ArticleEMBO molecular medicine2024
Neuraminidase inhibition promotes the collective migration of neurons and recovery of brain function.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Neuronal migration into injured tissue: mechanisms and therapeutic strategies for brain regeneration.Regenerative therapy · 2026Review
- Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026Review
- Relationship Between Regulation of Polysialic Acid Expression and Brain Diseases.Advances in experimental medicine and biology · 2026Review
- Neuroprotective Effects and Mechanisms ofInternational journal of molecular sciences · 2025Review
- A mathematical model suggests collectivity and inconstancy enhance the efficiency of neuronal migration in the adult brain.PLoS computational biology · 2025Article
- High spatial resolution gene expression profiling and characterization of neuroblasts migrating in the peri-injured cortex using photo-isolation chemistry.Frontiers in neuroscience · 2024Article
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Authors and funding
17 authors.
Funding
Abstract
In the injured brain, new neurons produced from endogenous neural stem cells form chains and migrate to injured areas and contribute to the regeneration of lost neurons. However, this endogenous regenerative capacity of the brain has not yet been leveraged for the treatment of brain injury. Here, we show that in healthy brain chains of migrating new neurons maintain unexpectedly large non-adherent areas between neighboring cells, allowing for efficient migration. In instances of brain injury, neuraminidase reduces polysialic acid levels, which negatively regulates adhesion, leading to increased cell-cell adhesion and reduced migration efficiency. The administration of zanamivir, a neuraminidase inhibitor used for influenza treatment, promotes neuronal migration toward damaged regions, fosters neuronal regeneration, and facilitates functional recovery. Together, these findings shed light on a new mechanism governing efficient neuronal migration in the adult brain under physiological conditions, pinpoint the disruption of this mechanism during brain injury, and propose a promising therapeutic avenue for brain injury through drug repositioning.
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Registered trials
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