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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: 30 June 2025 | Viewed by 2221

Special Issue Editor


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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 100 words) can be sent to the Editorial Office for announcement on this website.

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 (2 papers)

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Research

23 pages, 2007 KiB  
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
Viewed by 891
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
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27 pages, 3607 KiB  
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
Viewed by 1133
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
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