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Molecular Signaling Pathways in Brain Pathology 2.0

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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 (25 November 2023) | Viewed by 8809

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Special Issue Editor

Prof. Dr. Martin Berghoff

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Guest Editor

Department of Neurology, Justus Liebig University of Giessen, Giessen, Germany
Interests: neuroimmunology; multiple sclerosis; experimental autoimmune encephalomyelitis (EAE); FGF/FGFR signaling pathways; neuroinfectious diseases; Lyme borreliosis; encephalitis; meningitis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am serving as guest editor for the Special Issue “Molecular Signaling Pathways in Brain Pathology 2.0” in the International Journal of Molecular Sciences. In the past, diseases such as glioblastoma or multiple sclerosis have been associated with abnormal signaling including changes in FGF/FGFR pathways; patients with glioblastoma were or are being treated with FGFR tyrosine kinase inhibitors.

I would be pleased if you would be willing to contribute to this Special Issue by submitting an original research article or comprehensive review related to the above-mentioned topic.

The submission deadline will be 31 January 2023. Manuscripts may be submitted any time before the deadline, and they will be published online.

Dr. Martin Berghoff
Guest Editor

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

growth factors/-receptors
glioblastoma
multiple sclerosis
blood-brain-barrier
oligodendrocytes
neurons

Published Papers (4 papers)

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Research

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13 pages, 1672 KiB

Open AccessArticle

Astrocyte-Derived Exosomes Differentially Shape T Cells’ Immune Response in MS Patients

by Piotr Szpakowski, Dominika Ksiazek-Winiarek, Joanna Czpakowska, Mateusz Kaluza, Marta Milewska-Jedrzejczak and Andrzej Glabinski

Int. J. Mol. Sci. 2023, 24(8), 7470; https://doi.org/10.3390/ijms24087470 - 18 Apr 2023

Cited by 5 | Viewed by 1444

Abstract

Astrocytes, the most abundant group of glia cells in the brain, provide support for neurons and indicate multiple various functions in the central nervous system (CNS). Growing data additionally describe their role in the regulation of immune system activity. They exert their function not only by direct contact with other cell types, but also through an indirect method, e.g., by secreting various molecules. One such structure is extracellular vesicles, which are important mediators of crosstalk between cells. In our study, we observed that the impact of exosomes derived from astrocytes with various functional phenotype differently affect the immune response of CD4+ T cells, both from healthy individuals and from patients with multiple sclerosis (MS). Astrocytes, by modulating exosome cargo, impacts the release of IFN-γ, IL-17A and CCL2 in our experimental conditions. Considering the proteins concentration in cell culture supernatants and the cellular percentage of Th phenotypes, it could be stated that human astrocytes, by the release of exosomes, are able to modify the activity of human T cells. Full article

(This article belongs to the Special Issue Molecular Signaling Pathways in Brain Pathology 2.0)

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13 pages, 1227 KiB

Open AccessArticle

Is There Reduced Hemodynamic Brain Activation in Multiple Sclerosis Even with Undisturbed Cognition?

by Bianca Wagner, Clara L. Härig, Bertram Walter, Jens Sommer, Gebhard Sammer and Martin Berghoff

Int. J. Mol. Sci. 2023, 24(1), 112; https://doi.org/10.3390/ijms24010112 - 21 Dec 2022

Cited by 1 | Viewed by 1319

Abstract

Cognitive impairments related to changes in deep gray matter and other brain regions occur in up to 70% of people with multiple sclerosis. But do such brain changes also occur in patients without significant cognitive impairment? Eighteen participants with relapsing-remitting multiple sclerosis (RRMS) and fifteen healthy controls participated in this study. Cognitive status, depression, and fatigue were assessed using the Multiple Sclerosis Inventory of Cognition (MUSIC), Beck’s Depression Inventory (BDI-II), and the Fatigue Severity Scale (FSS). fMRI was recorded while a participant performed the modified attention network test (ANT). The effects of ANT executive attention network on hemodynamic activation of a priori defined regions of interest, including the hippocampus, anterior cingulate cortex (ACC), thalamus, caudate nucleus, pallidum, and putamen were studied. The individual lesion load was estimated. For fMRI data analysis a general linear model with randomization statistics including threshold-free cluster enhancement as implemented in the FSL software was used. Participants with RRMS showed reduced activation of the executive attention network in the hippocampus, pallidum, and ACC. The thalamus was involved in both group activations but did not differ between groups. In summary, functional changes in the brain can also be demonstrated in RRMS patients without cognitive deficits. The affected brain regions can best be assigned to the attention network for executive control. This association could likely serve as a biological indicator of susceptibility to imminent cognitive impairment in MS. Full article

(This article belongs to the Special Issue Molecular Signaling Pathways in Brain Pathology 2.0)

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12 pages, 3016 KiB

Open AccessArticle

Interferon Beta-1a versus Combined Interferon Beta-1a and Oligodendrocyte-Specific FGFR1 Deletion in Experimental Autoimmune Encephalomyelitis

by Ranjithkumar Rajendran, Vinothkumar Rajendran, Liza Gupta, Kian Shirvanchi, Darja Schunin, Srikanth Karnati, Mario Giraldo-Velásquez and Martin Berghoff

Int. J. Mol. Sci. 2022, 23(20), 12183; https://doi.org/10.3390/ijms232012183 - 12 Oct 2022

Cited by 2 | Viewed by 1567

Abstract

Recombinant beta interferons-1 (IFNβ-1) are used as first line therapies in patients with relapsing multiple sclerosis (MS), a chronic inflammatory and neurodegenerative disease of the CNS. IFNβ-1a/b has moderate effects on the prevention of relapses and slowing of disease progression. Fibroblast growth factors (FGFs) and FGF receptors (FGFRs) are known to play a key role in the pathology of MS and its model EAE. To investigate the effects of short-term treatment with s.c. IFNβ-1a versus the combined application of s.c. IFNβ-1a and oligodendrocyte-specific deletion of FGFR1 (Fgfr1^ind^−/− mice) in MOG_35-55-induced EAE. IFNβ-1a (30 mg/kg) was applied s.c. from days 0–7 p.i. of EAE in controls and Fgfr1^ind^−/− mice. FGFR signaling proteins associated with inflammation/degeneration in MS/EAE were analyzed by western blot in the spinal cord. Further, FGFR1 in Oli-neu oligodendrocytes were inhibited by PD166866 and treated with IFNβ-1a (400 ng/mL). Application of IFNβ-1a over 8 days resulted in less symptoms only at the peak of disease (days 9–11) compared to controls. Application of IFNβ-1a in Fgfr1^ind^−/− mice resulted in less symptoms primarily in the chronic phase of EAE. Fgfr1^ind^−/− mice treated with IFNβ-1a showed increased expression of pERK and BDNF. In Oli-neu oligodendrocytes, treatment with PD166866 and IFNβ-1a also showed an increased expression of pERK and BDNF/TrkB. These data suggest that the beneficial effects in the chronic phase of EAE and on signaling molecules associated with ERK and BDNF expression are caused by the modulation of FGFR1 and not by interferon beta-1a. FGFR may be a potential target for therapy in MS. Full article

(This article belongs to the Special Issue Molecular Signaling Pathways in Brain Pathology 2.0)

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Review

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17 pages, 1598 KiB

Open AccessReview

Blood–Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets

by Ruicheng Yang, Jundan Wang, Fen Wang, Huipeng Zhang, Chen Tan, Huanchun Chen and Xiangru Wang

Int. J. Mol. Sci. 2023, 24(3), 2852; https://doi.org/10.3390/ijms24032852 - 2 Feb 2023

Cited by 14 | Viewed by 3599

Abstract

Despite advances in supportive care and antimicrobial treatment, bacterial meningitis remains the most serious infection of the central nervous system (CNS) that poses a serious risk to life. This clinical dilemma is largely due to our insufficient knowledge of the pathology behind this disease. By controlling the entry of molecules into the CNS microenvironment, the blood–brain barrier (BBB), a highly selective cellular monolayer that is specific to the CNS’s microvasculature, regulates communication between the CNS and the rest of the body. A defining feature of the pathogenesis of bacterial meningitis is the increase in BBB permeability. So far, several contributing factors for BBB disruption have been reported, including direct cellular damage brought on by bacterial virulence factors, as well as host-specific proteins or inflammatory pathways being activated. Recent studies have demonstrated that targeting pathological factors contributing to enhanced BBB permeability is an effective therapeutic complement to antimicrobial therapy for treating bacterial meningitis. Hence, understanding how these meningitis-causing pathogens affect the BBB permeability will provide novel perspectives for investigating bacterial meningitis’s pathogenesis, prevention, and therapies. Here, we summarized the recent research progress on meningitis-causing pathogens disrupting the barrier function of BBB. This review provides handy information on BBB disruption by meningitis-causing pathogens, and helps design future research as well as develop potential combination therapies. Full article

(This article belongs to the Special Issue Molecular Signaling Pathways in Brain Pathology 2.0)

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