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Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy
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Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy

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 June 2025 | Viewed by 7202

Special Issue Editor

Dr. Chih Hung Lo

E-Mail Website
Guest Editor
Department of Biology & Interdisciplinary Neuroscience Program, Syracuse University, Syracuse, NY, USA
Interests: neuroinflammation; neurodegeneration; neuroimmunology; lysosome biology; receptor signalling; single-cell spatial analysis; drug discovery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation and neuronal cell death are hallmarks of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. While some of these neurological disorders are associated with the accumulation of toxic protein aggregates, including tau, β-amyloid, and α-synuclein, others are related to chronic inflammation and dysregulated immune cell functions. Impairments in lysosomal, autophagic, and mitochondrial functions have also been shown to play major roles in further promoting the accumulation of toxic protein aggregates, while the crosstalk of different organelles remains to be investigated. On the other hand, aberrant receptor signaling is detrimental to neurons and glial cells as it can trigger various types of cell death. Besides understanding the pathogenic molecular pathways, it is also important to elucidate cellular phenotypes and cell–cell interactions in these diseases, including neuron–glia and glia–immune interactions, especially through omics characterizations. Together, these molecular mechanisms will provide insights into novel therapeutic developments and biomarker discovery for translational neuroscience applications. We invite authors to submit original articles and review articles highlighting the latest advances in probing molecular mechanisms and developing novel therapies for neuroinflammation and neurodegeneration.

Dr. Chih Hung Lo
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.

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Keywords

  • neuroinflammation
  • neurodegeneration
  • neuroimmunology
  • toxic protein aggregates
  • autolysosomal dysfunction
  • metabolic defects
  • aberrant receptor signaling
  • neuron-glia interactions
  • glia-immune interactions
  • omics characterizations
  • therapeutic development
  • biomarker discovery

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Published Papers (5 papers)

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Research

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17 pages, 1813 KiB  
Article
Mapping Inflammatory Markers in Cerebrospinal Fluid Following Aneurysmal Subarachnoid Hemorrhage: An Age- and Sex-Matched Analysis
by Katharina Sophie Seyfried, Benedikt Kremer, Catharina Conzen-Dilger, Michael Veldeman, Ulf Bertram, Christian Blume, Christian Andreas Mueller, Tianshu Bi, Kerstin Jütten, Hans Clusmann and Anke Höllig
Int. J. Mol. Sci. 2025, 26(3), 1302; https://doi.org/10.3390/ijms26031302 (registering DOI) - 3 Feb 2025
Abstract
Despite extensive research on aneurysm treatment and neurocritical care, aneurysmal subarachnoid hemorrhage (SAH) is still a life-threatening disease, often leaving survivors with lasting neurological and cognitive impairments. Early brain injury (EBI) and delayed cerebral ischemia (DCI) are the main contributors to brain damage, [...] Read more.
Despite extensive research on aneurysm treatment and neurocritical care, aneurysmal subarachnoid hemorrhage (SAH) is still a life-threatening disease, often leaving survivors with lasting neurological and cognitive impairments. Early brain injury (EBI) and delayed cerebral ischemia (DCI) are the main contributors to brain damage, with neuroinflammation being a critical shared pathophysiological process. While numerous inflammatory markers and their temporal profiles in cerebrospinal fluid (CSF) have already been identified, comparisons with age- and sex-matched controls are limited. This study analyzed CSF from 17 SAH patients requiring an external ventricular drain (EVD) due to symptomatic hydrocephalus, sampled on days 4 and 10 post-ictus. An age- and sex-matched control group included 17 cerebrovascularly healthy patients requiring lumbar drains during aortic surgery. Chemokines and cytokines were quantified using immunoassays. Significantly elevated markers in SAH patients across both time points included MCP-1, CXCL-13, Eotaxin-1, CXCL-10, IL-8, and MIF. MIP-1α and MIP-1β showed significant differences at particular time points, indicating a distinct temporal profile for each parameter. These findings highlight neuroinflammation’s key role in intracranial and systemic pathophysiology following SAH, emphasizing its complexity and individual variability. Knowing demographic factors impact the specific manifestations of pathophysiological processes, the comparison with an age- and sex-matched control group is meaningful. Full article
(This article belongs to the Special Issue Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy)
19 pages, 8145 KiB  
Article
Adoptive Transfer of CX3CR1-Transduced Tregs Homing to the Forebrain in Lipopolysaccharide-Induced Neuroinflammation and 3xTg Alzheimer’s Disease Models
by Hyejin Yang, Juwon Yang, Namgyeong Park, Deok-Sang Hwang, Seon-Young Park, Soyoung Kim and Hyunsu Bae
Int. J. Mol. Sci. 2024, 25(24), 13682; https://doi.org/10.3390/ijms252413682 - 21 Dec 2024
Viewed by 620
Abstract
CX3CR1-transduced regulatory T cells (Tregs) have shown potential in reducing neuroinflammation by targeting microglial activation. Reactive microglia are implicated in neurological disorders, and CX3CR1-CX3CL1 signaling modulates microglial activity. The ability of CX3CR1-transduced Tregs to inhibit LPS-induced neuroinflammation was assessed in animal models. CX3CR1 [...] Read more.
CX3CR1-transduced regulatory T cells (Tregs) have shown potential in reducing neuroinflammation by targeting microglial activation. Reactive microglia are implicated in neurological disorders, and CX3CR1-CX3CL1 signaling modulates microglial activity. The ability of CX3CR1-transduced Tregs to inhibit LPS-induced neuroinflammation was assessed in animal models. CX3CR1 Tregs were administered to LPS-induced and 3xTg Alzheimer’s mouse models, resulting in reduced proinflammatory marker expression in both the cortices and hippocampi. In the 3xTg Alzheimer’s model, neuroinflammation was significantly reduced, demonstrating the efficacy of CX3CR1 Tregs even in chronic neuroinflammatory conditions. These findings highlight the therapeutic potential of CX3CR1 Treg therapy in modulating microglial activity and offer promising treatment strategies for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy)
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Review

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8 pages, 649 KiB  
Review
IgLON5-IgG: Innocent Bystander or Perpetrator?
by Jane Andersen, Bronte Jeffrey, Winny Varikatt, Michael Rodriguez, Ming-Wei Lin and David A. Brown
Int. J. Mol. Sci. 2024, 25(14), 7956; https://doi.org/10.3390/ijms25147956 - 21 Jul 2024
Viewed by 1576
Abstract
Anti-IgLON5 (IgLON5-IgG)-associated disease is a newly defined clinical entity. This literature review aims to evaluate its pathogenesis, which remains a pivotal question. Features that favour a primary neurodegenerative mechanism include the non-inflammatory tauopathy neuropathological signature and overrepresentation of microtubule-associated protein tau (MAPT [...] Read more.
Anti-IgLON5 (IgLON5-IgG)-associated disease is a newly defined clinical entity. This literature review aims to evaluate its pathogenesis, which remains a pivotal question. Features that favour a primary neurodegenerative mechanism include the non-inflammatory tauopathy neuropathological signature and overrepresentation of microtubule-associated protein tau (MAPT) H1/H1 genotype as seen in other sporadic tauopathies. In contrast, the cell-surface localisation of IgLON5, capability of anti-IgLON5 antibodies to exert direct in vitro pathogenicity and disrupt IgLON5 interactions with its binding partners, human leukocyte antigen (HLA)-DRB1*10:01 and HLA-DQB1*05:01 allele preponderance with high affinity binding of IgLON5 peptides, and responsiveness to immunotherapy favour a primary autoimmune process. The presentation and course of anti-IgLON5-associated disease is heterogenous; hence, we hypothesise that a multitude of immune mechanisms are likely simultaneously operational in this disease cohort. Full article
(This article belongs to the Special Issue Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy)
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16 pages, 1650 KiB  
Review
Exploring Fecal Microbiota Transplantation for Modulating Inflammation in Parkinson’s Disease: A Review of Inflammatory Markers and Potential Effects
by Karol Sadowski, Weronika Zając, Łukasz Milanowski, Dariusz Koziorowski and Monika Figura
Int. J. Mol. Sci. 2024, 25(14), 7741; https://doi.org/10.3390/ijms25147741 - 15 Jul 2024
Cited by 2 | Viewed by 2003
Abstract
Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by numerous motor and non-motor symptoms. Recent data highlight a potential interplay between the gut microbiota and the pathophysiology of PD. The degeneration of dopaminergic neurons in PD leads to motor symptoms (tremor, rigidity, [...] Read more.
Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by numerous motor and non-motor symptoms. Recent data highlight a potential interplay between the gut microbiota and the pathophysiology of PD. The degeneration of dopaminergic neurons in PD leads to motor symptoms (tremor, rigidity, and bradykinesia), with antecedent gastrointestinal manifestations, most notably constipation. Consequently, the gut emerges as a plausible modulator in the neurodegenerative progression of PD. Key molecular changes in PD are discussed in the context of the gut–brain axis. Evidence suggests that the alterations in the gut microbiota composition may contribute to gastroenteric inflammation and influence PD symptoms. Disturbances in the levels of inflammatory markers, including tumor necrosis factor-α (TNF α), interleukin -1β (IL-1β), and interleukin-6 (IL-6), have been observed in PD patients. These implicate the involvement of systemic inflammation in disease pathology. Fecal microbiota transplantation emerges as a potential therapeutic strategy for PD. It may mitigate inflammation by restoring gut homeostasis. Preclinical studies in animal models and initial clinical trials have shown promising results. Overall, understanding the interplay between inflammation, the gut microbiota, and PD pathology provides valuable insights into potential therapeutic interventions. This review presents recent data about the bidirectional communication between the gut microbiome and the brain in PD, specifically focusing on the involvement of inflammatory biomarkers. Full article
(This article belongs to the Special Issue Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy)
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24 pages, 1975 KiB  
Review
Function and Mechanism of Abscisic Acid on Microglia-Induced Neuroinflammation in Parkinson’s Disease
by Tingting Han, Yuxiang Xu, Haixuan Liu, Lin Sun, Xiangshu Cheng, Ying Shen and Jianshe Wei
Int. J. Mol. Sci. 2024, 25(9), 4920; https://doi.org/10.3390/ijms25094920 - 30 Apr 2024
Cited by 1 | Viewed by 1789
Abstract
Parkinson’s disease (PD), as a neurologically implemented disease with complex etiological factors, has a complex and variable pathogenesis. Accompanying further research, neuroinflammation has been found to be one of the possible factors in its pathogenesis. Microglia, as intrinsic immune cells in the brain, [...] Read more.
Parkinson’s disease (PD), as a neurologically implemented disease with complex etiological factors, has a complex and variable pathogenesis. Accompanying further research, neuroinflammation has been found to be one of the possible factors in its pathogenesis. Microglia, as intrinsic immune cells in the brain, play an important role in maintaining microenvironmental homeostasis in the brain. However, over-activation of neurotoxic microglia in PD promotes neuroinflammation, which further increases dopaminergic (DA) neuronal damage and exacerbates the disease process. Therefore, targeting and regulating the functional state of microglia is expected to be a potential avenue for PD treatment. In addition, plant extracts have shown great potential in the treatment of neurodegenerative disorders due to their abundant resources, mild effects, and the presence of multiple active ingredients. However, it is worth noting that some natural products have certain toxic side effects, so it is necessary to pay attention to distinguish medicinal ingredients and usage and dosage when using to avoid aggravating the progression of diseases. In this review, the roles of microglia with different functional states in PD and the related pathways inducing microglia to transform into neuroprotective states are described. At the same time, it is discussed that abscisic acid (ABA) may regulate the polarization of microglia by targeting them, promote their transformation into neuroprotective state, reduce the neuroinflammatory response in PD, and provide a new idea for the treatment of PD and the selection of drugs. Full article
(This article belongs to the Special Issue Neuroinflammation and Neurodegeneration: Molecular Mechanism and Novel Therapy)
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