CNS neuroscience & therapeutics · 2025
Alterations in Neuroinflammation, Microglia and Neuroplasticity in the Rat Hippocampus in a Combined Model of Periodontitis and Depression.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Robledo-Montaña Javier, Martín-Hernández David, Cuenca-Ortega Javier, Martínez María, Virto Leire, Ambrosio Nagore, Montero Eduardo, Marín María José, Herrera David, Sanz Mariano, Leza Juan C, Figuero Elena, García-Bueno Borja
Аннотация
AIMS: The exact causes of major depressive disorder (MDD) are still debated, but its connection with inflammatory diseases and stress is well established. Emerging evidence suggests a potential link between periodontitis (gum disease) and MDD.
METHODS: Periodontitis (P) was induced in rats through oral rinses with the pathogenic bacteria Porphyromonas gingivalis and Fusobacterium nucleatum for 12 weeks, followed by 3 weeks of chronic mild stress (CMS) to induce depressive-like behavior. Four experimental groups were established: periodontitis with CMS (P + CMS+), periodontitis without CMS (P + CMS-), CMS without periodontitis (P-CMS+), and control (P-CMS-). Inflammatory and synaptic plasticity-related mediators were quantified in hippocampal samples. The number, morphology, and inflammatory phenotype of microglia were also evaluated by ultrastructural and fractal analyses.
RESULTS: P + CMS+ animals compared with controls showed: (1) increased protein expression of TLR-4, phospho(p)-nuclear factor kappa B (p-NFκB)/NFκB ratio, and inducible nitric oxide synthase (iNOS); (2) decreased microglial number, shorter branch length, reduced complexity, and increased expression of iNOS; (3) decreased protein levels of BDNF and synaptophysin, and lower ratios of p-protein kinase B (p-Akt)/Akt and p-mammalian target of rapamycin (p-mTOR)/mTOR.
CONCLUSION: Alterations in neuroinflammation and neuroplasticity in the hippocampus may contribute to the comorbidity between periodontitis and MDD, warranting further investigation.
METHODS: Periodontitis (P) was induced in rats through oral rinses with the pathogenic bacteria Porphyromonas gingivalis and Fusobacterium nucleatum for 12 weeks, followed by 3 weeks of chronic mild stress (CMS) to induce depressive-like behavior. Four experimental groups were established: periodontitis with CMS (P + CMS+), periodontitis without CMS (P + CMS-), CMS without periodontitis (P-CMS+), and control (P-CMS-). Inflammatory and synaptic plasticity-related mediators were quantified in hippocampal samples. The number, morphology, and inflammatory phenotype of microglia were also evaluated by ultrastructural and fractal analyses.
RESULTS: P + CMS+ animals compared with controls showed: (1) increased protein expression of TLR-4, phospho(p)-nuclear factor kappa B (p-NFκB)/NFκB ratio, and inducible nitric oxide synthase (iNOS); (2) decreased microglial number, shorter branch length, reduced complexity, and increased expression of iNOS; (3) decreased protein levels of BDNF and synaptophysin, and lower ratios of p-protein kinase B (p-Akt)/Akt and p-mammalian target of rapamycin (p-mTOR)/mTOR.
CONCLUSION: Alterations in neuroinflammation and neuroplasticity in the hippocampus may contribute to the comorbidity between periodontitis and MDD, warranting further investigation.