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Biomolecules
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Molecular Events in Neurodegenerative and Neuroinflammatory Diseases in Italy: Implications...
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Molecular Events in Neurodegenerative and Neuroinflammatory Diseases in Italy: Implications for Treatments

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (20 June 2022) | Viewed by 10647

Special Issue Editors

Prof. Dr. Lucilla Parnetti

E-Mail Website
Guest Editor
Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy
Interests: Alzheimer disease; Parkinson disease; early diagnosis; cerebrospinal fluid biomarkers; alpha synuclein
Special Issues, Collections and Topics in MDPI journals
Dr. Massimiliano Di Filippo

E-Mail Website
Guest Editor
Section of Neurology, Department of Medicine, University of Perugia, 06123 Perugia, Italy
Interests: neurology; multiple sclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of State-of-the-Art in Italy about the ongoing research on the molecular events characterizing the pathogenesis of central nervous system degenerative, inflammatory and neuropsychiatric disorders. Indeed, the identification of biomolecular pathways taking place in different CNS disorders represents a key step for the development of new therapeutic targets, as well as for the definition of new diagnostic and/or prognostic biomarkers.

We invite research papers that will consolidate our understanding in this area.  The Special Issue will be entitled “Molecular events in neurodegenerative and neuroinflammatory diseases: implications for treatments” and will publish full Research Articles and Systematic Reviews.

Potential topics include, but are not limited to, the following research areas in the field of neurological disorders in both clinical and preclinical settings:

  • Molecular mechanisms underlying circuit dysfunction and neuronal death in the CNS
  • Protein misfolding, amyloid and alpha-syncuclein metabolism
  • Neurotransmitters, neuronal receptors and downstream pathways
  • Lipid mediators in CNS
  • Biofluids markers in neurodegenerative and neuroinflammatory disorders
  • Cytokines, antibodies, and immunological mechanisms in CNS disorders
  • Mechanisms of dysfunctional neuro-immune communication
  • Pathways regulating microglia and astrocyte functions
  • Novel diagnostic tools for CNS disorders

Prof. Dr. Lucilla Parnetti
Dr. Massimiliano Di Filippo
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

 

Published Papers (3 papers)

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Research

10 pages, 762 KiB  
Article
Inter-Laboratory Concordance of Cerebrospinal Fluid and Serum Kappa Free Light Chain Measurements
by Patrizia Natali, Roberta Bedin, Gaetano Bernardi, Elena Corsini, Eleonora Cocco, Lucia Schirru, Ilaria Crespi, Marta Lamonaca, Arianna Sala, Cinzia Nicolò, Massimiliano Di Filippo, Alfredo Villa, Viviana Nociti, Teresa De Michele, Paola Cavalla, Paola Caropreso, Francesca Vitetta, Maria Rosaria Cucinelli, Matteo Gastaldi, Tommaso Trenti, Patrizia Sola, Diana Ferraro and on behalf of RIREMS (Rising Researchers in MS)add Show full author list remove Hide full author list
Biomolecules 2022, 12(5), 677; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12050677 - 07 May 2022
Cited by 3 | Viewed by 1842
Abstract
The kappa index (K-Index), calculated by dividing the cerebrospinal fluid (CSF)/serum kappa free light chain (KFLC) ratio by the CSF/serum albumin ratio, is gaining increasing interest as a marker of intrathecal immunoglobulin synthesis. However, data on inter-laboratory agreement of these measures is lacking. [...] Read more.
The kappa index (K-Index), calculated by dividing the cerebrospinal fluid (CSF)/serum kappa free light chain (KFLC) ratio by the CSF/serum albumin ratio, is gaining increasing interest as a marker of intrathecal immunoglobulin synthesis. However, data on inter-laboratory agreement of these measures is lacking. The aim was to assess the concordance of CSF and serum KFLC measurements, and of K-index values, across different laboratories. KFLC and albumin of 15 paired CSF and serum samples were analyzed by eight participating laboratories. Four centers used Binding Site instruments and assays (B), three used Siemens instruments and assays (S), and one center used a Siemens instrument with a Binding Site assay (mixed). Absolute individual agreement was calculated using a two-way mixed effects intraclass correlation coefficient (ICC). Cohen’s kappa coefficient (k) was used to measure agreement on positive (≥5.8) K-index values. There was an excellent agreement in CSF KFLC measurements across all laboratories (ICC (95% confidence interval): 0.93 (0.87–0.97)) and of serum KFLC across B and S laboratories (ICC: 0.91 (0.73–0.97)), while ICC decreased (to 0.81 (0.53–0.93)) when including the mixed laboratory in the analysis. Concordance for a positive K-Index was substantial across all laboratories (k = 0.77) and within S laboratories (k = 0.71), and very good (k = 0.89) within B laboratories, meaning that patients rarely get discordant results on K-index positivity notwithstanding the testing in different laboratories and the use of different platforms/assays. Full article
(This article belongs to the Special Issue Molecular Events in Neurodegenerative and Neuroinflammatory Diseases in Italy: Implications for Treatments)
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13 pages, 1118 KiB  
Article
Neuroinflammation Is Associated with GFAP and sTREM2 Levels in Multiple Sclerosis
by Federica Azzolini, Luana Gilio, Luigi Pavone, Ennio Iezzi, Ettore Dolcetti, Antonio Bruno, Fabio Buttari, Alessandra Musella, Georgia Mandolesi, Livia Guadalupi, Roberto Furlan, Annamaria Finardi, Teresa Micillo, Fortunata Carbone, Giuseppe Matarese, Diego Centonze and Mario Stampanoni Bassi
Biomolecules 2022, 12(2), 222; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12020222 - 27 Jan 2022
Cited by 21 | Viewed by 3998
Abstract
Background: Astrocytes and microglia play an important role in the inflammatory process of multiple sclerosis (MS). We investigated the associations between the cerebrospinal fluid (CSF) levels of glial fibrillary acid protein (GFAP) and soluble triggering receptors expressed on myeloid cells-2 (sTREM-2), inflammatory [...] Read more.
Background: Astrocytes and microglia play an important role in the inflammatory process of multiple sclerosis (MS). We investigated the associations between the cerebrospinal fluid (CSF) levels of glial fibrillary acid protein (GFAP) and soluble triggering receptors expressed on myeloid cells-2 (sTREM-2), inflammatory molecules, and clinical characteristics in a group of patients with relapsing-remitting MS (RRMS). Methods: Fifty-one RRMS patients participated in the study. Clinical evaluation and CSF collection were performed at the time of diagnosis. The CSF levels of GFAP, sTREM-2, and of a large set of inflammatory and anti-inflammatory molecules were determined. MRI structural measures (cortical thickness, T2 lesion load, cerebellar volume) were examined. Results: The CSF levels of GFAP and sTREM-2 showed significant correlations with inflammatory cytokines IL-8, G-CSF, and IL-5. Both GFAP and sTREM-2 CSF levels positively correlated with age at diagnosis. GFAP was also higher in male MS patients, and was associated with an increased risk of MS progression, as evidenced by higher BREMS at the onset. Finally, a negative association was found between GFAP CSF levels and cerebellar volume in RRMS at diagnosis. Conclusions: GFAP and sTREM-2 represent suitable biomarkers of central inflammation in MS. Our results suggest that enhanced CSF expression of GFAP may characterize patients with a higher risk of progression. Full article
(This article belongs to the Special Issue Molecular Events in Neurodegenerative and Neuroinflammatory Diseases in Italy: Implications for Treatments)
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14 pages, 4561 KiB  
Article
Macrophage Plasticity and Polarization Are Altered in the Experimental Model of Multiple Sclerosis
by Alessandro Leuti, Emanuela Talamonti, Antonietta Gentile, Marta Tiberi, Alessandro Matteocci, Diego Fresegna, Diego Centonze and Valerio Chiurchiù
Biomolecules 2021, 11(6), 837; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11060837 - 04 Jun 2021
Cited by 22 | Viewed by 3976
Abstract
Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system. MS is characterized by infiltrations of leukocytes such as T and B lymphocytes and macrophages. Macrophages have been identified as major effectors of inflammation and demyelination in both MS and [...] Read more.
Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system. MS is characterized by infiltrations of leukocytes such as T and B lymphocytes and macrophages. Macrophages have been identified as major effectors of inflammation and demyelination in both MS and its animal model, experimental autoimmune encephalomyelitis (EAE). However, the activation and heterogeneity of macrophages in MS has been poorly investigated. Thus, in this study, we evaluated M1 and M2 macrophages immunophenotype from EAE and control mice by analyzing over 30 surface and intracellular markers through polychromatic flow cytometry, qRT-PCR, and ELISA assay. We showed that M1 macrophages possessed a higher proinflammatory profile in EAE compared to control mice, since they expressed higher levels of activation/co-stimulatory markers (iNOS, CD40, and CD80) and cytokines/chemokines (IL-6, IL-12, CCL2, and CXCL10), whereas M2 lost their M2-like phenotype by showing a decreased expression of their signature markers CD206 and CCL22, as well as a concomitant upregulation of several M1 makers. Furthermore, immunization of M1 and M2 macrophages with MOG35-55 led to a significant hyperactivation of M1 and a concomitant shift of anti-inflammatory M2 to pro-inflammatory M1 macrophages. Overall, we provide evidence for a phenotypic alteration of M1/M2 balance during MS, which can be of crucial importance not only for a better understanding of the immunopathology of this neurodegenerative disease but also to potentially develop new macrophage-centered therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Events in Neurodegenerative and Neuroinflammatory Diseases in Italy: Implications for Treatments)
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