The journal of gene medicine · 2025
Mechanism of Tourette Syndrome Induced by ABGA-Mediated CaMKII-TH Pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wu Xinnan, Hao Juanjuan, Jiang Keyu, Wu Min, Zhao Xin, Zhang Xin
Аннотация
BACKGROUND: In this study, we intend to investigate the mechanism by which anti-basal ganglia antibodies (ABGA) modulate dopamine release through the CaMKII-TH pathway, which leads to the onset of Tourette syndrome (TS).
METHODS: In the clinical experiment, serum samples were collected from 40 TS children and 40 healthy children. ELISA was performed to detect ABGA, anti-streptolysin O (ASO), and anti-deoxyribonuclease B (ADNB) levels in each group. In the animal experiment, the TS group was microinfused with ABGA-positive serum from TS children. The expression levels of striatal pCaMKIIα/CaMKIIα, pTH/TH, Drd1, Drd2, and dopamine (DA) were detected.
RESULTS: Clinical experiments showed positive correlation between serum ABGA, ASO, ADNB levels, and YGTSS scores. Animal experiments showed that the stereotype score and the expression levels of striatal pCaMKIIα/CaMKIIα, pTH/TH, Drd1, and DA were increased in the TS group. The expression levels of striatal Drd2 were reduced, accompanied by neuronal loss within the striatum in the TS group.
CONCLUSION: ABGA may contribute to the development of TS by increasing striatal dopamine levels through the activation of calcium-calmodulin dependent protein kinase II (CaMKIIα) phosphorylation and tyrosine hydroxylase (TH) phosphorylation.
METHODS: In the clinical experiment, serum samples were collected from 40 TS children and 40 healthy children. ELISA was performed to detect ABGA, anti-streptolysin O (ASO), and anti-deoxyribonuclease B (ADNB) levels in each group. In the animal experiment, the TS group was microinfused with ABGA-positive serum from TS children. The expression levels of striatal pCaMKIIα/CaMKIIα, pTH/TH, Drd1, Drd2, and dopamine (DA) were detected.
RESULTS: Clinical experiments showed positive correlation between serum ABGA, ASO, ADNB levels, and YGTSS scores. Animal experiments showed that the stereotype score and the expression levels of striatal pCaMKIIα/CaMKIIα, pTH/TH, Drd1, and DA were increased in the TS group. The expression levels of striatal Drd2 were reduced, accompanied by neuronal loss within the striatum in the TS group.
CONCLUSION: ABGA may contribute to the development of TS by increasing striatal dopamine levels through the activation of calcium-calmodulin dependent protein kinase II (CaMKIIα) phosphorylation and tyrosine hydroxylase (TH) phosphorylation.