Kristopher Thomas Kahle

This study integrates multi-omic data from mouse and human choroid plexus to identify conserved molecular programs of epithelial function across species.

This study shows that inhibiting the WNK-SPAK/OSR1 pathway reduces neuronal chloride intracellular levels and suppresses ictal-like discharges by enhancing chloride extrusion through NKCC1 and KCC2.

This study shows PTEN regulates neuronal growth and excitability through distinct mTORC1 and mTORC2 pathways, with implications for ASD and epilepsy.

This paper introduces an ultra-high-resolution MRI framework to map perivascular spaces (PVS) across the whole brain, revealing their hierarchical organization along vascular trees.

This study identifies somatic Ras-MAPK pathway variants in hippocampal tissue from patients with drug-resistant epilepsy, showing their association with clonal competition and worse surgical outcomes.

This study identifies TRIM71 as essential for hearing in humans and mice, showing it regulates the timing of auditory sensory organ development and prevents premature hair cell differentiation.

This review summarizes the genetic basis of hydrocephalus, including genes, pathways, and mechanisms, to highlight the complexity and global impact of its genetic contributions.

This study identifies SMARCC1 mutations as a cause of congenital hydrocephalus, showing they lead to neural progenitor dysfunction and a new syndrome called SaDDS.

This study shows PTEN mutations cause ventriculomegaly and cortical network dysfunction through neural precursor and interneuron dysregulation, with mTORC1 inhibition offering therapeutic potential.

The paper identifies genetic variants in RASA1 and EPHB4 associated with vein of Galen malformations through exome analysis and single-cell transcriptomics.

The paper uses FLIM to map dendritic chloride ion levels and identifies KCC2's role in creating chloride microdomains, revealing implications for ischemic stroke.

The paper measures chloride ion concentrations in neurons to show the existence of stable cytoplasmic chloride microdomains that affect GABAergic signaling.

This study shows that impaired KCC2 phosphorylation in mice leads to neuronal network dysfunction and neurodevelopmental issues, with some effects reversible by bumetanide treatment.

The paper identifies a zebrafish mutant with proportional overgrowth due to Kcc4a loss of function and shows its role in bioelectric signaling for growth regulation.