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New Insights into Chronic Inflammatory Demyelinating Polyneuropathy and Neuroimmunological Diseases
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New Insights into Chronic Inflammatory Demyelinating Polyneuropathy and Neuroimmunological Diseases

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 2026 | Viewed by 2787

Special Issue Editor

Dr. Fumitaka Shimizu

E-Mail Website
Guest Editor
Department of Neurology and Clinical Neuroscience, Graduate School of Medicine, Yamaguchi University, Ube 755-8505, Japan
Interests: neuroimmune disease; blood-brain barrier; blood-nerve barrier
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Research on neuroimmunological diseases based on molecular biological studies and experimental models is providing new insights into disease mechanisms and contributing to the development of novel therapeutic drugs and biologics for these diseases. This Special Issue seeks to focus on both basic molecular science and translational research on neuroimmunological diseases in order to overcome these intractable neurological diseases. This Special Issue is focused on chronic inflammatory demyelinating polyneuropathy and also addresses some neuroimmunological diseases.  Topics of interest include, but are not limited to, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), acute demyelinating encephalomyelitis (ADEM), autoimmune encephalitis, paraneoplastic neurological syndrome, Guillain–Barre syndrome (GBS), and other immune-mediated diseases related to neuropathy and myositis.  Research related to in vitro/in vivo models, including experimental autoimmune encephalitis (EAE), experimental autoimmune neuritis (EAN), the blood–brain barrier, the blood–nerve barrier, astrocytes, microglia, neurons and muscle, and pathological observations or new diagnostic biomarkers for these diseases is also welcome. Since IJMS is a journal about molecular science, pure clinical or model studies will unfortunately not be suitable for this journal.

Dr. Fumitaka Shimizu
Guest Editor

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Keywords

  • chronic inflammatory demyelinating polyneuropathy (CIDP)
  • multiple sclerosis (MS)
  • neuromyelitis optica spectrum disorder (NMOSD)
  • myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)
  • autoimmune encephalitis
  • paraneoplastic neurological syndrome
  • Guillain-Barre syndrome (GBS)
  • myositis
  • blood-brain barrier
  • blood-nerve barrier

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Published Papers (3 papers)

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Research

10 pages, 623 KB  
Article
A Long-Term Prospective Evaluation of the Predictive Value of Molecular Markers in Serum and Cerebrospinal Fluid in Patients in the Early Stage of Multiple Sclerosis
by Mariola Świderek-Matysiak, Magdalena Oset, Karolina Pendrasik, Dominika Świerczewska, Małgorzata Domowicz, Magdalena Namiecińska and Mariusz Stasiołek
Int. J. Mol. Sci. 2026, 27(7), 3155; https://doi.org/10.3390/ijms27073155 - 31 Mar 2026
Viewed by 330
Abstract
Various molecular biomarkers have been suggested as a method to improve the predictive value of prognosis in multiple sclerosis (MS). The characterization of such biomarkers would greatly enhance individual patient management. The aim of this study was to conduct a long-term, prospective evaluation [...] Read more.
Various molecular biomarkers have been suggested as a method to improve the predictive value of prognosis in multiple sclerosis (MS). The characterization of such biomarkers would greatly enhance individual patient management. The aim of this study was to conduct a long-term, prospective evaluation of the prognostic value of molecular biomarkers in serum and cerebrospinal fluid (CSF) in patients in the early stages of MS, before the first treatment initiation. The study included a total of 121 MS patients. Serum and CSF were obtained during diagnostic process. Concentrations of IFN γ, IL-6, CHI3L1, osteopontin, CXCL13, GFAP and neurofilament light chains (NfLs) were analyzed. The mean time of the observation of clinical and radiological MS activity was 60 months after start of MS treatment. Higher serum concentrations of NfLs (Z = 2.28; p = 0.02) and CXCL13 (Z = 2.14; p = 0.03) correlated with need to change the first MS therapy (88% due to ineffectiveness and 12% due to adverse events). Higher NfLs concentrations in the CSF specifically correlated with the occurrence of radiological activity (Z = 2.02; p = 0.04). Increased NfLs and IL-6 concentrations in the CSF correlated with disability progression assessed with the EDSS (Z = 2.81; Z = 2.87; p = 0.004; p = 0.003, respectively), as well as with clinical and/or radiological disease activity (Z = 2.80; Z = 2.43; p = 0.004; p = 0.014, respectively). High levels of NfLs and Il6 in the CSF of MS patients assessed before the therapy may be an indication to use a highly effective therapy as the first treatment for MS. Full article
(This article belongs to the Special Issue New Insights into Chronic Inflammatory Demyelinating Polyneuropathy and Neuroimmunological Diseases)
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13 pages, 8071 KB  
Article
Blood–Nerve Barrier Breakdown Induced by Immunoglobulin G in Typical and Multifocal Chronic Inflammatory Demyelinating Polyneuropathy and Multifocal Motor Neuropathy
by Fumitaka Shimizu, Ryota Sato, Yoichi Mizukami, Kenji Watanabe, Toshihiko Maeda, Takashi Kanda, Naoko Matsui, Sonoko Misawa, Yuishin Izumi, Satoshi Kuwabara and Masayuki Nakamori
Int. J. Mol. Sci. 2026, 27(2), 1088; https://doi.org/10.3390/ijms27021088 - 22 Jan 2026
Viewed by 616
Abstract
Impairment of the blood–nerve barrier (BNB) is associated with the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). This research analyzes the molecular mechanisms of immunoglobulin (Ig) G in patients with typical CIDP, CIDP variants (multifocal CIDP), and multifocal [...] Read more.
Impairment of the blood–nerve barrier (BNB) is associated with the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP) and multifocal motor neuropathy (MMN). This research analyzes the molecular mechanisms of immunoglobulin (Ig) G in patients with typical CIDP, CIDP variants (multifocal CIDP), and multifocal motor neuropathy in BNB-endothelial cells. IgG was purified from the sera of patients with typical CIDP (n = 15), multifocal CIDP (n = 14), multifocal motor neuropathy (MMN; n = 12), and healthy controls (HCs; n = 14). Molecular changes in the RNA-seq/high-content imaging system and permeability were evaluated after the incubation of human peripheral nerve microvascular endothelial cells (PnMECs) with IgG. RNA-seq and a pathway analysis using PnMECs showed that TNF-α, CCL20 (MIP-3α), and ICAM-1 were the centers of the upregulated gene pathways in patients with typical CIDP. TNF-α, VCAM-1, NF-κB, and CSF2 (GM-CSF) are important molecules in patients with multifocal CIDP. The high-content imaging system demonstrated that MIP-3, GM-CSF, and VCAM-1 increased after exposure to typical CIDP-IgG, claudin-5 decreased after exposure to IgG from patients with multifocal CIDP, and TNF-α and VCAM-1 increased after exposure to IgG from patients with MMN. The 10 kDa dextran permeability using coculture with PnMECs and pericytes increased after exposure to IgG from patients with typical CIDP and multifocal CIDP. This effect was reversed after incubation with GM-CSF neutralizing antibodies. Upregulation of MIP-3, GM-CSF, and VCAM-1 may contribute to the infiltration of leukocytes/lymphocytes/monocytes across the BNB into the PNS in typical CIDP. IgG from typical CIDP and multifocal CIDP may decrease barrier properties through autocrine GM-CSF from PnMECs. VCAM-1 upregulation through autocrine TNF secretion in PnMECs may induce lymphocyte entry across the BNB in MMN. Full article
(This article belongs to the Special Issue New Insights into Chronic Inflammatory Demyelinating Polyneuropathy and Neuroimmunological Diseases)
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10 pages, 2415 KB  
Article
5-Aminolevulinic Acid Ameliorates Chronic Experimental Autoimmune Neuritis Through a Dual Mechanism of Mitochondrial Protection and Immunomodulation
by Shingo Konno, Takafumi Uchi, Hideo Kihara and Toshiki Fujioka
Int. J. Mol. Sci. 2025, 26(17), 8512; https://doi.org/10.3390/ijms26178512 - 2 Sep 2025
Viewed by 1283
Abstract
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disorder characterized by inflammation and neurodegeneration, yet current therapies lack direct neuroprotective effects. We investigated the therapeutic potential of 5-aminolevulinic acid (5-ALA), a key precursor for mitochondrial heme synthesis, in a chronic experimental autoimmune neuritis [...] Read more.
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disorder characterized by inflammation and neurodegeneration, yet current therapies lack direct neuroprotective effects. We investigated the therapeutic potential of 5-aminolevulinic acid (5-ALA), a key precursor for mitochondrial heme synthesis, in a chronic experimental autoimmune neuritis (EAN) rat model of CIDP. Rats with established EAN received daily oral 5-ALA (100 mg/kg) or vehicle. Treatment efficacy was assessed by clinical scoring, nerve histopathology, and biochemical analyses of sciatic nerves. 5-ALA administration significantly ameliorated clinical disease severity. This was associated with local immunomodulation in the sciatic nerve, marked by reduced pro-inflammatory IFN-γ and increased anti-inflammatory IL-10 levels. Concurrently, 5-ALA exerted direct neuroprotective effects, evidenced by restored mitochondrial ATP production, decreased oxidative DNA damage, upregulated antioxidant heme oxygenase-1 (HO-1), and improved myelin sheath integrity. These findings suggest that 5-ALA may offer a dual therapeutic benefit by targeting both local inflammation and mitochondrial-mediated neuroprotection. By addressing key pathological mechanisms currently unmet by standard therapies, 5-ALA emerges as a promising disease-modifying candidate for CIDP. Full article
(This article belongs to the Special Issue New Insights into Chronic Inflammatory Demyelinating Polyneuropathy and Neuroimmunological Diseases)
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