The Effect Of Autotaxin In Periondontitis-Induced Cognitive Impairment
Autotaxin(ATX), encoded by the human ectonucleotide pyrophosphatase phosphodiesterase 2 gene, can exacerbate the progression of cognitive impairment by promoting neuroinflammation. This study was to explore the role and mechanism of ATX in the correlation between periodontitis and cognitive impairment. C57BL/6 male mice were divided into three groups: 1) Control group; 2) Periodontitis group; 3) Periodontitis plus ATX inhibitor(PF8380) group. We explored the influence of ATX on the learning and memory abilities of mice through behavioral experiments, and investigated the expression of ATX and IBA1 in the hippocampus of mice by using immunofluorescence. The expressions and secretions of ATX and inflammatory factors in tissue and plasma of mice were detected by qPCR and ELISA. Morris water maze test showed that on the fifth day of training, the latency of finding the platform by the mice in periodontitis group was significantly longer than that of periodontitis plus PF8380 group. Immunofluorescence revealed that ATX and IBA1 proteins highly expressed and co-localized with microglia in the hippocampus of periodontitis mice, but the expression of two proteins significantly decreased in periodontitis plus PF8380 group. The expressions and secretions of ATX, IL-1β, TNF-α and IL-6 increased in the peripheral blood, gingiva and brain of periodontitis mice, which can be reduced by PF8380. ATX axis may be involved in the process of periodontitis-induced cognitive impairment, which represents a potential pharmacological target to interfere with systemic inflammation and neuroinflammation.
Authors
- E. Liu
- Wei Zhou (ORCID: https://orcid.org/0000-0002-3224-7046)
Institutions
- Shanghai Jiao Tong University (CN)
- Shanghai Ninth People's Hospital (CN)
Publication Details
- Journal
- International Dental Journal
- Published
- 2025-10-01
- DOI
- https://doi.org/10.1016/j.identj.2025.104088
- Primary Topic
- Sphingolipid Metabolism and Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00