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Inflammaging and Brain Aging
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Inflammaging and Brain Aging

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

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 7198

Special Issue Editors

Prof. Dr. Babak Baban

E-Mail Website
Guest Editor
Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA
Interests: innate immunity; cannabinoids; cannabis; inflammation; neuroinflammation; immune regulation; microbiome
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. David C. Hess

E-Mail Website
Guest Editor
Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, USA
Interests: neurology

Special Issue Information

Dear Colleagues,

The concept of mild and chronic inflammation associated with biological aging, known as inflammaging, has revolutionized our understanding and views toward the complex process of aging for the last two decades. Given the pivotal role of the brain and central nervous system (CNS) in living and survival, it is a dire need to better understand the interactions between inflammatory responses and components of the CNS within and beyond the borders of brain–blood barriers. Therefore, the scope of the articles to be considered for the Special Issue is focused on novel concepts, research and methods elucidating and improving our current understanding of brain aging, immune and cellular senescence, immunobiography, genetic and immunogenetic, as well as molecular and cellular properties of inflammaging, along with their impact on CNS aging and age-associated/related neurological diseases and pathological events connected to this process.

Prof. Dr. Babak Baban
Prof. Dr. David C. Hess
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

  • inflammaging
  • brain aging
  • aging
  • senescence
  • CNS
  • immunobiography
  • age-related diseases

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Published Papers (3 papers)

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Research

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12 pages, 7458 KiB  
Article
Boosting Acetylcholine Signaling by Cannabidiol in a Murine Model of Alzheimer’s Disease
by Hesam Khodadadi, Évila Lopes Salles, Sahar Emami Naeini, Bidhan Bhandari, Hannah M. Rogers, Jules Gouron, William Meeks, Alvin V. Terry, Jr., Anilkumar Pillai, Jack C. Yu, John C. Morgan, Kumar Vaibhav, David C. Hess, Krishnan M. Dhandapani, Lei P. Wang and Babak Baban
Int. J. Mol. Sci. 2024, 25(21), 11764; https://doi.org/10.3390/ijms252111764 - 1 Nov 2024
Cited by 1 | Viewed by 1505
Abstract
Alzheimer’s disease (AD) is a challenging medical issue that requires efficacious treatment options to improve long-term quality of life. Cannabidiol (CBD) is a cannabis-derived phytocannabinoid with potential health benefits, including reports from our laboratory and others showing a therapeutic role in the pre-clinical [...] Read more.
Alzheimer’s disease (AD) is a challenging medical issue that requires efficacious treatment options to improve long-term quality of life. Cannabidiol (CBD) is a cannabis-derived phytocannabinoid with potential health benefits, including reports from our laboratory and others showing a therapeutic role in the pre-clinical treatment of AD; however, the mechanisms whereby CBD affects AD progression remain undefined. Innate lymphoid cells (ILCs) are recently discovered immune cells that initiate and orchestrate inflammatory responses. ILC2, a sub-class of ILCs, is proposed to have a role in cognitive function via unknown mechanisms. In this present study, we explored whether CBD ameliorates AD symptoms via the enhancement of acetylcholine (ACh), a cholinergic neurotransmitter involved in cognition that may regulate ILC2. 5xFAD mice were chronically treated by inhalation of a formulation of broad-spectrum CBD for seven months. ACh production, ILC2s profile, brain histopathology, and long-term behavior were assessed. Together, our studies showed that long-term inhalation of CBD improved cognitive function and reduced senile plaques in a murine AD model, effects that were associated with enhanced ACh production and altered ILC2s distribution within the CNS. These findings indicate that inhaled CBD could offer a cost-effective, non-invasive, and effective treatment for managing AD. The beneficial effects of CBD inhalation may be linked to increased ACh production and an altered distribution of ILC2s, highlighting the need for further research in this area. Full article
(This article belongs to the Special Issue Inflammaging and Brain Aging)
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14 pages, 2809 KiB  
Communication
A Brain Anti-Senescence Transcriptional Program Triggered by Hypothalamic-Derived Exosomal microRNAs
by Josefa Krarup, Lucas Araya, Felipe Álvarez, Daniel A. Bórquez and Pamela J. Urrutia
Int. J. Mol. Sci. 2024, 25(10), 5467; https://doi.org/10.3390/ijms25105467 - 17 May 2024
Cited by 3 | Viewed by 2439
Abstract
In contrast to the hypothesis that aging results from cell-autonomous deterioration processes, the programmed longevity theory proposes that aging arises from a partial inactivation of a “longevity program” aimed at maintaining youthfulness in organisms. Supporting this hypothesis, age-related changes in organisms can be [...] Read more.
In contrast to the hypothesis that aging results from cell-autonomous deterioration processes, the programmed longevity theory proposes that aging arises from a partial inactivation of a “longevity program” aimed at maintaining youthfulness in organisms. Supporting this hypothesis, age-related changes in organisms can be reversed by factors circulating in young blood. Concordantly, the endocrine secretion of exosomal microRNAs (miRNAs) by hypothalamic neural stem cells (htNSCs) regulates the aging rate by enhancing physiological fitness in young animals. However, the specific molecular mechanisms through which hypothalamic-derived miRNAs exert their anti-aging effects remain unexplored. Using experimentally validated miRNA–target gene interactions and single-cell transcriptomic data of brain cells during aging and heterochronic parabiosis, we identify the main pathways controlled by these miRNAs and the cell-type-specific gene networks that are altered due to age-related loss of htNSCs and the subsequent decline in specific miRNA levels in the cerebrospinal fluid (CSF). Our bioinformatics analysis suggests that these miRNAs modulate pathways associated with senescence and cellular stress response, targeting crucial genes such as Cdkn2a, Rps27, and Txnip. The oligodendrocyte lineage appears to be the most responsive to age-dependent loss of exosomal miRNA, leading to significant derepression of several miRNA target genes. Furthermore, heterochronic parabiosis can reverse age-related upregulation of specific miRNA-targeted genes, predominantly in brain endothelial cells, including senescence promoting genes such as Cdkn1a and Btg2. Our findings support the presence of an anti-senescence mechanism triggered by the endocrine secretion of htNSC-derived exosomal miRNAs, which is associated with a youthful transcriptional signature. Full article
(This article belongs to the Special Issue Inflammaging and Brain Aging)
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Review

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31 pages, 2854 KiB  
Review
Sex as a Determinant of Age-Related Changes in the Brain
by Dmitriy E. Burmistrov, Sergey V. Gudkov, Claudio Franceschi and Maria V. Vedunova
Int. J. Mol. Sci. 2024, 25(13), 7122; https://doi.org/10.3390/ijms25137122 - 28 Jun 2024
Cited by 4 | Viewed by 2573
Abstract
The notion of notable anatomical, biochemical, and behavioral distinctions within male and female brains has been a contentious topic of interest within the scientific community over several decades. Advancements in neuroimaging and molecular biological techniques have increasingly elucidated common mechanisms characterizing brain aging [...] Read more.
The notion of notable anatomical, biochemical, and behavioral distinctions within male and female brains has been a contentious topic of interest within the scientific community over several decades. Advancements in neuroimaging and molecular biological techniques have increasingly elucidated common mechanisms characterizing brain aging while also revealing disparities between sexes in these processes. Variations in cognitive functions; susceptibility to and progression of neurodegenerative conditions, notably Alzheimer’s and Parkinson’s diseases; and notable disparities in life expectancy between sexes, underscore the significance of evaluating aging within the framework of gender differences. This comprehensive review surveys contemporary literature on the restructuring of brain structures and fundamental processes unfolding in the aging brain at cellular and molecular levels, with a focus on gender distinctions. Additionally, the review delves into age-related cognitive alterations, exploring factors influencing the acceleration or deceleration of aging, with particular attention to estrogen’s hormonal support of the central nervous system. Full article
(This article belongs to the Special Issue Inflammaging and Brain Aging)
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