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Autonomic ganglionic injection of α-synuclein fibrils as a model of pure autonomic failure α-synucleinopathy

Wang, Xue Jing (author)
First Affiliated Hospital of Zhengzhou University
Ma, Ming Ming (author)
First Affiliated Hospital of Zhengzhou University
Zhou, Le Bo (author)
First Affiliated Hospital of Zhengzhou University
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Jiang, Xiao Yi (author)
First Affiliated Hospital of Zhengzhou University
Hao, Miao Miao (author)
First Affiliated Hospital of Zhengzhou University
Teng, Robert K.F. (author)
Shenzhen University
Wu, Erxi (author)
Baylor University Medical Centre
Tang, Bei Sha (author)
Central South University, China
Li, Jia Yi (author)
Lund University,Lunds universitet,Neural plasticitet och reparation,Forskargrupper vid Lunds universitet,Neural Plasticity and Repair,Lund University Research Groups,China Medical University, Shenyang
Teng, Jun Fang (author)
First Affiliated Hospital of Zhengzhou University
Ding, Xue Bing (author)
Central South University, China,First Affiliated Hospital of Zhengzhou University
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 (creator_code:org_t)
2020-02-18
2020
English.
In: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11:1
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • α-Synucleinopathies are characterized by autonomic dysfunction and motor impairments. In the pure autonomic failure (PAF), α-synuclein (α-Syn) pathology is confined within the autonomic nervous system with no motor features, but mouse models recapitulating PAF without motor dysfunction are lacking. Here, we show that in TgM83+/− mice, inoculation of α-Syn preformed fibrils (PFFs) into the stellate and celiac ganglia induces spreading of α-Syn pathology only through the autonomic pathway to both the central nervous system (CNS) and the autonomic innervation of peripheral organs bidirectionally. In parallel, the mice develop autonomic dysfunction, featured by orthostatic hypotension, constipation, hypohidrosis and hyposmia, without motor dysfunction. Thus, we have generated a mouse model of pure autonomic dysfunction caused by α-Syn pathology. This model may help define the mechanistic link between transmission of pathological α-Syn and the cardinal features of autonomic dysfunction in α-synucleinopathy.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Neurosciences (hsv//eng)

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