NeuralCipher Research overview
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Abstract Background/Aims: This study aims to elucidate how hyperactivated enteric glial cells (EGCs) trigger Parkinson's disease (PD) pathogenesis and whether the exogenous gut–brain regulatory hormone oxytocin canalleviate the phenotypes of PD. Methods: Prodromal and clinical PD mouse models were established via the intragastric administration of rotenone (ROT). The intestinal and motor functions of the mice were assessed. The expression of glial fibrillary acidic protein (GFAP), oxytocin receptor (OXTR) and tyrosine hydroxylase (TH) in the colon and midbrain was detected by immunofluorescence staining. The levels of α-synuclein (α-syn), oxytocin (OXT), and inflammatory factors in the serum and colon were measured by ELISA, western blotting and qPCR. Exogenous OXT and the EGC inhibitor fluorocitrate (FC) were administered, and the rescue effect on PD mice was assessed via neurobehavioral assays. Results: ROT administration induced constipation and motor PD symptoms in mice. The expression of GFAP and α-syn in the colon of PD mice wasincreased, whereasthe OXT and OXTR levels were decreased. Exogenous OXT or FC administration inhibited EGChyperactivation, reduced inflammatory factorlevels and α-syn accumulation, and ultimately alleviated the prodromal and clinical PD phenotypes. Conclusions: EGC hyperactivation plays a crucial role in PD pathogenesis, and exogenous OXT or FC could ameliorate the prodromal and clinical PD phenotypes.
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