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SCN2A Expression Reduces Seizures in Mice

by Lisa Park - Tech Editor

Summary of the Research on SCN2A haploinsufficiency and CRISPRa Treatment

This article details a study investigating a potential treatment for ​conditions⁣ linked to haploinsufficiency of the‍ SCN2A gene – autism, intellectual disability, and drug-resistant epilepsy. Here’s a breakdown of the key ‌findings:

the Problem:

* SCN2A encodes a sodium channel crucial for neuron interaction.
* ‍ Having only​ one functional copy of the gene​ (haploinsufficiency) leads to neurological issues.
* Mice with ⁣ SCN2A haploinsufficiency exhibit immature synapses and⁣ increased seizure susceptibility.

The Solution & Method:

*​ ​ Researchers used CRISPRa (CRISPR activation) – a technique that enhances ‍ gene expression, rather than altering the genome ‌- to boost the‍ expression of‍ the remaining functional SCN2A copy in mice.
* ⁢ They aimed to restore ​protein ‍levels to those‌ found in mice with two normal copies of the gene.
* CRISPRa ⁢was delivered via an adeno-associated‍ virus, either directly to the brain ⁤or intravenously.

The Results:

* Restored Synapse Function: CRISPRa treatment successfully restored synapse function in the SCN2A haploinsufficient ⁢mice.
* ‍ Reduced Seizure Susceptibility: The mice became less susceptible to seizures induced by a chemoconvulsant, reaching levels similar to those of ⁣healthy mice.
* Late-Life Effectiveness: Importantly, the treatment was‍ effective even when administered to mice equivalent to 10-year-old children developmentally (30 ‌days old in mice).
* No Negative⁤ Side Effects: No adverse effects were observed. Even in mice with already normal SCN2A levels, overexpression didn’t cause harm.
* Controlled Expression: The researchers believe CRISPRa offers a safer approach than traditional ‌gene‍ therapy because it utilizes the cell’s natural regulatory mechanisms for gene expression.

Meaning & Future Implications:

* The study⁢ is highly relevant to autism spectrum disorder due⁢ to the established link between SCN2A and ‌autism.
* While the study didn’t‌ directly address core autism symptoms, it provides a promising avenue for potential treatment.
* ‍ The success of CRISPRa in a late-life model⁢ suggests a potential therapeutic window for individuals already exhibiting symptoms.

Key People Involved:

* Kevin Bender: Led the research.
* Nadav Ahituv: ‍ Study investigator and ‍director of the Institute for⁢ Human Genetics at UCSF.

Publication: The findings were published in‍ Nature on September ⁤17th.

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