association between sclerostin and vascular diseases is summarized in this review. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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10 pages, 501 KiB  
Review
Molecular Aspects and Treatment of Iron Deficiency in the Elderly
by Antonino Davide Romano, Annalisa Paglia, Francesco Bellanti, Rosanna Villani, Moris Sangineto, Gianluigi Vendemiale and Gaetano Serviddio
Int. J. Mol. Sci. 2020, 21(11), 3821; https://doi.org/10.3390/ijms21113821 - 28 May 2020
Cited by 14 | Viewed by 6956
Abstract
Iron deficiency (ID) is the most frequent nutritional deficiency in the whole population worldwide, and the second most common cause of anemia in the elderly. The prevalence of anemia is expecting to rise shortly, because of an ageing population. Even though WHO criteria [...] Read more.
Iron deficiency (ID) is the most frequent nutritional deficiency in the whole population worldwide, and the second most common cause of anemia in the elderly. The prevalence of anemia is expecting to rise shortly, because of an ageing population. Even though WHO criteria define anemia as a hemoglobin serum concentration <12 g/dL in women and <13 g/dL in men, several authors propose different and specific cut-off values for the elderly. Anemia in aged subjects impacts health and quality of life, and it is associated with several negative outcomes, such as longer time of hospitalization and a higher risk of disability. Furthermore, it is an independent risk factor of increased morbidity and mortality. Even though iron deficiency anemia is a common disorder in older adults, it should be not considered as a normal ageing consequence, but a sign of underlying dysfunction. Relating to the molecular mechanism in Iron Deficiency Anemia (IDA), hepcidin has a key role in iron homeostasis. It downregulates the iron exporter ferroportin, inhibiting both iron absorption and release. IDA is frequently dependent on blood loss, especially caused by gastrointestinal lesions. Thus, a diagnostic algorithm for IDA should include invasive investigation such as endoscopic procedures. The treatment choice is influenced by the severity of anemia, underlying conditions, comorbidities, and the clinical state of the patient. Correction of anemia and iron supplementation should be associated with the treatment of the causal disease. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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17 pages, 964 KiB  
Review
Molecular Basis of Bone Aging
by Addolorata Corrado, Daniela Cici, Cinzia Rotondo, Nicola Maruotti and Francesco Paolo Cantatore
Int. J. Mol. Sci. 2020, 21(10), 3679; https://doi.org/10.3390/ijms21103679 - 23 May 2020
Cited by 46 | Viewed by 10432
Abstract
A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes [...] Read more.
A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue and structural levels; they include alterations of bone cell differentiation and activity, oxidative stress, genetic damage and the altered responses of bone cells to various biological signals and to mechanical loading. The molecular mechanisms responsible for these changes remain greatly unclear and many data derived from in vitro or animal studies appear to be conflicting and heterogeneous, probably due to the different experimental approaches; nevertheless, understanding the main physio-pathological processes that cause bone senescence is essential for the development of new potential therapeutic options for treating age-related bone loss. This article reviews the current knowledge concerning the molecular mechanisms underlying the pathogenesis of age-related bone changes. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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24 pages, 1073 KiB  
Review
Molecular Mechanisms of Premature Aging in Hemodialysis: The Complex Interplay between Innate and Adaptive Immune Dysfunction
by Vincenzo Losappio, Rossana Franzin, Barbara Infante, Giulia Godeas, Loreto Gesualdo, Alberto Fersini, Giuseppe Castellano and Giovanni Stallone
Int. J. Mol. Sci. 2020, 21(10), 3422; https://doi.org/10.3390/ijms21103422 - 12 May 2020
Cited by 29 | Viewed by 3945
Abstract
Hemodialysis (HD) patient are known to be susceptible to a wide range of early and long-term complication such as chronic inflammation, infections, malnutrition, and cardiovascular disease that significantly affect the incidence of mortality. A large gap between the number of people with end-stage [...] Read more.
Hemodialysis (HD) patient are known to be susceptible to a wide range of early and long-term complication such as chronic inflammation, infections, malnutrition, and cardiovascular disease that significantly affect the incidence of mortality. A large gap between the number of people with end-stage kidney disease (ESKD) and patients who received kidney transplantation has been identified. Therefore, there is a huge need to explore the underlying pathophysiology of HD complications in order to provide treatment guidelines. The immunological dysregulation, involving both the innate and adaptive response, plays a crucial role during the HD sessions and in chronic, maintenance treatments. Innate immune system mediators include the dysfunction of neutrophils, monocytes, and natural killer (NK) cells with signaling mediated by NOD-like receptor P3 (NLRP3) and Toll-like receptor 4 (TLR4); in addition, there is a significant activation of the complement system that is mediated by dialysis membrane-surfaces. These effectors induce a persistent, systemic, pro-inflammatory, and pro-coagulant milieu that has been described as inflammaging. The adaptive response, the imbalance in the CD4+/CD8+ T cell ratio, and the reduction of Th2 and regulatory T cells, together with an altered interaction with B lymphocyte by CD40/CD40L, have been mainly implicated in immune system dysfunction. Altogether, these observations suggest that intervention targeting the immune system in HD patients could improve morbidity and mortality. The purpose of this review is to expand our understanding on the role of immune dysfunction in both innate and adaptive response in patients undergoing hemodialysis treatment. Full article
(This article belongs to the Special Issue Molecular Research in Gerontology and Geriatrics)
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