Philipp Boehm‐Sturm

This paper develops a harmonized MRI QC framework using phantoms to identify sources of variability across field strengths and sites, showing that field strength alone does not fully characterize MRI performance.

The paper investigates resilience and susceptibility to social defeat stress in mice using brain imaging, identifying structural and network-level differences associated with coping mechanisms.

OTTER maps mouse and human brain regions using optimal transport, revealing evolutionary differences in association cortex and enabling cross-species predictions.

The paper identifies a metabolically defined penumbra in hyperacute stroke using multimodal molecular profiling in a mouse model.

This study identifies Nurr1 as a critical transcription factor for claustrum development and function, showing its role in neuronal positioning and behavior regulation.

The paper shows chronic heterochromatin loss in neurons leads to ERV de-repression, inflammation, and cognitive decline in mice.

This study develops a new MRI protocol using 2DG-CESL to measure glucose metabolism in a rat stroke model and shows it provides a biomarker of disturbed metabolism with high effect size.

The paper uses machine learning to analyze movement in mouse stroke models, revealing distinct motor deficits based on lesion location.

This paper predicts stroke outcomes in mice using MRI and behavioral data, finding that lesion volume and topology are key predictors of subacute and residual deficits.

This paper develops an automated deep learning method for ischemic stroke lesion segmentation in mouse MRI, achieving high agreement with manual segmentation.

This study investigates functional connectivity changes in murine models of NMDAR antibody-associated pathology using rs-fMRI, finding impaired connectivity in hippocampal regions similar to human patients.

The paper demonstrates that patient-derived monoclonal GABAA receptor antibodies cause catatonia and seizures in rodents, providing a model for autoimmune encephalitis and supporting antibody depletion as a treatment.

The paper examines structural and functional connectivity changes in a mouse model of vascular cognitive impairment, finding altered network connectivity and behavioural deficits.

This study shows that inhibiting HDAC1 and HDAC3 with RGFP109 improves motor function and corrects gene expression in a Huntington's disease mouse model.

This study shows that Ube3b regulates dendritic branching and synaptic function by ubiquitinating Ppp3cc, contributing to intellectual disability-like phenotypes in a KOS mouse model.