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The Role of Neuroinflammation in Neurodegenerative Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 658

Special Issue Editor


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Guest Editor
Department of Neuroscience, UCB Biopharma SPRL, 1420 Braine-l'Alleud, Belgium
Interests: neuroinflammation; neurodevelopment; neurogenesis; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation, characterized by the activation of glial cells and the release of inflammatory mediators, has emerged as a key player in the pathogenesis of disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. This Special Issue will bring together cutting-edge research that elucidates the molecular mechanisms driving neuroinflammation, its impact on neuronal function and survival, and the potential for targeting these pathways in therapeutic strategies. Contributions will include original research articles, reviews, and perspectives that address how neuroinflammatory processes influence disease progression, and the development of novel biomarkers and interventions.

This Special Issue aims to foster a deeper understanding of neuroinflammation's role in neurodegeneration, paving the way for innovative treatments that could alter the course of these debilitating diseases.

Dr. Wenqiang Fan
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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

  • molecular neuropathology
  • neuroinflammation
  • multiple sclerosis
  • neurodegenerative diseases
  • dementias

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Published Papers (1 paper)

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Research

11 pages, 1679 KiB  
Article
Empagliflozin Attenuates High-Glucose-Induced Astrocyte Activation and Inflammation via NF-κB Pathway
by Dong Hee Kim, Min Jin Lee, Dasol Kang, Ji Young Lee, Sujin Park, Ah Reum Khang, Ji Hyun Bae, Joo Yeon Kim, Su Hyun Kim, Yang Ho Kang and Dongwon Yi
Curr. Issues Mol. Biol. 2024, 46(11), 12417-12427; https://doi.org/10.3390/cimb46110737 - 4 Nov 2024
Viewed by 546
Abstract
Sodium-glucose cotransporter-2 (SGLT2) inhibitors regulate blood glucose levels in patients with type 2 diabetes mellitus and may also exert anti-inflammatory and anti-atherosclerotic effects by promoting M2 macrophage polarization. Although SGLT2 is expressed in brain regions that influence glucose balance and cognitive function, its [...] Read more.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors regulate blood glucose levels in patients with type 2 diabetes mellitus and may also exert anti-inflammatory and anti-atherosclerotic effects by promoting M2 macrophage polarization. Although SGLT2 is expressed in brain regions that influence glucose balance and cognitive function, its roles in the central nervous system are unclear. This study investigated the effects of empagliflozin (EMPA), an SGLT2 inhibitor, on hypothalamic inflammation associated with metabolic diseases. Mice were subjected to a high-fat diet (HFD) for varying durations (3 d, 3 weeks, and 16 weeks) and treated with EMPA for 3 weeks (NFD, NFD + EMPA, HFD, HFD + EMPA; n = 5/group). EMPA regulated the expression of astrocyte markers and pro-inflammatory cytokine mRNA in the hypothalamus of HFD-induced mice, which was linked to regulation of the NF-κB pathway. Under hyperglycemic conditions, EMPA may mitigate hypothalamic inflammation by modulating astrocyte activation via the NF-κB pathway. Our findings demonstrated that EMPA possesses therapeutic potential beyond merely lowering blood glucose levels, opening new avenues for addressing inflammation and providing neuroprotection in metabolic disease management. Full article
(This article belongs to the Special Issue The Role of Neuroinflammation in Neurodegenerative Diseases)
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