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Anti-Inflammatory Strategies and Cell Models for Alzheimer’s Disease

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 November 2025 | Viewed by 1643

Special Issue Editor


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Guest Editor
Laboratory of Animal Physiology, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
Interests: antioxidants; sperm physiology; signaling pathways; oxidative stress

Special Issue Information

Dear Colleagues,

Neuroinflammation has been implicated in the development of a variety of CNS diseases, including late-onset Alzheimer’s disease (LOAD). The development of inflammation is a complex process involving multiple molecular interactions that remain to be further characterized in the CNS. The development of neuroinflammation may represent an important link between the early stages of LOAD and its pathological outcomes. It is thought that LOAD risk factors, including genetic, biological, and environmental factors, may all contribute to the impairment of normal CNS regulation and function. The links between risk factors and the development of neuroinflammation are numerous and involve many complex interactions that lead to vascular damage, oxidative stress, and ultimately neuroinflammation. Once this chain of events is initiated, the neuroinflammatory process becomes overactivated, resulting in further cellular damage and loss of neuronal function. Furthermore, neuroinflammation is associated with the formation of amyloid plaques and neurofibrillary tangles, which are pathological hallmarks of LOAD. Elevated levels of inflammatory markers are associated with late cognitive impairment. Based on this knowledge, new therapies aimed at limiting the onset of neuroinflammation could halt or even reverse the progression of the disease. Alzheimer's disease (AD) is characterized by multiple cellular and molecular insults. Therefore, there is a growing and justifiable interest in multi-targeted molecular therapies. This Special Issue welcomes discussions on inflammation in AD as well as on cell models.

Dr. Sophia Lavrentiadou
Guest Editor

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Keywords

  • Alzheimer’s disease
  • neuroinflammation
  • anti-inflammatory strategies
  • cell models

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Published Papers (1 paper)

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Research

27 pages, 3932 KiB  
Article
Evaluation of the Anti-Amyloid and Anti-Inflammatory Properties of a Novel Vanadium(IV)–Curcumin Complex in Lipopolysaccharides-Stimulated Primary Rat Neuron-Microglia Mixed Cultures
by Georgios Katsipis, Sophia N. Lavrentiadou, George D. Geromichalos, Maria P. Tsantarliotou, Eleftherios Halevas, George Litsardakis and Anastasia A. Pantazaki
Int. J. Mol. Sci. 2025, 26(1), 282; https://doi.org/10.3390/ijms26010282 - 31 Dec 2024
Cited by 2 | Viewed by 1395
Abstract
Lipopolysaccharides (LPS) are bacterial mediators of neuroinflammation that have been detected in close association with pathological protein aggregations of Alzheimer’s disease. LPS induce the release of cytokines by microglia and mediate the upregulation of inducible nitric oxide synthase (iNOS)—a mechanism also associated with [...] Read more.
Lipopolysaccharides (LPS) are bacterial mediators of neuroinflammation that have been detected in close association with pathological protein aggregations of Alzheimer’s disease. LPS induce the release of cytokines by microglia and mediate the upregulation of inducible nitric oxide synthase (iNOS)—a mechanism also associated with amyloidosis. Curcumin is a recognized natural medicine but has extremely low bioavailability. V-Cur, a novel hemocompatible Vanadium(IV)-curcumin complex with higher solubility and bioactivity than curcumin, is studied here. Co-cultures consisting of rat primary neurons and microglia were treated with LPS and/or curcumin or V-Cur. V-Cur disrupted LPS-induced overexpression of amyloid precursor protein (APP) and the in vitro aggregation of human insulin (HI), more effectively than curcumin. Cell stimulation with LPS also increased full-length, inactive, and total iNOS levels, and the inflammation markers IL-1β and TNF-α. Both curcumin and V-Cur alleviated these effects, with V-Cur reducing iNOS levels more than curcumin. Complementary insights into possible bioactivity mechanisms of both curcumin and V-Cur were provided by In silico molecular docking calculations on Aβ1-42, APP, Aβ fibrils, HI, and iNOS. This study renders curcumin-based compounds a promising anti-inflammatory intervention that may be proven a strong tool in the effort to mitigate neurodegenerative disease pathology and neuroinflammatory conditions. Full article
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