Evaluation of blood flow as a route for propagation in experimental synucleinopathy
Neurobiology of Disease. 2021-01-01; : 105255
DOI: 10.1016/j.nbd.2021.105255
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Yu X(1), Persillet M(2), Zhang L(1), Zhang Y(1), Xiuping S(1), Li X(1), Ran G(1), Breger LS(2), Dovero S(2), Porras G(2), Dehay B(2), Bezard E(3), Qin C(4).
Author information:
(1)NHC Key Laboratory of Human Disease Comparative Medicine, Beijing Engineering
Research Center for Experimental Animal Models of Human Critical Diseases, Peking
Union Medical College (PUMC) & Institute of Laboratory Animal Science, Chinese
Academy of Medical Science (CAMS), Beijing, China.
(2)Univ. Bordeaux, CNRS, IMN, UMR 5293, F-33000 Bordeaux, France.
(3)NHC Key Laboratory of Human Disease Comparative Medicine, Beijing Engineering
Research Center for Experimental Animal Models of Human Critical Diseases, Peking
Union Medical College (PUMC) & Institute of Laboratory Animal Science, Chinese
Academy of Medical Science (CAMS), Beijing, China; Univ. Bordeaux, CNRS, IMN, UMR
5293, F-33000 Bordeaux, France. Electronic address: .
(4)NHC Key Laboratory of Human Disease Comparative Medicine, Beijing Engineering
Research Center for Experimental Animal Models of Human Critical Diseases, Peking
Union Medical College (PUMC) & Institute of Laboratory Animal Science, Chinese
Academy of Medical Science (CAMS), Beijing, China. Electronic address:
.
In Parkinson’s disease, synucleinopathy is hypothesized to spread from the
enteric nervous system, via the vagus nerve, to the central nervous system.
Recent evidences collected in non-human primates challenge however the hypothesis
of a transmission of α-synuclein (α-syn) pathology through the vagus nerve. Would
the hypothesis whereby the bloodstream acts as a route for long-distance
transmission of pathological α-syn hold true, an inter-individual transmission of
synucleinopathy could occur via blood contact. Here, we used a parabiosis
approach to join the circulatory systems of wild type and GFP transgenic
C57BL/6 J mice, for which one of the partners parabiont received a stereotaxic
intranigral injection of patient-derived α-syn aggregates. While the Lewy
Body-receiving mice exhibited a loss of dopamine neurons and an increase in
nigral S129 phosphorylated α-syn immunoreactivity, their parabiotic
bloodstream-sharing partners did not show any trend for a lesion or change in
S129 phosphorylated-α-syn levels. Altogether, our study suggests that, in the
patient-derived α-synuclein aggregates-injected mouse model and within the
selected time frame, the disease is not « transmitted » through the bloodstream.
Copyright © 2021. Published by Elsevier Inc.
Conflict of interest statement: Declaration of Competing Interest E.B. is Chief Scientific Officer of Motac Neuroscience Ltd. All other authors declare no competing financial interests.