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Scientists identify new protein role in brain development

5. oktober 2025
Rapporteret af AI

A recent study has revealed how a specific protein influences neural connections during early brain growth. Researchers from the University of California found that disrupting this protein leads to impaired synapse formation in animal models. The discovery could pave the way for better understanding neurodevelopmental disorders.

In a study published on October 3, 2025, in the journal Nature Neuroscience, scientists detailed the function of the protein dubbed NeuroLink-1 in regulating synapse development. The research, led by Dr. Elena Ramirez at the University of California, San Diego, used mouse models to observe how NeuroLink-1 binds to synaptic vesicles, facilitating their transport and integration into neural circuits.

The timeline of the experiment began with genetic modification of mice to knock out the NeuroLink-1 gene. Over a 14-day observation period post-birth, the modified mice exhibited a 40% reduction in dendritic spine density compared to controls, as measured by electron microscopy. 'This protein acts as a molecular scaffold, ensuring proper wiring of the brain during critical developmental windows,' Dr. Ramirez stated in the paper's abstract.

Background context highlights that synapse formation is essential for learning and memory, with disruptions linked to conditions like autism spectrum disorder and schizophrenia. Previous studies had identified broad synaptic proteins, but this is the first to pinpoint NeuroLink-1's specific role in vesicle trafficking. The team analyzed over 500 neural samples, confirming the protein's expression peaks at embryonic day 18 in mice, equivalent to the third trimester in human gestation.

Implications include potential therapeutic targets for neurodevelopmental issues. Co-author Dr. Marcus Lee noted, 'Targeting NeuroLink-1 pathways might help restore synaptic balance in affected individuals.' However, the study emphasizes that human applications require further clinical trials, as animal models do not fully replicate human brain complexity.

The research was funded by the National Institutes of Health and involved collaboration with bioinformatics experts to map protein interactions. No major contradictions were noted in the source, which aligns with prior synaptic biology literature.

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