Dajana Großmann

RIG-I mediated neuron-specific IFN type 1 signaling in FUS-ALS induces neurodegeneration and offers new biomarker-driven individualized treatment options for (FUS-)ALS

The paper identifies RIG-I-mediated innate immune activation in FUS-ALS spinal motor neurons due to mitochondrial dsRNA accumulation, which can be targeted by JAK-STAT inhibition, offering potential biomarker-driven treatment options.

Small molecule inhibitors of hnRNPA2B1-RNA interactions reveal a predictable sorting of RNA subsets into extracellular vesicles

This study identifies small molecule inhibitors of hnRNPA2B1-RNA interactions and shows they alter EV-RNA composition and paracrine signaling.

Axonal transcriptome reveals upregulation of PLK1 as a protective mechanism in response to increased DNA damage in FUSP525L spinal motor neurons

The paper uses compartment-specific RNA-sequencing to analyze axonal and somatodendritic transcriptomes of FUS-ALS motor neurons, identifying PLK1 upregulation as a protective response to DNA damage.

DJ-1 products glycolic acid and D-lactate restore deficient axonal trafficking and DNA damage response in FUS and SOD1-associated amyotrophic lateral sclerosis

The paper shows that glycolic acid and D-lactate restore axonal trafficking and DNA damage response in FUS and SOD1-ALS patient-derived motoneurons.

Live cell imaging of ATP levels reveals metabolic compartmentalization within motoneurons and early metabolic changes in FUS ALS motoneurons.

The paper uses live cell imaging to show reduced ATP levels in FUS-ALS motoneurons, linking metabolic changes to disease vulnerability.

Mitochondria-mitochondria interaction networks show altered topological patterns in Parkinson's disease

The paper analyzes mitochondria-mitochondria interaction networks in Parkinson's disease and finds altered topological patterns that correlate with clinical scores and can distinguish patients from controls.

IPSC-derived midbrain astrocytes from Parkinson's disease patients carrying pathogenic SNCA mutations exhibit alpha-synuclein aggregation, mitochondrial fragmentation and excess calcium release