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Immunity in Neurodegenerative Diseases: Systemic Immune Imbalance, Neuroinflammation, and Beyond

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: 31 May 2024 | Viewed by 1690

Special Issue Editors


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Guest Editor
Department of Biotechnology, University of Rijeka, 51000 Rijeka, Croatia
Interests: adaptive and innate immunity; neuroimmunity; cellular signaling; immunology; T cells

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Guest Editor
Department of Neurobiology, Faculty of Life Sciences, Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 69978, Israel
Interests: neuroinflammation; astrocyte; microglia; Alzheimer’s disease; animal model
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Special Issue Information

Dear Colleagues,

Although immune reactions in the central nervous system (CNS) were in the past uniformly branded as noxious, it is now increasingly clear that the immune system closely monitors the CNS and exerts a major protective role. It does so both from within the CNS parenchyma, primarily through the only resident immune cell there (microglia), and from afar, via numerous peripheral immune cell subsets. The latter can oftentimes act without crossing the blood–brain barrier. This shows the immense power of communication between the immune system and the CNS that operates through numerous passages (the choroid plexus, brain-draining lymph vessels, and skull bone marrow channels), neuroimmune units in the gut and skin, the vagus nerve, and others. Notably, in many pathologic conditions, the immune system can turn neurotoxic and become the primary source of neuronal damage and ultimately death. Neuroinflammation is being identified as one of the most important pathological hallmarks in different brain pathologies. It can be seen in a wide variety of diseases ranging from brain trauma to neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease, amyotrophic lateral sclerosis, and frontotemporal dementia. Recent years have brought new insights on various neuroprotective and neurotoxic functions exerted not only by the microglia, border-associated macrophages, and (exceptionally limited) adaptive immune cells in the CNS, but also by various peripheral immune subsets, including but not limited to regulatory CD4 T cells, NK cells, neuromuscular junction macrophages, and mast cells. These two opposite functions have a range of implications on processes of neurodevelopment, synaptogenesis, neuroplasticity, chronic stress, and neurodegeneration.

We encourage the submission of original research and review articles that cover the following topics:

  1. Genetics and molecular mechanisms of neurodegeneration linked to immune functions.
  2. The role of CNS resident immune cells in neuroprotection and neurotoxicity.
  3. The systemic immune imbalance in neurodegenerative diseases.
  4. The link between ageing and neuroinflammation.
  5. Neuro-immune axis.
  6. Peripheral vs. central mediators of neuroinflammation.
  7. Preventive and therapeutic strategies targeting immune system in neurodegenerative diseases.

Dr. Ivana Munitic
Prof. Dr. Frenkel Dan
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

  • neurodegeneration
  • CNS immunosurveillance
  • neuroinflammation
  • neuro-immune axis
  • glia
  • T cells
  • phagocytosis
  • immunomodulation
  • autoimmunity
  • immunodeficiency

Published Papers (1 paper)

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Research

16 pages, 3242 KiB  
Article
Boosting Mitochondrial Biogenesis Diminishes Foam Cell Formation in the Post-Stroke Brain
by Sanna H. Loppi, Marco A. Tavera-Garcia, Natalie E. Scholpa, Boaz K. Maiyo, Danielle A. Becktel, Helena W. Morrison, Rick G. Schnellmann and Kristian P. Doyle
Int. J. Mol. Sci. 2023, 24(23), 16632; https://doi.org/10.3390/ijms242316632 - 23 Nov 2023
Viewed by 1363
Abstract
Following ischemic stroke, the degradation of myelin and other cellular membranes surpasses the lipid-processing capabilities of resident microglia and infiltrating macrophages. This imbalance leads to foam cell formation in the infarct and areas of secondary neurodegeneration, instigating sustained inflammation and furthering neurological damage. [...] Read more.
Following ischemic stroke, the degradation of myelin and other cellular membranes surpasses the lipid-processing capabilities of resident microglia and infiltrating macrophages. This imbalance leads to foam cell formation in the infarct and areas of secondary neurodegeneration, instigating sustained inflammation and furthering neurological damage. Given that mitochondria are the primary sites of fatty acid metabolism, augmenting mitochondrial biogenesis (MB) may enhance lipid processing, curtailing foam cell formation and post-stroke chronic inflammation. Previous studies have shown that the pharmacological activation of the β2-adrenergic receptor (β2-AR) stimulates MB. Consequently, our study sought to discern the effects of intensified β2-AR signaling on MB, the processing of brain lipid debris, and neurological outcome using a mouse stroke model. To achieve this goal, aged mice were treated with formoterol, a long-acting β2-AR agonist, daily for two and eight weeks following stroke. Formoterol increased MB in the infarct region, modified fatty acid metabolism, and reduced foam cell formation. However, it did not reduce markers of post-stroke neurodegeneration or improve recovery. Although our findings indicate that enhancing MB in myeloid cells can aid in the processing of brain lipid debris after stroke, it is important to note that boosting MB alone may not be sufficient to significantly impact stroke recovery. Full article
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