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Background: Tooth loss is closely related to cognitive impairment, especially affecting cognitive functions involving hippocampus. The most well-known function of the hippocampus is learning and memory, and the mechanism behind is neuroplasticity, which strongly depends on the level of brain-derived neurotrophic factor (BDNF). While research has delved into the possible mechanisms behind the loss of teeth leading to cognitive dysfunction, there are few studies on the plasticity of sensory neural pathway after tooth loss, and the changes in related indicators of synaptic plasticity still need to be further explored., Methods: In this study, the bilateral maxillary molars were extracted in Sprague-Dawley rats of two age ranges (young and middle age) to establish occlusal support loss model; then, the spatial cognition was tested by Morris Water Maze (MWM). Quantitative real-time PCR (qPCR) and Western Blotting (WB) were used to detect BDNF, AKT, and functional proteins (viz., PSD95 and NMDAR) of hippocampal synapses. Golgi staining was used to observe changes in ascending nerve pathway. IF was used to confirm the location of BDNF and AKT expressed in hippocampus., Results: MWM showed that the spatial cognitive level of rats dropped after occlusal support loss. qPCR, WB, and IF suggested that the BDNF/AKT pathway was down-regulated in the hippocampus. Golgi staining showed the neurons of ascending sensory pathway decreased in numbers., Conclusion: Occlusal support loss caused plastic changes in ascending nerve pathway and induced cognitive impairment in rats by down-regulating BDNF and synaptic plasticity., (© 2024 The Author(s). CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)

Background: Both animal studies and prospective observational studies on patients with neurodegenerative disease have reported a positive link between oral diseases and cognitive function. However, the effect of early tooth loss on hippocampal morphology remains unknown. Methods: In this study, 6-week-old, male, juvenile Sprague–Dawley (SD) rats were randomized into the control (C) and tooth loss (TL) groups. In the TL group, all right maxillary molars of SD rats were extracted, while in the C group, no teeth were extracted. After 3 months, the learning and memory behavior were examined by Morris Water Maze (MWM), and the protein expression and mechanic signaling pathways were analyzed by real-time polymerase chain reaction, and cresyl violet staining. Results: Two days after the operation, the body weight of both groups recovered and gradually returned to the level before operation. Three months after tooth extraction, the completion time of the C group in the MWM was significantly shorter than the TL group. The mRNA expression of BDNF, TrkB, AKT1 , and NR2B in the C group were significantly higher than in the TL group. The pyramidal neurons in the TL group was fewer than in the C group. Conclusion: Tooth loss in the juvenile SD rats will reduce the number of pyramidal neurons in the hippocampus, inhibit the expression of BDNF, TrkB, AKT1 , and NR2B , and eventually lead to cognitive dysfunction. [ABSTRACT FROM AUTHOR]