Molecular and Cellular Mechanism in Neuroinflammation Research
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: 31 January 2026 | Viewed by 8
Special Issue Editor
Special Issue Information
Dear Colleagues,
In the current Special Issue, the focus is on the molecular aspects of neuroinflammation characterized by the molecular interactions between coding and non-coding molecular constituents of cells within the central and peripheral nervous systems.
Never in history have research opportunities presented themselves in such an appealing way, namely with the multifactorial mechanisms of neuroinflammation being faced with the multimodal armamentarium of their analysis, including multiomics approaches, all reinforced with pathway prediction and machine learning tools that, among others, reveal new interactions and functions of researched pathways with the importance for the progression of disease.
Novel methods to study those disorders will enable the deciphering of complex expression and interaction patterns of genes and non-coding molecules, alongside the epigenetic makeup, sometimes advanced to the level of the molecular machinery of a single cell.
In addition, prospective contributions based on long-established research techniques used to investigate cellular mechanisms and interactions of the acute phase proteins, nucleic acids, functional and structural metabolites, inflammatory mediators, etc., all advancing the knowledge on neuroinflammation are welcome. Importantly, the results of those laborious investigations oftentimes share striking accordance with the results obtained via multiomics assays.
Contributions from all fields of modern neurology, including but not limited to studies of neuro-oncological entities, neurodegenerative diseases, and cerebrovascular diseases are also welcome.
The role of neuroinflammation as induced by a pathogenic agent that changes the cell microenvironment for more efficient disease development is emerging. It is becoming increasingly clear that immune system malfunction may shape the very landscape of neuroinflammatory disorders. This includes the deficient or excessive function of immune cells, molecular hijacking or dysregulation of immune checkpoint proteins, unfavorable polarization of inflammatory and immune cells, and the death of normal cells. In this respect, novel therapies are meant to correct the immune system for indiscriminate/excessive actions, hence suppressing the harms of inflammation while allowing inflammation-dependent defense mechanisms and tissue repair to thrive.
Multi-disciplinary applied research on neuroinflammation should intensify as important questions remain to be answered, e.g., what characteristics novel therapeutics should have to withstand harsh neuroinflammatory microenvironments and what the optimal delivery system should be. The results will hopefully be soon followed by therapies tailored with this regard. Novel therapeutics are awaited to effectively oppose the impact of neuroinflammation on cell injury, thereby abrogating the mechanisms of neurologic disorders or restraining the progression of these diseases and enabling successful neurorehabilitation.
Dr. Robert P. Ostrowski
Guest Editor
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Keywords
- non-coding RNA
- nucleic acids
- inflammatory cells
- inflammatory mediators
- neurotransmitters
- neuroinflammation
- immune cells
- neurodegenerative diseases
- cerebrovascular diseases
- brain tumors
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