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Neuroinflammatory Processes in Neurodegenerative Diseases 2.0
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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: closed (31 July 2023) | Viewed by 9483

Special Issue Editors

Prof. Dr. Fabrizio Michetti

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Guest Editor
Department of Neuroscience, Università Cattolica S. Cuore, Rome, Italy
Interests: neurodegeneration; neuroinflammation; multiple sclerosis; amyotrophic lateral sclerosis; animal models of neural diseases; neural biomarkers; calcium-binding neuroproteins; S100B protein
Special Issues, Collections and Topics in MDPI journals
Dr. Gabriele Di Sante

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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
Dr. M. Elisabetta Clementi

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Guest Editor
National Research Council (CNR), Istituto di Scienze e Tecnologie Chimiche “Giulio Natta” (SCITEC)—c/o Istituto di Biochimica e Biochimica Clinica Università Cattolica del Sacro Cuore, Largo F. Vito 1, 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.

Keywords

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

Published Papers (5 papers)

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Research

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23 pages, 2577 KiB  
Article
Alteration of Blood Immune Biomarkers in MCI Patients with Different APOE Genotypes after Cognitive Training: A 1 Year Follow-Up Cohort Study
by Olga Abramova, Yana Zorkina, Valeriya Ushakova, Dmitry Gryadunov, Anna Ikonnikova, Elena Fedoseeva, Marina Emelyanova, Aleksandra Ochneva, Irina Morozova, Konstantin Pavlov, Timur Syunyakov, Alisa Andryushchenko, Victor Savilov, Marat Kurmishev, Denis Andreuyk, Svetlana Shport, Olga Gurina, Vladimir Chekhonin, Georgy Kostyuk and Anna Morozova
Int. J. Mol. Sci. 2023, 24(17), 13395; https://doi.org/10.3390/ijms241713395 - 29 Aug 2023
Cited by 1 | Viewed by 1024
Abstract
Many studies aim to detect the early phase of dementia. One of the major ways to achieve this is to identify corresponding biomarkers, particularly immune blood biomarkers. The objective of this study was to identify such biomarkers in patients with mild cognitive impairment [...] Read more.
Many studies aim to detect the early phase of dementia. One of the major ways to achieve this is to identify corresponding biomarkers, particularly immune blood biomarkers. The objective of this study was to identify such biomarkers in patients with mild cognitive impairment (MCI) in an experiment that included cognitive training. A group of patients with MCI diagnoses over the age of 65 participated in the study (n = 136). Measurements of cognitive functions (using the Mini-Mental State Examination scale and Montreal Cognitive Assessment) and determination of 27 serum biomarkers were performed twice: on the first visit and on the second visit, one year after the cognitive training. APOE genotypes were also determined. Concentrations of EGF (F = 17; p = 0.00007), Eotaxin (F = 7.17; p = 0.008), GRO (F = 13.42; p = 0.0004), IL-8 (F = 8.16; p = 0.005), MCP-1 (F = 13.46; p = 0.0001) and MDC (F = 5.93; p = 0.016) increased after the cognitive training in MCI patients. All these parameters except IL-8 demonstrated a weak correlation with other immune parameters and were poorly represented in the principal component analysis. Differences in concentrations of IP-10, FGF-2, TGFa and VEGF in patients with MCI were associated with APOE genotype. Therefore, the study identified several immune blood biomarkers that could potentially be associated with changes in cognitive function. Full article
(This article belongs to the Special Issue Neuroinflammatory Processes in Neurodegenerative Diseases 2.0)
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14 pages, 2547 KiB  
Article
Biochemical and Anthropometric Parameters for the Early Recognition of the Intrauterine Growth Restriction and Preterm Neonates at Risk of Impaired Neurodevelopment
by Maria Cristina Aisa, Benito Cappuccini, Alessandro Favilli, Alessandro Datti, Vincenza Nardicchi, Giuliana Coata and Sandro Gerli
Int. J. Mol. Sci. 2023, 24(14), 11549; https://doi.org/10.3390/ijms241411549 - 17 Jul 2023
Cited by 2 | Viewed by 947
Abstract
Background: S100B and Tau are implicated with both brain growth and injury. Their urinary levels in 30-to-40-day-old full-term, preterm, IUGR, and preterm-IUGR subjects were measured to investigate their possible relationship with future delayed neurodevelopment. Methods: Values were related to the neuro-behavioral outcome at [...] Read more.
Background: S100B and Tau are implicated with both brain growth and injury. Their urinary levels in 30-to-40-day-old full-term, preterm, IUGR, and preterm-IUGR subjects were measured to investigate their possible relationship with future delayed neurodevelopment. Methods: Values were related to the neuro-behavioral outcome at two years of age, as well as to brain volumes and urinary NGF assessed at the same postnatal time point. Results: Using the Griffiths III test, cognitive and motor performances were determined to establish subgroups characterized by either normal or impaired neuro-behavior. The latter included preterm, IUGR, and preterm-IUGR individuals who exhibited significantly higher and lower S100B and Tau levels, respectively, along with markedly reduced cerebral volumes and urinary NGF, as previously demonstrated. Contrary to NGF, however, Tau and S100B displayed a weak correlation with brain volumes. Conclusions: Delayed cognitive and motor performances observed in two-year-old preterm and IUGR-born individuals were also found to be associated with anomalous urinary levels of S100B and Tau, assessed at 30–40 days of the postnatal period, and their changes did not correlate with brain growth. Thus, our data suggests that, in addition to cerebral volumes and NGF, urinary S100B and Tau can also be considered as valuable parameters for the early detection of future neurodevelopmental abnormalities. Full article
(This article belongs to the Special Issue Neuroinflammatory Processes in Neurodegenerative Diseases 2.0)
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15 pages, 3861 KiB  
Article
Pharmacokinetics and Tissue Distribution of Bee Venom-Derived Phospholipase A2 Using a Sandwich ELISA after Subcutaneous Injection of New Composition Bee Venom in Rats
by Soon Uk Chae, Seong Jun Jo, Chae Bin Lee, Sangyoung Lee, Ji-Hyun Park, Jin-Su Jung, Eui-Suk Park, Hyunsu Bae and Soo Kyung Bae
Int. J. Mol. Sci. 2023, 24(12), 10214; https://doi.org/10.3390/ijms241210214 - 16 Jun 2023
Viewed by 1716
Abstract
Bee venom is a traditional drug used to treat the nervous system, musculoskeletal system, and autoimmune diseases. A previous study found that bee venom and one of its components, phospholipase A2, can protect the brain by suppressing neuroinflammation and can also be used [...] Read more.
Bee venom is a traditional drug used to treat the nervous system, musculoskeletal system, and autoimmune diseases. A previous study found that bee venom and one of its components, phospholipase A2, can protect the brain by suppressing neuroinflammation and can also be used to treat Alzheimer’s disease. Thus, new composition bee venom (NCBV), which has an increased phospholipase A2 content of up to 76.2%, was developed as a treatment agent for Alzheimer’s disease by INISTst (Republic of Korea). The aim of this study was to characterize the pharmacokinetic profiles of phospholipase A2 contained in NCBV in rats. Single subcutaneous administration of NCBV at doses ranging from 0.2 mg/kg to 5 mg/kg was conducted, and pharmacokinetic parameters of bee venom-derived phospholipase A2 (bvPLA2) increased in a dose-dependent manner. Additionally, no accumulation was observed following multiple dosings (0.5 mg/kg/week), and other constituents of NCBV did not affect the pharmacokinetic profile of bvPLA2. After subcutaneous injection of NCBV, the tissue-to-plasma ratios of bvPLA2 for the tested nine tissues were all <1.0, indicating a limited distribution of the bvPLA2 within the tissues. The findings of this study may help understand the pharmacokinetic characteristics of bvPLA2 and provide useful information for the clinical application of NCBV. Full article
(This article belongs to the Special Issue Neuroinflammatory Processes in Neurodegenerative Diseases 2.0)
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13 pages, 1638 KiB  
Article
Depletion of Arg1-Positive Microglia/Macrophages Exacerbates Cerebral Ischemic Damage by Facilitating the Inflammatory Response
by Ting Li, Jin Zhao and Hao Gao
Int. J. Mol. Sci. 2022, 23(21), 13055; https://doi.org/10.3390/ijms232113055 - 27 Oct 2022
Cited by 7 | Viewed by 2183
Abstract
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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Review

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15 pages, 926 KiB  
Review
The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker
by Fabrizio Michetti, Maria Elisabetta Clementi, Rosa Di Liddo, Federica Valeriani, Francesco Ria, Mario Rende, Gabriele Di Sante and Vincenzo Romano Spica
Int. J. Mol. Sci. 2023, 24(11), 9605; https://doi.org/10.3390/ijms24119605 - 31 May 2023
Cited by 7 | Viewed by 3056
Abstract
S100B is a calcium-binding protein mainly concentrated in astrocytes in the nervous system. Its levels in biological fluids are recognized as a reliable biomarker of active neural distress, and more recently, mounting evidence points to S100B as a Damage-Associated Molecular Pattern molecule, which, [...] Read more.
S100B is a calcium-binding protein mainly concentrated in astrocytes in the nervous system. Its levels in biological fluids are recognized as a reliable biomarker of active neural distress, and more recently, mounting evidence points to S100B as a Damage-Associated Molecular Pattern molecule, which, at high concentration, triggers tissue reactions to damage. S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease. In addition, in experimental models of diseases such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, multiple sclerosis, traumatic and vascular acute neural injury, epilepsy, and inflammatory bowel disease, alteration of S100B levels correlates with the occurrence of clinical and/or toxic parameters. In general, overexpression/administration of S100B worsens the clinical presentation, whereas deletion/inactivation of the protein contributes to the amelioration of the symptoms. Thus, the S100B protein may be proposed as a common pathogenic factor in different disorders, sharing different symptoms and etiologies but appearing to share some common pathogenic processes reasonably attributable to neuroinflammation. Full article
(This article belongs to the Special Issue Neuroinflammatory Processes in Neurodegenerative Diseases 2.0)
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