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Effects of Chronic Inflammation on Brain Ageing and Sensory Decline
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Effects of Chronic Inflammation on Brain Ageing and Sensory Decline

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 13104

Special Issue Editor

Dr. Srdjan Vlajkovic

E-Mail Website
Guest Editor
Department of Physiology and The Eisdell Moore Centre, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
Interests: sensory systems; auditory neuroscience; inner ear diseases; inner ear therapeutics; hearing loss; inflammation; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

'Inflammaging' describes the relationship between low-grade chronic inflammation and accelerated ageing. It contributes to the pathogenesis of several age-related diseases, including those affecting the brain and sensory systems. Inflammaging is the long-term result of the chronic stimulation of the innate immune system, which can become damaging during ageing. Genetic and environmental factors that promote inflammation contribute to increased susceptibility to age-related disorders, whilst healthy ageing could partly relate to reduced levels of chronic inflammation.

This Special Issue aims to elucidate the role of chronic inflammation in the age-related brain and sensory disorders and propose novel strategies to protect the brain and sensory function. We invite investigators to contribute original research articles and review articles that will address the molecular mechanisms, biomarkers and prospective therapies of age-related inflammatory disorders in the brain and sensory organs. Please note that pure clinical or model studies are unsuitable for this journal, but clinical submissions with biomolecular studies are welcome.

Prof. Dr. Srdjan Vlajkovic
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

  • brain
  • sensory systems
  • inflammation
  • ageing
  • neurodegenerative disorders
  • age-related hearing loss
  • age-related macular degeneration
  • neuroprotection

Published Papers (4 papers)

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Research

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16 pages, 4402 KiB  
Article
Effects of Combined Gentamicin and Furosemide Treatment on Cochlear Macrophages
by Liana Sargsyan, Austin R. Swisher, Alisa P. Hetrick and Hongzhe Li
Int. J. Mol. Sci. 2022, 23(13), 7343; https://doi.org/10.3390/ijms23137343 - 1 Jul 2022
Viewed by 1619
Abstract
Combining aminoglycosides and loop diuretics often serves as an effective ototoxic approach to deafen experimental animals. The treatment results in rapid hair cell loss with extended macrophage presence in the cochlea, creating a sterile inflammatory environment. Although the early recruitment of macrophages is [...] Read more.
Combining aminoglycosides and loop diuretics often serves as an effective ototoxic approach to deafen experimental animals. The treatment results in rapid hair cell loss with extended macrophage presence in the cochlea, creating a sterile inflammatory environment. Although the early recruitment of macrophages is typically neuroprotective, the delay in the resolution of macrophage activity can be a complication if the damaged cochlea is used as a model to study subsequent therapeutic strategies. Here, we applied a high dose combination of systemic gentamicin and furosemide in C57 BL/6 and CBA/CaJ mice and studied the ototoxic consequences in the cochlea, including hair cell survival, ribbon synaptic integrity, and macrophage activation up to 15-day posttreatment. The activity of macrophages in the basilar membrane was correlated to the severity of cochlear damage, particularly the hair cell damage. Comparatively, C57 BL/6 cochleae were more vulnerable to the ototoxic challenge with escalated macrophage activation. In addition, the ribbon synaptic deterioration was disproportionately limited when compared to the degree of outer hair cell loss in CBA/CaJ mice. The innate and differential otoprotection in CBA/CaJ mice appears to be associated with the rapid activation of cochlear macrophages and a certain level of synaptogenesis after the combined gentamicin and furosemide treatment. Full article
(This article belongs to the Special Issue Effects of Chronic Inflammation on Brain Ageing and Sensory Decline)
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Review

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0 pages, 3066 KiB  
Review
Neuroinflammation in Parkinson’s Disease: From Gene to Clinic: A Systematic Review
by Carlos Castillo-Rangel, Gerardo Marin, Karla Aketzalli Hernández-Contreras, Micheel Merari Vichi-Ramírez, Cristofer Zarate-Calderon, Osvaldo Torres-Pineda, Dylan L. Diaz-Chiguer, David De la Mora González, Erick Gómez Apo, Javier Alejandro Teco-Cortes, Flor de María Santos-Paez, María de los Ángeles Coello-Torres, Matías Baldoncini, Gervith Reyes Soto, Gonzalo Emiliano Aranda-Abreu and Luis I. García
Int. J. Mol. Sci. 2023, 24(6), 5792; https://doi.org/10.3390/ijms24065792 - 17 Mar 2023
Cited by 12 | Viewed by 3564
Abstract
Parkinson’s disease is a neurodegenerative disease whose progression and clinical characteristics have a close bidirectional and multilevel relationship with the process of neuroinflammation. In this context, it is necessary to understand the mechanisms involved in this neuroinflammation–PD link. This systematic search was, hereby, [...] Read more.
Parkinson’s disease is a neurodegenerative disease whose progression and clinical characteristics have a close bidirectional and multilevel relationship with the process of neuroinflammation. In this context, it is necessary to understand the mechanisms involved in this neuroinflammation–PD link. This systematic search was, hereby, conducted with a focus on the four levels where alterations associated with neuroinflammation in PD have been described (genetic, cellular, histopathological and clinical-behavioral) by consulting the PubMed, Google Scholar, Scielo and Redalyc search engines, including clinical studies, review articles, book chapters and case studies. Initially, 585,772 articles were included, and, after applying the inclusion and exclusion criteria, 84 articles were obtained that contained information about the multilevel association of neuroinflammation with alterations in gene, molecular, cellular, tissue and neuroanatomical expression as well as clinical-behavioral manifestations in PD. Full article
(This article belongs to the Special Issue Effects of Chronic Inflammation on Brain Ageing and Sensory Decline)
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20 pages, 7393 KiB  
Review
Relationships between Inflammation and Age-Related Neurocognitive Changes
by Run Jin, Aidan Kai Yeung Chan, Jingsong Wu and Tatia Mei Chun Lee
Int. J. Mol. Sci. 2022, 23(20), 12573; https://doi.org/10.3390/ijms232012573 - 20 Oct 2022
Cited by 5 | Viewed by 2363
Abstract
The relationship between inflammation and age-related neurocognitive changes is significant, which may relate to the age-related immune dysfunctions characterized by the senescence of immune cells and elevated inflammatory markers in the peripheral circulation and the central nervous system. In this review, we discuss [...] Read more.
The relationship between inflammation and age-related neurocognitive changes is significant, which may relate to the age-related immune dysfunctions characterized by the senescence of immune cells and elevated inflammatory markers in the peripheral circulation and the central nervous system. In this review, we discuss the potential mechanisms, including the development of vascular inflammation, neuroinflammation, organelle dysfunctions, abnormal cholesterol metabolism, and glymphatic dysfunctions as well as the role that the key molecules play in the immune-cognition interplay. We propose potential therapeutic pharmacological and behavioral strategies for ameliorating age-related neurocognitive changes associated with inflammation. Further research to decipher the multidimensional roles of chronic inflammation in normal and pathological aging processes will help unfold the pathophysiological mechanisms underpinning neurocognitive disorders. The insight gained will lay the path for developing cost-effective preventative measures and the buffering or delaying of age-related neurocognitive decline. Full article
(This article belongs to the Special Issue Effects of Chronic Inflammation on Brain Ageing and Sensory Decline)
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16 pages, 768 KiB  
Review
Age-Related Hearing Loss: The Link between Inflammaging, Immunosenescence, and Gut Dysbiosis
by Dagmara Kociszewska and Srdjan Vlajkovic
Int. J. Mol. Sci. 2022, 23(13), 7348; https://doi.org/10.3390/ijms23137348 - 1 Jul 2022
Cited by 16 | Viewed by 4624
Abstract
This article provides a theoretical overview of the association between age-related hearing loss (ARHL), immune system ageing (immunosenescence), and chronic inflammation. ARHL, or presbyacusis, is the most common sensory disability that significantly reduces the quality of life and has a high economic impact. [...] Read more.
This article provides a theoretical overview of the association between age-related hearing loss (ARHL), immune system ageing (immunosenescence), and chronic inflammation. ARHL, or presbyacusis, is the most common sensory disability that significantly reduces the quality of life and has a high economic impact. This disorder is linked to genetic risk factors but is also influenced by a lifelong cumulative effect of environmental stressors, such as noise, otological diseases, or ototoxic drugs. Age-related hearing loss and other age-related disorders share common mechanisms which often converge on low-grade chronic inflammation known as “inflammaging”. Various stimuli can sustain inflammaging, including pathogens, cell debris, nutrients, and gut microbiota. As a result of ageing, the immune system can become defective, leading to the accumulation of unresolved inflammatory processes in the body. Gut microbiota plays a central role in inflammaging because it can release inflammatory mediators and crosstalk with other organ systems. A proinflammatory gut environment associated with ageing could result in a leaky gut and the translocation of bacterial metabolites and inflammatory mediators to distant organs via the systemic circulation. Here, we postulate that inflammaging, as a result of immunosenescence and gut dysbiosis, accelerates age-related cochlear degeneration, contributing to the development of ARHL. Age-dependent gut dysbiosis was included as a hypothetical link that should receive more attention in future studies. Full article
(This article belongs to the Special Issue Effects of Chronic Inflammation on Brain Ageing and Sensory Decline)
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