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Research paper

Mouse models of human PIK3CA-related brain overgrowth have acutely treatable epilepsy

PIK3CA signaling is directly epileptogenic independent of dysplasia; acute AKT inhibition suppresses seizures in mouse models; establishes PI3K-AKT signaling as a druggable target in malformation-associated pediatric epilepsy.

Indexed context

Roy A, et al.

pik3camouse-modelpediatric-epilepsyakt-inhibition

Markdown path

content/research/papers/2015-roy-pik3ca-mouse-epilepsy.md

Findings

PIK3CA signaling is directly epileptogenic independent of dysplasia; acute AKT inhibition suppresses seizures in mouse models; establishes PI3K-AKT signaling as a druggable target in malformation-associated pediatric epilepsy.

Why it may matter for Levi

Supports the mechanistic basis for precision therapy in PI3K-AKT-mTOR-axis disorders and provides rationale for specific drug selection once a molecular diagnosis is made. Reinforces that a PIK3CA-positive result would open an actionable therapeutic path, not a dead end.

Paper text

Mouse models of human PIK3CA-related brain overgrowth have acutely treatable epilepsy

Roy A, et al. — eLife (2015). https://elifesciences.org/articles/12703

Findings summary

PIK3CA signaling is directly epileptogenic independent of dysplasia; acute AKT inhibition suppresses seizures in mouse models; establishes PI3K-AKT signaling as a druggable target in malformation-associated pediatric epilepsy.

Relevance to Levi

Supports the mechanistic basis for precision therapy in PI3K-AKT-mTOR-axis disorders and provides rationale for specific drug selection once a molecular diagnosis is made. Reinforces that a PIK3CA-positive result would open an actionable therapeutic path, not a dead end.

Provenance

  • Ingested 2026-04-16 as part of the batch literature pass supporting the Root Cause Theories, diagnostics, and treatments workspaces.
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