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Special Issue "Neuroinflammatory Processes in Neurodegenerative Diseases 2.0"

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 July 2023 | Viewed by 1014

Special Issue Editors

Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
Interests: neurodegeneration; neuroinflammation; multiple sclerosis; amyotrophic lateral sclerosis; animal models of neural diseases; neural biomarkers; calcium-binding neuroproteins; S100B protein
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Dr. Gabriele Di Sante
Guest Editor
Department of Medicine and Surgery, Section of Human, Clinical and Forensic Anatomy, University of Perugia, 06132 Perugia, Italy
Interests: neurodegeneration; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Istituto di Scienze e Tecnologie Chimiche “Giulio Natta” (SCITEC-CNR), 00168 Rome, Italy
Interests: apoptosis; oxidative stress; nutraceutical
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pathological conditions of the nervous system in which neurons degenerate are collectively defined as neurodegenerative diseases. Different diseases are developed, essentially depending on the location of the neuronal population(s) involved. Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, and multiple sclerosis are among the most pressing neurodegenerative diseases, owing to their devastating consequences. Despite the different etiologies, a growing role is recognized in processes collectively referred to as neuroinflammation. During these processes, the neuron environment is affected, principally by non-neuronal neural cells, such as microglia and astrocytes, and also the blood–brain barrier, and immune cells entering the nervous system, which mediate damage and repair. In this respect, emerging evidence also indicates that trillions of microorganisms that inhabit the gut (gut microbiota) may influence neuroinflammatory responses. They represent the most relevant source of proteins, pathogen-related motives, and “foreign” DNAs, continuously interacting with the immune system.

This Special Issue will provide an up-to-date overview, gathering research or review manuscripts addressing inflammatory processes that mechanistically participate in inducing different neurodegenerative diseases, including molecular signaling pathways, mechanisms able to modulate immune cell trafficking, the role of microbiota, and also considering the role of environment and genetics as drivers. Studies on inflammatory biomarkers as tools for diagnosing/monitoring neurodegenerative diseases are also welcome.

Prof. Dr. Fabrizio Michetti
Dr. Gabriele Di Sante
Dr. M. Elisabetta Clementi
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.


  • neuroinflammation
  • neurodegeneration
  • astrocytes
  • microglia
  • immune cells
  • blood–brain barrier
  • microbiota
  • damage/danger-associated molecular patterns
  • pattern recognition receptors

Published Papers (1 paper)

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Depletion of Arg1-Positive Microglia/Macrophages Exacerbates Cerebral Ischemic Damage by Facilitating the Inflammatory Response
Int. J. Mol. Sci. 2022, 23(21), 13055; https://doi.org/10.3390/ijms232113055 - 27 Oct 2022
Cited by 1 | Viewed by 789
Stroke is a serious worldwide disease that causes death and disability, more than 80% of which is ischemic stroke. The expression of arginase 1 (Arg1), a key player in regulating nitrogen homeostasis, is altered in the peripheral circulation after stroke. Growing evidence indicates [...] Read more.
Stroke is a serious worldwide disease that causes death and disability, more than 80% of which is ischemic stroke. The expression of arginase 1 (Arg1), a key player in regulating nitrogen homeostasis, is altered in the peripheral circulation after stroke. Growing evidence indicates that ischemic stroke also induces upregulated Arg1 expression in the central nervous system, especially in activated microglia and macrophages. This implies that Arg1 may affect stroke progression by modulating the cerebral immune response. To investigate the effect of Arg1+ microglia/macrophages on ischemic stroke, we selectively eliminated cerebral Arg1+ microglia/macrophages by mannosylated clodronate liposomes (MCLs) and investigated their effects on behavior, neurological deficits, and inflammatory responses in mice after ischemic stroke. More than half of Arg1+ cells, mainly Arg1+ microglia/macrophages, were depleted after MCLs administration, resulting in a significant deterioration of motility in mice. After the elimination of Arg1+ microglia/macrophages, the infarct volume expanded and neuronal degenerative lesions intensified. Meanwhile, the absence of Arg1+ microglia/macrophages significantly increased the production of pro-inflammatory cytokines and suppressed the expression of anti-inflammatory factors, thus profoundly altering the immune microenvironment at the lesion site. Taken together, our data demonstrate that depletion of Arg1+ microglia/macrophages exacerbates neuronal damage by facilitating the inflammatory response, leading to more severe ischemic injury. These results suggest that Arg1+ microglia/macrophages, as a subpopulation regulating inflammation, is beneficial in controlling the development of ischemia and promoting recovery from injury. Regulation of Arg1 expression on microglia/macrophages at the right time may be a potential target for the treatment of ischemic brain injury. Full article
(This article belongs to the Special Issue Neuroinflammatory Processes in Neurodegenerative Diseases 2.0)
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