ArticleCell death & disease2024
Ventricular Netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mirror movements: mechanisms, diagnosis, and emerging therapeutic strategies.Acta neurologica Belgica · 2026Review
- Astrocytic Netrin-1 modulates stress-induced anxiety susceptibility in mice through ADAM17-mediated TNFα shedding.Journal of neuroinflammation · 2026Article
- Corticospinal Tract Development, Evolution, and Skilled Movements.Movement disorders : official journal of the Movement Disorder Society · 2025Review
- Netrin-1 Is an Important Mediator in Microglia Migration.International journal of molecular sciences · 2024Article
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Authors and funding
17 authors.
Funding
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Abstract
The corticospinal tract (CST) is the principal neural pathway responsible for conducting voluntary movement in the vertebrate nervous system. Netrin-1 is a well-known guidance molecule for midline crossing of commissural axons during embryonic development. Families with inherited Netrin-1 mutations display congenital mirror movements (CMM), which are associated with malformations of pyramidal decussation in most cases. Here, we investigated the role of Netrin-1 in CST formation by generating conditional knockout (CKO) mice using a Gfap-driven Cre line. A large proportion of CST axons spread laterally in the ventral medulla oblongata, failed to decussate and descended in the ipsilateral spinal white matter of Ntn1
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