Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model

Abstract Demyelination leads to a loss of neurons, which results in, among other consequences, a severe reduction in locomotor function, and underlies several diseases in humans including multiple sclerosis and polyneuropathies. Considerable clinical progress has been made in counteracting demyelina...

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Autores principales:	Suhyun Kim, Dong-Won Lee, Melitta Schachner, Hae-Chul Park
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/978469672c0e40a787afdf155c4e2fff
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spelling	oai:doaj.org-article:978469672c0e40a787afdf155c4e2fff2021-12-02T13:18:01ZSmall compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model10.1038/s41598-021-85412-12045-2322https://doaj.org/article/978469672c0e40a787afdf155c4e2fff2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85412-1https://doaj.org/toc/2045-2322Abstract Demyelination leads to a loss of neurons, which results in, among other consequences, a severe reduction in locomotor function, and underlies several diseases in humans including multiple sclerosis and polyneuropathies. Considerable clinical progress has been made in counteracting demyelination. However, there remains a need for novel methods that reduce demyelination while concomitantly achieving remyelination, thus complementing the currently available tools to ameliorate demyelinating diseases. In this study, we used an established zebrafish demyelination model to test selected compounds, following a screening in cell culture experiments and in a mouse model of spinal cord injury that was aimed at identifying beneficial functions of the neural cell adhesion molecule L1. In comparison to mammalian nervous system disease models, the zebrafish allows testing of potentially promotive compounds more easily than what is possible in mammals. We found that our selected compounds tacrine and duloxetine significantly improved remyelination in the peripheral and central nervous system of transgenic zebrafish following pharmacologically induced demyelination. Given that both molecules are known to positively affect functions other than those related to L1 and in other disease contexts, we propose that their combined beneficial function raises hope for the use of these compounds in clinical settings.Suhyun KimDong-Won LeeMelitta SchachnerHae-Chul ParkNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Suhyun Kim Dong-Won Lee Melitta Schachner Hae-Chul Park Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
description	Abstract Demyelination leads to a loss of neurons, which results in, among other consequences, a severe reduction in locomotor function, and underlies several diseases in humans including multiple sclerosis and polyneuropathies. Considerable clinical progress has been made in counteracting demyelination. However, there remains a need for novel methods that reduce demyelination while concomitantly achieving remyelination, thus complementing the currently available tools to ameliorate demyelinating diseases. In this study, we used an established zebrafish demyelination model to test selected compounds, following a screening in cell culture experiments and in a mouse model of spinal cord injury that was aimed at identifying beneficial functions of the neural cell adhesion molecule L1. In comparison to mammalian nervous system disease models, the zebrafish allows testing of potentially promotive compounds more easily than what is possible in mammals. We found that our selected compounds tacrine and duloxetine significantly improved remyelination in the peripheral and central nervous system of transgenic zebrafish following pharmacologically induced demyelination. Given that both molecules are known to positively affect functions other than those related to L1 and in other disease contexts, we propose that their combined beneficial function raises hope for the use of these compounds in clinical settings.
format	article
author	Suhyun Kim Dong-Won Lee Melitta Schachner Hae-Chul Park
author_facet	Suhyun Kim Dong-Won Lee Melitta Schachner Hae-Chul Park
author_sort	Suhyun Kim
title	Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
title_short	Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
title_full	Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
title_fullStr	Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
title_full_unstemmed	Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
title_sort	small compounds mimicking the adhesion molecule l1 improve recovery in a zebrafish demyelination model
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/978469672c0e40a787afdf155c4e2fff
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_version_	1718393345951137792

Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model

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