Csaba Konràd

This study investigates mitochondrial phenotypes in motor neurons derived from familial ALS patients using direct conversion of fibroblasts, identifying metabolic and functional differences across mutations.

This study shows mitochondrial dysfunction and oxidative stress occur before neuronal loss in DRPLA patient-derived neurons, and phenylbutyrate treatment improves survival.

This study shows that expressing alternative oxidase (AOX) reduces reverse electron transfer and oxidative stress in ischemia-reperfusion brain injury, preserving complex I function and providing neuroprotection.

The paper uses machine learning on fibroblast morphometry to predict stress but finds limited ability to distinguish ALS from controls.

The paper maps Tau interactomes in neurons using APEX and AP-MS to reveal activity-dependent interactions and FTD mutation effects on mitochondrial associations in neurodegenerative diseases.

The paper identifies a subclass of sporadic ALS patients with metabolic defects in trans-sulfuration, characterized by increased cysteine and glutathione synthesis and distinct metabolic responses.

The paper identifies a distinct metabolomic subtype in sporadic ALS patients through metabolite profiling and multi-omics integration, showing increased cysteine metabolism and potential therapeutic targets.