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Neuroinflammation: Advancements in Pathophysiology and Therapies (2nd Edition)
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Neuroinflammation: Advancements in Pathophysiology and Therapies (2nd Edition)

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: 20 December 2025 | Viewed by 6223

Special Issue Editor

Dr. David Martín-Hernández

E-Mail Website
Guest Editor
1. Centro de Investigación Biomédica en Red de Salud Mental, Instituto de Salud Carlos III (CIBERSAM, ISCIII), 28029 Madrid, Spain
2. Departamento de Farmacología y Toxicología, Facultad de Medicina, Instituto de Investigación Hospital 12 de Octubre (i+12), Instituto Universitario de Investigación en Neuroquímica (IUIN), Universidad Complutense de Madrid (UCM), 28040 Madrid, Spain
Interests: neuropsychopharmacology; inflammation; microbiome; glía; barrier function; psychiatric diseases; schizophrenia; depression
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Special Issue Information

Dear Colleagues,

Neuroinflammation stands as a pervasive phenomenon that cuts across various conditions that affect the central nervous system (CNS), encompassing neurological, neurodegenerative, cardiovascular, and psychiatric disorders. Furthermore, neuroinflammation might also have a role in physiological processes such as aging. In essence, inflammation is a homeostatic mechanism triggered by stimuli of diverse nature to protect the organism. However, if the inflammatory process falters in eliminating potential menaces and persists over time, it can hamper normal CNS function and contribute to disease development. Despite the etiological responsibilities of neuroinflammation sparking an intense debate, its concurrence and consequences represent a harmful threat and may exacerbate the progression and severity of CNS diseases. In this context, a wealth of meta-analyses and an expanding body of clinical and preclinical data underscore the efficacy of anti-inflammatory treatments in some facets of these pathologies, supporting the fact that uncontrolled and chronic neuroinflammation endangers the CNS. Nevertheless, the precise molecular mechanisms underpinning neuroinflammation, its significance for the pathophysiology of certain diseases, and the search for novel therapies aimed at modulating neuroinflammation for clinical improvement remain limited, thereby necessitating further research.

This Special Issue aims to provide a broad overview of the latest cutting-edge advancements in neuroinflammation research, emphasizing its role in the pathophysiology of diseases and innovative treatment strategies. We welcome original research articles, reviews, brief reports, or any other contributions dealing with the following:

  • Molecular, cellular, and tissue-level mechanisms governing neuroinflammation and their regulatory pathways;
  • Neuroinflammation in the pathophysiology of CNS or systemic diseases;
  • Emerging pharmacological approaches for managing or modulating neuroinflammation.

We hope that Special Issue will serve as a trove of recent and current knowledge for newcomers and experienced scientists in this dynamic field.

Dr. David Martín-Hernández
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 250 words) can be sent to the Editorial Office for assessment.

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

  • neuroinflammation
  • CNS diseases
  • pathophysiology
  • therapeutic strategies
  • pharmacological treatments
  • neurological disorders
  • neurodegenerative diseases
  • cardiovascular diseases
  • psychiatric disorders

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Related Special Issue

Published Papers (3 papers)

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Research

25 pages, 2889 KB  
Article
Prolonged Aggressive Experience Accelerates Resolution of Inflammation in Blood and Microglia After Repeated LPS Treatment
by Anastasia Mutovina, Anna Sapronova, Kseniya Ayriyants, Yulia Ryabushkina, Julia Khantakova, Polina Mezhevalova, Polina Ritter and Natalya Bondar
Int. J. Mol. Sci. 2025, 26(24), 12007; https://doi.org/10.3390/ijms262412007 - 13 Dec 2025
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Abstract
This study investigated how prolonged aggression in male CD1 mice alters responses to chronic LPS (lipopolysaccharide)-induced inflammation. Experience of aggression induced pathological aggression in 36% of mice. Following LPS, aggressors resolved systemic inflammation within five days—evidenced by normalized locomotor activity, WBC (white blood [...] Read more.
This study investigated how prolonged aggression in male CD1 mice alters responses to chronic LPS (lipopolysaccharide)-induced inflammation. Experience of aggression induced pathological aggression in 36% of mice. Following LPS, aggressors resolved systemic inflammation within five days—evidenced by normalized locomotor activity, WBC (white blood cells), and lymphocyte counts—while controls remained inflamed. LPS did not alter established aggression or anxiety. Furthermore, aggressors demonstrated accelerated inflammation resolution in the brain, showing a higher proportion of resting microglia and a lower percentage of activated microglia following LPS-induced inflammation compared to control animals. Gene expression analysis revealed a more pronounced inflammatory response in the hypothalamus than in the nucleus accumbens. Aggressive mice exhibited a profile associated with inflammation resolution, indicated by increased expression of the Trem2 gene. These differential immune responses may be modulated by the dopaminergic system. Elevated Drd1 gene expression in the hypothalamus could possibly contribute to the anti-inflammatory signaling, while changes in nucleus accumbens dopaminergic activity, involving D2 receptor activation, appear linked to the development of pathological aggression. Thus, this study demonstrates that prolonged aggression induces persistent changes in behavioral, neuroimmune, and neuroendocrine systems in male CD1 mice. Aggressive animals develop a distinct neuroimmune phenotype characterized by accelerated resolution of both systemic and brain inflammation following LPS challenge. Full article
(This article belongs to the Special Issue Neuroinflammation: Advancements in Pathophysiology and Therapies (2nd Edition))
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23 pages, 2007 KB  
Article
LRRK2 in Drosophila Melanogaster Model: Insights into Cellular Dysfunction and Neuroinflammation in Parkinson’s Disease
by Cristina Ciampelli, Grazia Galleri, Manuela Galioto, Paolo Mereu, Monica Pirastru, Roberto Bernardoni, Diego Albani, Claudia Crosio and Ciro Iaccarino
Int. J. Mol. Sci. 2025, 26(5), 2093; https://doi.org/10.3390/ijms26052093 - 27 Feb 2025
Cited by 1 | Viewed by 2715
Abstract
Parkinson’s disease (PD) is a fatal neurodegenerative disease for which there are no still effective treatments able to stop or slow down neurodegeneration. To date, pathological mutations in the leucine-rich repeat kinase 2 (LRRK2) gene have been identified as the major genetic cause [...] Read more.
Parkinson’s disease (PD) is a fatal neurodegenerative disease for which there are no still effective treatments able to stop or slow down neurodegeneration. To date, pathological mutations in the leucine-rich repeat kinase 2 (LRRK2) gene have been identified as the major genetic cause of PD, although the molecular mechanism responsible for the loss of dopaminergic neurons is still cryptic. In this review, we explore the contribution of Drosophila models to the elucidation of LRRK2 function in different cellular pathways in either neurons or glial cells. Importantly, recent studies have shown that LRRK2 is highly expressed in immunocompetent cells, including astrocytes and microglia in the brain, compared to neuronal expression. LRRK2 mutations are also strongly associated with the development of inflammatory diseases and the production of inflammatory molecules. Using Drosophila models, this paper shows that a genetic reduction of the inflammatory response protects flies from the neurodegeneration induced by LRRK2 pathological mutant expression. Full article
(This article belongs to the Special Issue Neuroinflammation: Advancements in Pathophysiology and Therapies (2nd Edition))
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27 pages, 3607 KB  
Article
Predicting the Beneficial Effects of Cognitive Stimulation and Transcranial Direct Current Stimulation in Amnestic Mild Cognitive Impairment with Clinical, Inflammation, and Human Microglia Exposed to Serum as Potential Markers: A Double-Blind Placebo-Controlled Randomized Clinical Trial
by Ruth Alcalá-Lozano, Rocio Carmona-Hernández, Ana Gabriela Ocampo-Romero, Adriana Leticia Sosa-Millán, Erik Daniel Morelos-Santana, Diana Zapata Abarca, Dana Vianey Castro-de-Aquino, Edith Araceli Cabrera-Muñoz, Gerardo Bernabé Ramírez-Rodríguez, Ana Luisa Sosa Ortiz, Eduardo A. Garza-Villarreal, Ricardo Saracco-Alvarez and Jorge Julio González Olvera
Int. J. Mol. Sci. 2025, 26(4), 1754; https://doi.org/10.3390/ijms26041754 - 19 Feb 2025
Cited by 2 | Viewed by 3073
Abstract
In amnestic mild cognitive impairment (aMCI), neuroinflammation evolves during disease progression, affecting microglial function and potentially accelerating the pathological process. Currently, no effective treatment exists, leading to explorations of various symptomatic approaches, though few target the underlying physiological mechanisms. Modulating inflammatory processes may [...] Read more.
In amnestic mild cognitive impairment (aMCI), neuroinflammation evolves during disease progression, affecting microglial function and potentially accelerating the pathological process. Currently, no effective treatment exists, leading to explorations of various symptomatic approaches, though few target the underlying physiological mechanisms. Modulating inflammatory processes may be critical in slowing disease progression. Cognitive stimulation (CS) and transcranial direct current stimulation (tDCS) applied to the left dorsolateral prefrontal cortex (l-DLPFC) show promise, but the results are heterogeneous. Thus, a randomized, double-blind, placebo-controlled clinical trial is currently underway. The first-stage results were examined after three weeks of intervention in two groups: active tDCS combined with CS and sham tDCS combined with CS. Twenty-two participants underwent two assessments: T0 (baseline) and T1 (after 15 sessions of tDCS, active or sham, and 9 sessions of CS). The results demonstrated that CS improved cognition, increased brain-derived neurotrophic factor (BDNF) levels, and reduced peripheral proinflammatory cytokine levels (interleukin IL-6 and chemokine CX3CL1) in serum. This decrease in IL-6 may promote microglial proliferation and survival as a modulatory effect response, while the increase in BDNF might suggest a regulatory mechanism in microglia–neuron interaction responses. However, tDCS did not enhance the cognitive or modulatory effects of CS, suggesting that longer interventions might be required to achieve substantial benefits. Full article
(This article belongs to the Special Issue Neuroinflammation: Advancements in Pathophysiology and Therapies (2nd Edition))
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