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Microglia in Neurological Disorders: Potential Therapeutic Targets and Underlying Mechanisms
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Microglia in Neurological Disorders: Potential Therapeutic Targets and Underlying Mechanisms

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: 30 November 2025 | Viewed by 680

Special Issue Editor

Prof. Dr. Masashi Tanaka

E-Mail Website
Guest Editor
Department of Physical Therapy, Health Science University, 7187 Kodachi, Fujikawaguchiko-machi, Minamitsuru-gun, Yamanashi 401-0380, Japan
Interests: cerebral amyloid angiopathy; Alzheimer's disease; amyloid-β fibril formation; taxifolin; microglia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Microglia are innate immune cells that exhibit various functions in the central nervous system (CNS). The phagocytosis of cell debris, apoptotic cells, and cytotoxic factors (e.g., amyloid-β) contributes to CNS integrity, and interactions with neurons affect neuronal functions, such as synaptic plasticity. Therefore, microglial dysfunction has been reported to be closely implicated in the pathogenesis of neurological disorders, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis; however, the mechanistic details remain unclear. Growing evidence has further shown that neuroinflammation by activated microglia exacerbates the pathologies of these disorders. Moreover, recent studies have reported that microglial phenotypes are influenced by various factors, including aging, gut microbiota, and metabolic diseases. These findings highlight microglia as a promising therapeutic target for preventing and improving neurological disorders.

This Special Issue aims to provide novel insights into the underlying mechanisms and therapeutic strategies for neurological disorders, focusing on microglial functions. We welcome original articles, reviews, and commentaries that cover all aspects of this research topic.

Prof. Dr. Masashi Tanaka
Guest Editor

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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.

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Keywords

  • cerebral amyloid angiopathy
  • Alzheimer's disease
  • amyloid-β fibril formation

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Published Papers (2 papers)

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Research

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11 pages, 840 KB  
Communication
Fully Automated Measurement of GFAP in CSF Using the LUMIPULSE® System: Implications for Alzheimer’s Disease Diagnosis and Staging
by Hisashi Nojima, Mai Yamamoto, Jo Kamada, Tomohiro Hamanaka and Katsumi Aoyagi
Int. J. Mol. Sci. 2025, 26(17), 8134; https://doi.org/10.3390/ijms26178134 - 22 Aug 2025
Viewed by 322
Abstract
Glial fibrillary acidic protein (GFAP) has been shown to be a reliable biomarker for detecting neurological disorders. Recently, we developed the Lumipulse G GFAP plasma assay, which is a commercially available tool. Compared to existing assays, the LUMIPLSE G platform offers the high-throughput, [...] Read more.
Glial fibrillary acidic protein (GFAP) has been shown to be a reliable biomarker for detecting neurological disorders. Recently, we developed the Lumipulse G GFAP plasma assay, which is a commercially available tool. Compared to existing assays, the LUMIPLSE G platform offers the high-throughput, rapid, and fully automated quantification of biomarkers, enabling more standardized and accessible clinical study. In this study, we evaluated this assay using cerebrospinal fluid (CSF) samples. Assessing GFAP in CSF may provide more direct insights into central nervous system pathology than plasma and could improve the characterization of Alzheimer’s disease (AD) stages and support treatment monitoring. The LUMIPULSE G system is a chemiluminescent enzyme immunoassay (CLEIA) platform equipped with full automation, utilizing specialized cartridges to process samples within 30 min. The assay, which employs a pair of proprietary monoclonal antibodies targeting GFAP, was evaluated for clinical performance using 30 CSF samples from patients diagnosed with AD, patients with mild cognitive impairment (MCI), and cognitively unimpaired (CU) individuals, with 10 samples from each group. In addition, levels of β-amyloid 1–40 (Aβ40), β-amyloid 1–42 (Aβ42), and pTau181 were simultaneously measured. The Lumipulse G GFAP assay significantly differentiated (p < 0.05) between the amyloid accumulation and non-amyloid accumulation groups, as classified based on the CSF Aβ test. Furthermore, GFAP showed a moderate correlation with pTau181 (r = 0.588), as determined based on Spearman’s rank correlation coefficient. Moreover, receiver operating characteristic (ROC) analysis was performed to determine the performance of GFAP in distinguishing amyloid-positive and amyloid-negative subjects, with an area under the curve (AUC) of 0.72 (0.50–0.93). When stratified by CSF pTau181 positivity, GFAP demonstrated an improved diagnostic accuracy, achieving an AUC of 0.86 (95% CI: 0.68–1.00). This study demonstrates that the Lumipulse G GFAP assay, when applied to CSF samples, has the potential to differentiate AD from non-AD cases, particularly suggesting its utility in detecting tau-related pathology. While GFAP has previously been established as a biomarker for AD, our findings highlight that combining GFAP with other biomarkers such as Aβ40, Aβ42, and pTau181 may enhance the understanding of AD pathogenesis, disease staging, and possibly treatment responses. These findings suggest that GFAP may serve as a complementary biomarker reflecting astroglial reactivity associated with tau positivity, alongside established biomarkers such as Aβ40, Aβ42, and pTau181. However, since GFAP levels may also be elevated in other neurological disorders beyond AD, further investigation into these conditions is required. Full article
(This article belongs to the Special Issue Microglia in Neurological Disorders: Potential Therapeutic Targets and Underlying Mechanisms)
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Review

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29 pages, 1602 KB  
Review
Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia–Reperfusion Injury: From Inflammatory Response to Neurorepair
by Zhendong Li, Man Li, Zhi Fang and Haijun Wang
Int. J. Mol. Sci. 2025, 26(17), 8336; https://doi.org/10.3390/ijms26178336 - 28 Aug 2025
Viewed by 217
Abstract
Cerebral ischemia–reperfusion injury (CIRI) is a complex pathological process that arises when blood flow is restored to the brain after ischemia, often resulting in significant neuronal damage and triggering secondary inflammatory responses. This review explores the immune mechanisms underlying CIRI, focusing on the [...] Read more.
Cerebral ischemia–reperfusion injury (CIRI) is a complex pathological process that arises when blood flow is restored to the brain after ischemia, often resulting in significant neuronal damage and triggering secondary inflammatory responses. This review explores the immune mechanisms underlying CIRI, focusing on the activation and polarization of resident central nervous system (CNS) cells—particularly microglia and astrocytes—and the infiltration of peripheral immune cells such as neutrophils, monocytes/macrophages, and T lymphocytes. We discuss the central role of microglia in the neuroinflammatory cascade, their polarization between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes, and how this process influences neuronal damage and tissue repair. This review highlights the roles of the complement system, inflammasome activation, and blood–brain barrier disruption as key drivers of inflammation and neuronal injury. Additionally, we elaborate on the dynamic interactions between resident and infiltrating immune cells, which amplify inflammation and impede post-ischemic recovery. Finally, we discuss emerging therapeutic strategies targeting immune modulation, including cytokine regulation, microglial reprogramming, and targeted drug delivery systems, which offer promising avenues for improving outcomes in ischemic stroke. Full article
(This article belongs to the Special Issue Microglia in Neurological Disorders: Potential Therapeutic Targets and Underlying Mechanisms)
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