Inflammation in Neurogenerative Diseases: Mechanisms and Therapeutic Frontiers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 5036

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Guest Editor
Department of Ophthalmology, University of Virginia School of Medicine, Charlottesville, VA 22903, USA
Interests: neurodegenerative diseases; inflammation; eye diseases; gene therapy
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Special Issue Information

Dear Colleagues,

Chronic inflammation plays a critical role in the development and progression of many neurodegenerative diseases, including Alzheimer’s, Parkinson’s, multiple sclerosis, and age-related macular degeneration. Increasing evidence points to the complex involvement of immune responses, both in the brain and from the periphery, including the actions of microglia, astrocytes, and other immune cells, in driving neuronal damage and loss.

This Special Issue, entitled "Inflammation in Neurogenerative Diseases: Mechanisms and Therapeutic Frontiers", invites contributions that explore how inflammation shapes the course of neurodegenerative diseases and what we can do to intervene. We are particularly interested in studies that uncover new mechanisms of neuroinflammation, identify promising biomarkers, and propose innovative therapies—ranging from gene therapy and immunomodulation to nanomedicine.

Dr. Shao-Bin Wang
Guest Editor

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Keywords

  • neuroinflammation
  • neurodegenerative diseases
  • biomarkers mitochondria dysfunction
  • microglia
  • immune response
  • therapeutic development
  • gene therapy

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Published Papers (2 papers)

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Review

15 pages, 1682 KB  
Review
The Role of Non-LTR Retrotransposons in Sterile Inflammation: Mechanisms and Therapeutic Potential
by Hua Yang, Xin Chen, Tamara Saksida, Melita Vidaković, Sizhuo Chen, Vuk Savkovic, Mingyue Chen, Shaobin Wang and Zhenhuan Zhao
Biomedicines 2026, 14(2), 272; https://doi.org/10.3390/biomedicines14020272 - 26 Jan 2026
Viewed by 1834
Abstract
Non-long terminal repeat (Non-LTR) retrotransposons are mobile genetic elements that replicate through a “copy-and-paste” mechanism, enabling their expansion within the genome. Aberrant activation of these elements can induce genomic instability, elicit cellular stress responses, and activate inflammasome signaling, leading to tissue injury and [...] Read more.
Non-long terminal repeat (Non-LTR) retrotransposons are mobile genetic elements that replicate through a “copy-and-paste” mechanism, enabling their expansion within the genome. Aberrant activation of these elements can induce genomic instability, elicit cellular stress responses, and activate inflammasome signaling, leading to tissue injury and disease. The central process of sterile inflammation involves the release and recognition of damage-associated molecular patterns (DAMPs), endogenous molecules that initiate inflammatory responses and form a common basis for many sterile inflammatory disorders. Recent studies have identified non-LTR retrotransposons as key endogenous triggers of DAMP-like signaling that drive sterile inflammation in both neuronal and non-neuronal tissues, contributing to the development of neurodegenerative and other chronic inflammatory diseases. In this review, we summarize recent advances in understanding how non-LTR retrotransposons, particularly LINE and SINE elements, influence sterile inflammation and disease pathogenesis. We highlight how their mobilization reshapes genomic architecture and gene regulation, and how the resulting signaling cascades promote chronic inflammation, immune dysregulation, and tissue injury. We also discuss emerging therapeutic strategies aimed at suppressing retrotransposon activity or interrupting downstream inflammatory signaling for treating sterile inflammation-related diseases. Full article
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45 pages, 1192 KB  
Review
Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications
by Mario García-Domínguez
Biomedicines 2026, 14(1), 115; https://doi.org/10.3390/biomedicines14010115 - 6 Jan 2026
Cited by 11 | Viewed by 2789
Abstract
Neuroinflammation is a defining feature of many neurological disorders, including neurodegenerative diseases, traumatic brain injury, and demyelinating conditions. Glial cells play a central role in this process by initiating, modulating, and resolving inflammatory responses in the CNS. This review examines the diverse roles [...] Read more.
Neuroinflammation is a defining feature of many neurological disorders, including neurodegenerative diseases, traumatic brain injury, and demyelinating conditions. Glial cells play a central role in this process by initiating, modulating, and resolving inflammatory responses in the CNS. This review examines the diverse roles of glial cells in neuroinflammation, focusing on their molecular and cellular interactions, context-dependent activation states, and phenotypic plasticity. It discusses how microglial activation can result in both neuroprotective and neurotoxic effects, while astrocytes contribute to immune regulation, blood–brain barrier integrity, and neuronal survival. The review also highlights interactions between glial cells and peripheral immune components, which may exert synergistic or antagonistic effects. Finally, it outlines emerging preclinical and clinical strategies targeting glial pathways to modulate several neuroinflammatory outcomes, emphasizing that a detailed understanding of glial dynamics is essential for developing effective CNS therapies. Full article
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