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Molecular Research in Neuroimmunological Disorders
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Molecular Research in Neuroimmunological Disorders

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 (30 April 2023) | Viewed by 7820

Special Issue Editor

Dr. Paolo Immovilli

E-Mail Website
Guest Editor
The Neurology Unit, Emergency Department, Guglielmo da Saliceto Hospital, Via Taverna 39, 29121 Piacenza, Italy
Interests: multiple sclerosis; stroke
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the last few decades, we have observed substantial progress in the knowledge about pathogenesis and treatment of neuroimmunological disorders, which led to a paradigm shift in neuroimmunological therapy, especially in the field of multiple sclerosis (MS). Interferons, glatiramer acetate, mitoxantrone and cyclophosphamide were the main molecules available to treat MS before 2006; since then, research has led to the approval of about 20 different molecules.

The increasing number of treatments available were achieved with great effort in basic and translational research; molecular research in neuroimmunological disorders led to important new achievements in the immunopathogenesis, biomarkers, PET neuroimaging, and treatment of MS, acute disseminated encephalomyelitis (ADEM), neuromyelitis optica (NMO), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), autoimmune encephalitis, and experimental autoimmune encephalomyelitis (EAE). Neuroinflammatory molecular research has also extended to other fields of the neurosciences, such as stroke.

The aim of this Special Issue is to fulfill the knowledge gaps in molecular research regarding basic, translational, and pharmacological molecular research in the field of neuroimmunological disorders. Original research articles, reviews and short communications are equally welcome, provided that they present new insights in the field of neuroimmunology.

Dr. Paolo Immovilli
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

  • neuroimmunological disorders
  • neurofilaments
  • cytokine
  • multiple sclerosis
  • autoimmune encephalitis
  • acute disseminated encephalomyelitis
  • ADEM
  • neuromyelitis optica
  • myelin oligodendrocyte glycoprotein antibody-associated disease
  • MOGAD
  • experimental autoimmune encephalomyelitis
  • EAE
  • stroke neuroprotection

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Published Papers (2 papers)

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23 pages, 10460 KiB  
Article
Genetically Engineered Artificial Microvesicles Carrying Nerve Growth Factor Restrains the Progression of Autoimmune Encephalomyelitis in an Experimental Mouse Model
by Reem Alatrash, Maria Golubenko, Ekaterina Martynova, Ekaterina Garanina, Yana Mukhamedshina, Svetlana Khaiboullina, Albert Rizvanov, Ilnur Salafutdinov and Svetlana Arkhipova
Int. J. Mol. Sci. 2023, 24(9), 8332; https://doi.org/10.3390/ijms24098332 - 5 May 2023
Cited by 2 | Viewed by 3229
Abstract
Multiple sclerosis (MS) is an incurable, progressive chronic autoimmune demyelinating disease. Therapy for MS is based on slowing down the processes of neurodegeneration and suppressing the immune system of patients. MS is accompanied by inflammation, axon-degeneration and neurogliosis in the central nervous system. [...] Read more.
Multiple sclerosis (MS) is an incurable, progressive chronic autoimmune demyelinating disease. Therapy for MS is based on slowing down the processes of neurodegeneration and suppressing the immune system of patients. MS is accompanied by inflammation, axon-degeneration and neurogliosis in the central nervous system. One of the directions for a new effective treatment for MS is cellular, subcellular, as well as gene therapy. We investigated the therapeutic potential of adipose mesenchymal stem cell (ADMSC) derived, cytochalasin B induced artificial microvesicles (MVs) expressing nerve growth factor (NGF) on a mouse model of multiple sclerosis experimental autoimmune encephalomyelitis (EAE). These ADMSC-MVs-NGF were tested using histological, immunocytochemical and molecular genetic methods after being injected into the tail vein of animals on the 14th and 21st days post EAE induction. ADMSC-MVs-NGF contained the target protein inside the cytoplasm. Their injection into the caudal vein led to a significant decrease in neurogliosis at the 14th and 21st days post EAE induction. Artificial ADMSC-MVs-NGF stimulate axon regeneration and can modulate gliosis in the EAE model. Full article
(This article belongs to the Special Issue Molecular Research in Neuroimmunological Disorders)
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17 pages, 4248 KiB  
Article
Hericium erinaceus Promotes Anti-Inflammatory Effects and Regulation of Metabolites in an Animal Model of Cerebellar Ataxia
by Sze Chun Chau, Pit Shan Chong, Hongkai Jin, Ka Chun Tsui, Sharafuddin Khairuddin, Anna Chung Kwan Tse, Sze Yuen Lew, George Lim Tipoe, Chi Wai Lee, Man-Lung Fung, Kah Hui Wong and Lee Wei Lim
Int. J. Mol. Sci. 2023, 24(7), 6089; https://doi.org/10.3390/ijms24076089 - 23 Mar 2023
Cited by 5 | Viewed by 4026
Abstract
Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although previous study demonstrated the neuroprotective effects of Hericium erinaceus (H.E.), the mechanisms of H.E. treatment on the neuroinflammatory response, neurotransmission, and related metabolites remain largely unknown. We demonstrated that [...] Read more.
Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although previous study demonstrated the neuroprotective effects of Hericium erinaceus (H.E.), the mechanisms of H.E. treatment on the neuroinflammatory response, neurotransmission, and related metabolites remain largely unknown. We demonstrated that 3-AP rats treated with 25 mg/kg H.E. extracts had improved motor coordination and balance in the accelerated rotarod and rod tests. We showed that the H.E. treatment upregulated the expression of Tgfb1, Tgfb2, and Smad3 genes to levels comparable to those in the non-3-AP control group. Interestingly, we also observed a significant correlation between Tgfb2 gene expression and rod test performance in the 3-AP saline group, but not in the non-3-AP control or H.E.+3-AP groups, indicating a relationship between Tgfb2 gene expression and motor balance in the 3-AP rat model. Additionally, we also found that the H.E. treatment increased mitochondrial COX-IV protein expression and normalized dopamine-serotonin neurotransmission and metabolite levels in the cerebellum of the H.E.+3-AP group compared to the 3-AP saline group. In conclusion, our findings suggest that the H.E. treatment improved motor function in the 3-AP rat model, which was potentially mediated through neuroprotective mechanisms involving TGFB2-Smad3 signaling via normalization of neurotransmission and metabolic pathways. Full article
(This article belongs to the Special Issue Molecular Research in Neuroimmunological Disorders)
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