Term: Not started yet

Heterozygous variants in the transcription factor SOX11 have been linked to a rare neurodevelopmental syndrome featuring intellectual disability and microcephaly. This project investigates the novel concept that SOX11 plays an essential role for mitotic spindle function through a non-transcriptional mechanism and that disruption of this mechanism contributes to the pathogenesis of SOX11-linked neurodevelopmental disorders.

Term: 01.06.2026 – 30.11.2028

This project investigates the role of oligodendroglia in schizophrenia, focusing on neural circuit dysfunction using a mouse model of psychosis. It assesses oligodendroglial function and prefrontal sphingolipid metabolism during psychosis induction and treatment, examines the impact of myelination on neural coding in cognitive circuits and studies the excitability of oligodendroglia in behaving mice. This research aims to advance understanding of schizophrenia pathogenesis and treatment.

Term: 01.07.2026 – 31.12.2028

Inflammatory bowel diseases impair gut neuro-immune circuits. While gut-innervating neurons are vulnerable to inflammation, satellite glia offer protection. Emerging evidence links glial plasticity to SOX10, but its regulation in gut-innervating ganglia remains unclear. We will investigate cytokine-driven modulation of SOX10 in glia of the myenteric, superior mesenteric, and dorsal root ganglia to uncover mechanisms of inflammation-induced plasticity and neuro-immune adaptation in colitis.

Term: 01.05.2026 – 31.10.2028

Neurodegenerative disorders (NDs) frequently affect complex neurons with long axons. We hypothesize that axon length represents a molecularly defined source of intrinsic vulnerability to synapse loss, an early pathological feature of many NDs. We aim to identify these molecular signals, assay multiple ND-linked models and validate drivers of axon length-dependent synapse loss in human cells to provide insight into conserved molecular mechanisms as an entry point for early treatment of NDs.