Nat Comm . . . For the first time, zheng Dayi's team constructed a mouse model of simple autonomic neurodysfunction induced by alpha-synaptic nucleoprotein fibrosis.

Synaptic α - synuclein (α - synuclein) is the main marker of synaptic atrophy in Parkinson's disease.in the early stage and progression of this kind of disease, serious autonomic nervous dysfunction is often accompanied by abnormal myocardial, vascular smooth muscle, visceral movement and gland secretion.among them, pure autonomic failure (PAF) is a rare, sporadic, slow progressive α - synuclein disease characterized by autonomic dysfunction but no dyskinesia.PAF is often characterized by postural hypotension, accompanied by Hypohidrosis, constipation, urinary disorders, erectile dysfunction and other autonomic nervous dysfunction. The clinical diagnosis is difficult, and the quality of life of patients is poor, and there is no effective treatment method [1,2].the characteristic pathological changes of PAF are α - syn positive inclusion bodies at the early stage of the disease, that is, extensive involvement of autonomic nerve conduction pathway. The autopsy results of PAF patients showed that α - syn positive inclusions were found in substantia nigra, locus coeruleus, periaqueductal gray matter, dorsal vagal nucleus, medial lateral nucleus (IML), sympathetic ganglia, sympathetic and parasympathetic nerve fibers [3-7].studying PAF and constructing PAF disease model may be a breakthrough to explore the pathological mechanism of autonomic nervous dysfunction in α - synuclein disease.previous studies have confirmed that α - synfibrillar bodies can act as "seeds" to induce abnormal folding of normal α - synuclein, form α - syn positive inclusion bodies, and spread from one cell to another, suggesting that the formation and dissemination of α - synuclein positive inclusions in the nervous system is the common core pathological mechanism of α - synuclein disease [8-10].on February 18, 2020, the research group of Teng Junfang / Wang Xuejing / Ding Xuebing, the First Affiliated Hospital of Zhengzhou University, published the title of autonomous injection of α - synuclein fabrics as a model of pure automatic failure α - synuclein pathway This study fills in the blank of a-syn-induced phenotype animal model of autonomic nerve dysfunction, which is helpful to further explore the pathological mechanism of α - synuclein disease-related autonomic nerve dysfunction.the research team first prepared α - syn fiber bodies from α - syn monomer, and then microinjected them into stellate ganglion and celiac ganglion of tgm83 heterozygous transgenic mice to induce the deposition of α - syn inclusion bodies in the autonomic nervous system of the model mice.the results showed that α - syn positive inclusions were found in locus coeruleus, Barrington nucleus, dorsal vagal nucleus, spinal cord IML and cardiovascular, gastrointestinal, skin and sweat glands of peripheral nervous system.with the aggravation of pathological changes, postural hypotension, gastrointestinal dysfunction, sweating disorder and olfactory disturbance gradually appeared in the model mice, but no dyskinesia.in conclusion, the first PAF mouse model at home and abroad was successfully constructed by injecting α - synfilament into the sympathetic ganglia of mice, which provides a potential animal model for revealing the pathological mechanism of autonomic nervous dysfunction associated with α - synuclein disease.it is reported that Teng Junfang, Ding Xuebing, Wang Xuejing, the First Affiliated Hospital of Zhengzhou University, and Li Jiayi of Lunde University in Sweden, and Tang Beisha of Xiangya Hospital of Central South University are the corresponding authors of this paper, while Wang Xuejing (the First Affiliated Hospital of Zhengzhou University) and Ma Mingming (people's Hospital of Zhengzhou University, people's Hospital of Henan Province) are co authors of this paper. 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