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The Role of Neuroinflammation in Neurodegenerative Diseases
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The Role of Neuroinflammation in Neurodegenerative Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 12712

Special Issue Editor

Dr. Wenqiang Fan

E-Mail Website
Guest Editor
Department of Neuroscience, UCB Biopharma SPRL, 1420 Braine-l'Alleud, Belgium
Interests: neuroinflammation; neurodevelopment; neurogenesis; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation, characterized by the activation of glial cells and the release of inflammatory mediators, has emerged as a key player in the pathogenesis of disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. This Special Issue will bring together cutting-edge research that elucidates the molecular mechanisms driving neuroinflammation, its impact on neuronal function and survival, and the potential for targeting these pathways in therapeutic strategies. Contributions will include original research articles, reviews, and perspectives that address how neuroinflammatory processes influence disease progression, and the development of novel biomarkers and interventions.

This Special Issue aims to foster a deeper understanding of neuroinflammation's role in neurodegeneration, paving the way for innovative treatments that could alter the course of these debilitating diseases.

Dr. Wenqiang Fan
Guest Editor

Manuscript Submission Information

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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. Current Issues in Molecular Biology 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 2200 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.

Keywords

  • molecular neuropathology
  • neuroinflammation
  • multiple sclerosis
  • neurodegenerative diseases
  • dementias

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Published Papers (6 papers)

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Research

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14 pages, 1664 KB  
Article
Depletion of IGFALS Serum Level up to 3 Months After Cardiac Surgery, with Exploration of Potential Relationships to Surrogates of Organ Failures and Clinical Outcomes
by Krzysztof Laudanski, Mohamed A. Mahmoud, Hossam Gad and Daniel A. Diedrich
Curr. Issues Mol. Biol. 2025, 47(8), 581; https://doi.org/10.3390/cimb47080581 - 23 Jul 2025
Viewed by 302
Abstract
The insulin-like growth factor binding protein, acid-labile subunit (IGFALS), plays a crucial role in glucose metabolism and immune regulation, key processes in recovery from surgery. Here, we studied the perioperative serum IGFALS dynamics and explored potential clinical implications. A total of 79 patients [...] Read more.
The insulin-like growth factor binding protein, acid-labile subunit (IGFALS), plays a crucial role in glucose metabolism and immune regulation, key processes in recovery from surgery. Here, we studied the perioperative serum IGFALS dynamics and explored potential clinical implications. A total of 79 patients undergoing elective cardiac surgery with implementation of cardiopulmonary bypass had their serum isolated at baseline, 24 h, seven days, and three months postoperatively to assess serum concentrations of IGFALS and insulin growth factor 1 (IGF-1). Markers of perioperative injury included troponin I (TnI), high-mobility group box 1 (HMGB-1), and heat shock protein 60 (Hsp-60). Inflammatory status was assessed via interleukin-6 (IL-6) and interleukin-8 (IL-8). Additionally, we measured in vitro cytokine production to viral stimulation of whole blood and monocytes. Surrogates of neuronal distress included neurofilament light chain (NF-L), total tau (τ), phosphorylated tau at threonine 181 (τp181), and amyloid β40 and β42. Renal impairment was defined by RIFLE criteria. Cardiac dysfunction was denoted by serum N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Serum IGFALS levels declined significantly after surgery and remained depressed even at 3 months. Administration of acetaminophen and acetylsalicylic acid differentiated IGFALS levels at the 24 h postoperatively. Serum IGFALS 24 h post-operatively correlated with production of cytokines by leukocytes after in vitro viral stimulation. Serum amyloid-β1-42 was significantly associated with IGFALS at baseline and 24 h post-surgery Patients discharged home had higher IGFALS levels at 28 days and 3 months than those discharged to healthcare facilities or who died. These findings suggest that IGFALS may serve as a prognostic biomarker for recovery trajectory and postoperative outcomes in cardiac surgery patients. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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18 pages, 1584 KB  
Article
A Theoretical and Practical Analysis of Membrane Protein Genes Altered in Neutrophils in Parkinson’s Disease
by Araliz López Pintor, Miriam Nolasco López, José Daniel Lozada-Ramírez, Martín Alejandro Serrano-Meneses, Alicia Ortega Aguilar, Dante Oropeza Canto, César Flores-de los Ángeles, Victor Hugo Anaya-Muñoz and Aura Matilde Jiménez-Garduño
Curr. Issues Mol. Biol. 2025, 47(6), 459; https://doi.org/10.3390/cimb47060459 - 13 Jun 2025
Viewed by 1032
Abstract
Parkinson’s disease (PD) is a major health concern, with no accurate or early diagnostic test available for most patients. Chronic inflammation is a recognized contributor to PD pathogenesis; thus, membrane proteins of inflammatory cells such as neutrophils present an accessible target for detecting [...] Read more.
Parkinson’s disease (PD) is a major health concern, with no accurate or early diagnostic test available for most patients. Chronic inflammation is a recognized contributor to PD pathogenesis; thus, membrane proteins of inflammatory cells such as neutrophils present an accessible target for detecting early molecular changes. In this study, we conducted a theoretical analysis using the GSE99039 database to identify differentially expressed genes (DEGs) in leukocytes from PD patients. From this, we selected nine top candidates for digital polymerase chain reaction (dPCR) analysis in isolated neutrophils from nine PD patients and nine matched controls. Our results revealed significant upregulation of ORAI3 and CLCN2. Unexpectedly, both ACTB (β-actin) and SNCA (alpha-synuclein) were also upregulated in neutrophils. Notably, this study provides the first evidence of CLCN2 expression in neutrophils and demonstrates the significant upregulation of four genes via dPCR. These genes may serve as potential biomarkers for future research on PD detection. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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11 pages, 1679 KB  
Article
Empagliflozin Attenuates High-Glucose-Induced Astrocyte Activation and Inflammation via NF-κB Pathway
by Dong Hee Kim, Min Jin Lee, Dasol Kang, Ji Young Lee, Sujin Park, Ah Reum Khang, Ji Hyun Bae, Joo Yeon Kim, Su Hyun Kim, Yang Ho Kang and Dongwon Yi
Curr. Issues Mol. Biol. 2024, 46(11), 12417-12427; https://doi.org/10.3390/cimb46110737 - 4 Nov 2024
Viewed by 2822
Abstract
Sodium-glucose cotransporter-2 (SGLT2) inhibitors regulate blood glucose levels in patients with type 2 diabetes mellitus and may also exert anti-inflammatory and anti-atherosclerotic effects by promoting M2 macrophage polarization. Although SGLT2 is expressed in brain regions that influence glucose balance and cognitive function, its [...] Read more.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors regulate blood glucose levels in patients with type 2 diabetes mellitus and may also exert anti-inflammatory and anti-atherosclerotic effects by promoting M2 macrophage polarization. Although SGLT2 is expressed in brain regions that influence glucose balance and cognitive function, its roles in the central nervous system are unclear. This study investigated the effects of empagliflozin (EMPA), an SGLT2 inhibitor, on hypothalamic inflammation associated with metabolic diseases. Mice were subjected to a high-fat diet (HFD) for varying durations (3 d, 3 weeks, and 16 weeks) and treated with EMPA for 3 weeks (NFD, NFD + EMPA, HFD, HFD + EMPA; n = 5/group). EMPA regulated the expression of astrocyte markers and pro-inflammatory cytokine mRNA in the hypothalamus of HFD-induced mice, which was linked to regulation of the NF-κB pathway. Under hyperglycemic conditions, EMPA may mitigate hypothalamic inflammation by modulating astrocyte activation via the NF-κB pathway. Our findings demonstrated that EMPA possesses therapeutic potential beyond merely lowering blood glucose levels, opening new avenues for addressing inflammation and providing neuroprotection in metabolic disease management. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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Review

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17 pages, 1839 KB  
Review
The Clock and the Brain: Circadian Rhythm and Alzheimer’s Disease
by Samaneh Ghorbani Shirkouhi, Ashkan Karimi, Seyed Sepehr Khatami, Ashkan Asgari Gashtrodkhani, Farzin Kamari, Morten Blaabjerg and Sasan Andalib
Curr. Issues Mol. Biol. 2025, 47(7), 547; https://doi.org/10.3390/cimb47070547 - 15 Jul 2025
Viewed by 847
Abstract
Alzheimer’s Disease (AD) is the most common type of dementia. The circadian system, which is controlled by the master clock in the Suprachiasmatic Nucleus (SCN) of the hypothalamus, is crucial for various physiological processes. Studies have shown that changes in the circadian rhythms [...] Read more.
Alzheimer’s Disease (AD) is the most common type of dementia. The circadian system, which is controlled by the master clock in the Suprachiasmatic Nucleus (SCN) of the hypothalamus, is crucial for various physiological processes. Studies have shown that changes in the circadian rhythms can deteriorate neurodegenerative diseases. Changes in the SCN are associated with cognitive decline in AD. The cognitive impairments in AD, especially memory dysfunctions, may be related to Circadian Rhythm Disturbances (CRDs). Moreover, rhythmic expression of clock genes is disrupted in AD patients. There is a circadian pattern of inflammatory processes in AD, and dysregulation of core clock genes promotes neuroinflammation. The present narrative review addresses the intricate link between CRDs and AD, revisiting the relevant cellular and molecular mechanisms. The association between CRDs and AD highlights the need for further investigation of the underlying mechanisms. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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32 pages, 1237 KB  
Review
Neuroinflammation: Mechanisms, Dual Roles, and Therapeutic Strategies in Neurological Disorders
by Mario García-Domínguez
Curr. Issues Mol. Biol. 2025, 47(6), 417; https://doi.org/10.3390/cimb47060417 - 4 Jun 2025
Viewed by 1373
Abstract
Neuroinflammation represents a fundamental component in the development and progression of a wide range of neurological disorders, including neurodegenerative diseases, psychiatric conditions, and cerebral injuries. This review examines the complex mechanisms underlying neuroinflammatory responses, with a focus on the interactions between glial cells [...] Read more.
Neuroinflammation represents a fundamental component in the development and progression of a wide range of neurological disorders, including neurodegenerative diseases, psychiatric conditions, and cerebral injuries. This review examines the complex mechanisms underlying neuroinflammatory responses, with a focus on the interactions between glial cells and neurons. The dualistic role of neuroinflammation is further investigated, highlighting its ability to promote neuroprotection in acute phases while also contributing to neuronal injury and degeneration during chronic activation. This review also considers innovative therapeutic approaches designed to target neuroinflammatory processes, like drug-based treatments and immune-modulating therapies. A thorough understanding of the regulatory balance within neuroinflammatory networks is essential for the development of effective treatments for several neurological pathologies. Finally, this review provides an integrative summary of current evidence and highlights emerging directions in neuroinflammation research. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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17 pages, 744 KB  
Review
Mechanisms and Emerging Regulators of Neuroinflammation: Exploring New Therapeutic Strategies for Neurological Disorders
by Mi Eun Kim and Jun Sik Lee
Curr. Issues Mol. Biol. 2025, 47(1), 8; https://doi.org/10.3390/cimb47010008 - 26 Dec 2024
Cited by 15 | Viewed by 5828
Abstract
Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative [...] Read more.
Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Multiple Sclerosis. This review explores the cellular and molecular mechanisms underlying neuroinflammation, focusing on the roles of microglia, astrocytes, and peripheral immune cells. Key signaling pathways, including NF-κB, JAK-STAT, and the NLRP3 inflammasome, are discussed alongside emerging regulators such as non-coding RNAs, epigenetic modifications, and the gut–brain axis. The therapeutic landscape is evolving, with traditional anti-inflammatory drugs like NSAIDs and corticosteroids offering limited efficacy in chronic conditions. Immunomodulators, gene and RNA-based therapeutics, and stem cell methods have all shown promise for more specific and effective interventions. Additionally, the modulation of metabolic states and gut microbiota has emerged as a novel strategy to regulate neuroinflammation. Despite significant progress, challenges remain in translating these findings into clinically viable therapies. Future studies should concentrate on integrated, interdisciplinary methods to reduce chronic neuroinflammation and slowing the progression of neurodegenerative disorders, providing opportunities for revolutionary advances in CNS therapies. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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