Moyamoya disease is a chronic progressive occlusive cerebrovascular disease characterized by progressive occlusion of the terminal internal carotid artery with formation of an abnormal vascular network at the skull base. The pathogenesis of the disease is not fully understood and is mainly thought to be associated with genetic factors, environmental factors and immune inflammatory response. The discovery of relevant biomarkers may provide hope for elucidation of pathogenesis of moyamoya disease and the early diagnosis and treatment of it. From the perspectives of coding gene, non-coding RNA and protein related to moyamoya disease, the possible molecular mechanisms involved in the occurrence and development of moyamoya disease are elaborated to further clarify their value as biomarkers of moyamoya disease.

Abstract: To explore the inflammatory changes and the changes of β-amyloid in the brain of rats with experimental periodontitis induced by ligation. Methods: Eighteen Sprague Dawley rats were randomly divided into 3 groups(n=6): the negative control group, chronic periodontitis group and chronic periodontitis treated with intraperitoneal injection of TAK-242 group. The experimental periodontitis model was established by ligation of the necks of bilateral maxillary first molar and inoculation ofPorphyromonas gingivalis(P.gingivalis). At the end of the second month after the successful modeling, the samples were collected from the rats. The damage of the alveolar bone was analyzed by Micro-CT. The mRNA expression levels of interleukin(IL)-6, IL-1β and tumor necrosis factor-α(TNF-α) in gingival tissue and hippocampal tissue, the mRNA expression level of Toll like receptors-4(TLR4), leukocyte differentiation antigen 14(CD14) and NF-κB in hippocampal tissue of rats were detected by qPCR. The protein expression levels of IL-6, IL-1β, TNF-α, myloid-beta protein-40(Aβ40) and Aβ42in hippocampal tissue of rats were evaluated by ELISA. Results: Experimental periodontitis model of rats could be successfully established by ligation of the neck of the rat's bilateral maxillary first molars and inoculation with porphyromonas gingivalis. The results of qPCR and ELISA showed that experimental periodontitis up-regulated the expression levels of inflammatory factors(IL-6, IL-1β and TNF-α) in hippocampus of rats and the result of ELISA showed that the level of Aβ42in hippocampus of experimental periodontitis rats increased. But the pretreatment with TAK-242 intraperitoneal injection could reduce the up-regulated the expression of inflammatory factors and Aβ42by down-regulating the TLR4/NF-κB signaling pathway. Conclusion Experimental periodontitis in rats induced by ligation combined with inoculation of porphyromonas gingivalis can result in inflammation in the brain and promote the accumulation of Aβ42in the brain, and it is reasonable to speculate that inflammation may play an important role in the correlation between periodontitis and systemic diseases such as Alzheimer's disease.