ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2025
IL-17 A Exacerbated Neuroinflammatory and Neurodegenerative Biomarkers in Intranasal Amyloid-Beta Model of Alzheimer's Disease.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Chrysin Ameliorated Neurochemical and Behavioural Changes Mediated By Combined Exposure of Interleukin-17 A With Amyloid BetaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Vessel-associated microglia are differentially activated and distributed in relation to systemic infection and Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- Fecal Microbiota Transplantation from APP/PS1 Mice Induces Th17-Related Inflammatory Parameters and Pathological Changes in the Gut-Brain Axis of Healthy C57BL/6J Mice.International journal of molecular sciences · 2026Article
- Electroacupuncture Alleviates Cerebral Ischemia-Reperfusion Injury by Downregulating IL-17 A and Inhibiting Neurotoxic Astrocyte Activation.Neurochemical research · 2025Article
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Authors and funding
5 authors.
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Abstract
Proinflammatory cytokines, especially interleukin-17 A (IL-17 A) have been found to be significantly associated with AD patients. IL-17 A amplifies neuroinflammation during AD pathology. This study highlighted the ability of IL-17 A to exacerbate amyloid-beta-induced pathology in animals. The AD pathology was induced with repeated intranasal administration of Aβ along with recombinant mouse IL-17 A (rmIL-17) at 1, 2 and 4 µg/kg for seven alternate days. Although, the combination of rmIL-17 and Aβ did not have severe effects on memory of the animals, but it drastically increased the IL-17 A mediated signaling, level of proinflammatory cytokines, oxidative stress and reduced antioxidants in the hippocampus and cortex regions of the animal brains. Interestingly, combining rmIL-17 with Aβ also triggered the expression of AD structural markers like pTau, amyloid-beta and BACE1 in the brain regions. Furthermore, rmIL-17 with Aβ exposure stimulated astrocytes and microglia leading to activation of proinflammatory signaling in the brain of the animals. These results showed the propensity of IL-17 A to promote severity of AD pathology and suggest IL-17 A as potent therapeutic target to control AD progression.
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