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Molecular Mechanism and Regulation in Neuroinflammation, 2nd Edition
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Molecular Mechanism and Regulation in Neuroinflammation, 2nd Edition

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 10045

Editor

Dr. Hung-Pei Tsai

E-Mail Website
Guest Editor
Division of Neurosurgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung 80756, Taiwan
Interests: neuropathic pain; subarachnoid hemorrhage; nerve repair; brain tumor; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is defined as an inflammatory response within the brain or spinal cord, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. This inflammation is mediated by the production of cytokines, chemokines, reactive oxygen species, and second messengers. These mediators are produced by resident CNS glial cells (microglia and astrocytes), endothelial cells, and immune cells of peripheral origin. These neuroinflammatory responses have immunological, physiological, biochemical, and psychological consequences. From a pathological point of view, in the central nervous system, neuroinflammation is associated with damage from direct penetrating physical injury (e.g., traumatic brain injury (TBI), spinal cord injury (SCI), etc.), neurodegenerative multiple sclerosis (MS) and other biochemical diseases (e.g., Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS)), tumors (gliomas), or senescence. The development of solutions to slow or suppress this neuroinflammation is highly warranted. Following the first edition, the research topics of this Special Issue still aim to cover promising, recent, and novel molecular regulation and research mechanisms for the diagnosis and treatment of neuroinflammation.

Dr. Hung-Pei Tsai
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-anonymized 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 2400 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

  • microglia
  • glial cells
  • cytokines
  • blood–brain barrier
  • traumatic brain injury
  • aging
  • Alzheimer's disease
  • parkinson's disease
  • amyotrophic lateral sclerosis
  • multiple sclerosis

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Published Papers (3 papers)

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Review

23 pages, 665 KB  
Review
The Mast Cell–Substance P Neuroimmune Axis in Allergic Contact Dermatitis and Atopic Dermatitis: Molecular Mechanisms and Pathophysiological Perspectives
by Ernesto Aitella, Gianluca Azzellino, Ciro Romano, Massimo De Martinis and Lia Ginaldi
Curr. Issues Mol. Biol. 2026, 48(9), 928; https://doi.org/10.3390/cimb48090928 - 10 Sep 2026
Abstract
Recent advances in cutaneous neuroimmunology have substantially expanded our understanding of inflammatory skin diseases, revealing an intricate bidirectional network linking peripheral sensory neurons, resident immune cells, and structural skin components. Among the mediators orchestrating this communication, substance P (SP) and mast cells have [...] Read more.
Recent advances in cutaneous neuroimmunology have substantially expanded our understanding of inflammatory skin diseases, revealing an intricate bidirectional network linking peripheral sensory neurons, resident immune cells, and structural skin components. Among the mediators orchestrating this communication, substance P (SP) and mast cells have emerged as pivotal regulators connecting neuronal activation with immune responses, vascular dysfunction, chronic inflammation, and persistent pruritus. Beyond the canonical neurokinin-1 receptor (NK1R), the identification of the Mas-related G protein-coupled receptor X2 (MRGPRX2) has fundamentally reshaped mast-cell biology by establishing an IgE-independent pathway of neuropeptide-induced activation. This narrative review examines the molecular mechanisms underlying the mast cell–SP neuroimmune axis and discusses its contribution to the pathogenesis of allergic contact dermatitis and atopic dermatitis. Unlike the traditional approach, which primarily considers atopic dermatitis as the reference model for cutaneous neuroimmune interactions, allergic contact dermatitis may provide a useful model for examining how neuroimmune amplification integrates with delayed T-cell-mediated inflammation. These concepts are subsequently applied to atopic dermatitis, where they operate within the broader context of type 2 inflammation, epidermal barrier dysfunction, and chronic pruritus. Rather than replacing classical immunopathogenic models, this emerging neuroimmune perspective complements them by identifying bidirectional communication between sensory neurons and mast cells as a dynamic amplifier of adaptive immune responses. This integrated perspective not only provides a unifying interpretation of inflammatory dermatitis but also offers a conceptual basis for exploring similar neuroimmune mechanisms across other immune-mediated skin disorders and for generating future mechanism-based therapeutic hypotheses. Full article
(This article belongs to the Special Issue Molecular Mechanism and Regulation in Neuroinflammation, 2nd Edition)
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22 pages, 4021 KB  
Review
Insulin-like Growth Factor 1 Impact on Alzheimer’s Disease: Role in Inflammation, Stress, and Cognition
by Jonathan Zegarra-Valdivia, Harold Arana-Nombera, Leandro Perez-Fernandez, Milagros del Rocío Casimiro, Viviana Gallegos-Manayay, María del Rosario Oliva-Piscoya, Reyna Alamo-Medina, Eduardo Abanto-Saldaña, María Celinda Cruz-Ordinola, Carmen Paredes-Manrique and Brenda Chino-Vilca
Curr. Issues Mol. Biol. 2025, 47(4), 233; https://doi.org/10.3390/cimb47040233 - 27 Mar 2025
Cited by 6 | Viewed by 5014
Abstract
Alzheimer’s disease (AD) is a leading cause of dementia, characterized by multifactorial interactions involving genetic, inflammatory, and metabolic dysregulation. Insulin-like growth factor 1 (IGF-I) plays a critical role in maintaining brain homeostasis through neurogenesis, synaptogenesis, and neuroprotection. However, disruptions in IGF-I signaling have [...] Read more.
Alzheimer’s disease (AD) is a leading cause of dementia, characterized by multifactorial interactions involving genetic, inflammatory, and metabolic dysregulation. Insulin-like growth factor 1 (IGF-I) plays a critical role in maintaining brain homeostasis through neurogenesis, synaptogenesis, and neuroprotection. However, disruptions in IGF-I signaling have been implicated in hallmark AD processes such as beta-amyloid accumulation, glucose metabolism disturbances, oxidative stress, chronic inflammation, and neuronal death. This review aims to comprehensively analyze the mechanisms by which IGF-I influences AD pathology, emphasizing its potential as both an early detection biomarker and a therapeutic target. By synthesizing clinical and preclinical study findings, we explore how chronic stress, systemic inflammation, and lifestyle factors disrupt IGF-I pathways, accelerating cognitive and social impairments. Special attention is given to high-level cognitive processes, including executive functions and social cognition, which are particularly vulnerable to these disruptions. Highlighting the interplay between IGF-I, neuroinflammation, and stress, this work underscores the need for affordable and accessible diagnostic tools and therapeutic strategies. This review contributes to a deeper understanding of IGF-I’s multifaceted role in AD, offering new insights for addressing the growing global burden of dementia. Full article
(This article belongs to the Special Issue Molecular Mechanism and Regulation in Neuroinflammation, 2nd Edition)
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23 pages, 903 KB  
Review
The Therapeutic Potential of MicroRNA-21 in the Treatment of Spinal Cord Injury
by Ahmed Hasan, Alessio Ardizzone, Domenico Giosa, Sarah Adriana Scuderi, Elsa Calcaterra, Emanuela Esposito and Anna Paola Capra
Curr. Issues Mol. Biol. 2025, 47(2), 70; https://doi.org/10.3390/cimb47020070 - 21 Jan 2025
Cited by 11 | Viewed by 4340
Abstract
Spinal cord injury (SCI) involves complex pathological processes that often result in significant and long-term neurological deficits. Increasingly, research has identified microRNA-21 (miR-21) as a pivotal regulator in SCI, with studies focusing on its roles in inflammation, apoptosis, and tissue repair. This review [...] Read more.
Spinal cord injury (SCI) involves complex pathological processes that often result in significant and long-term neurological deficits. Increasingly, research has identified microRNA-21 (miR-21) as a pivotal regulator in SCI, with studies focusing on its roles in inflammation, apoptosis, and tissue repair. This review synthesizes current findings on miR-21’s involvement in post-injury molecular events, emphasizing its interactions with regulatory targets such as Phosphatase and Tensin Homolog (PTEN) and Programmed Cell Death Protein 4 (PDCD4), as well as its broader effects on inflammatory and apoptotic signaling pathways. Evidence from both in vitro and in vivo studies suggests that modulating miR-21 influences lesion size, cellular dynamics, and functional recovery, highlighting its potential as a therapeutic target for SCI. Nonetheless, the clinical translation of miR-21-based therapies poses significant challenges, including the need to optimize dosages, delivery mechanisms, and long-term safety profiles. Further research is crucial to fully delineate miR-21’s therapeutic potential and determine its feasibility for integration into SCI treatment protocols. This review aims to provide a comprehensive overview of miR-21’s roles in SCI pathology, offering insights into the molecular mechanisms underlying recovery and the emerging potential of miR-21 in SCI management to enhance outcomes and quality of life for affected patients. Full article
(This article belongs to the Special Issue Molecular Mechanism and Regulation in Neuroinflammation, 2nd Edition)
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