Albert Christian Ludolph

This study shows that β-adrenergic receptors regulate spinal motoneuron excitability through homeostatic feedback in both wild-type and presymptomatic SOD1 mice.

The paper identifies a protective variant CREB3R119G that reduces ALS risk and progression by modulating CREB3 activity in vulnerable neurons.

This study identifies FUS's role in muscle differentiation and structure through phase separation-mediated recruitment of ETV5 and MEF2, showing its dysfunction in FUS-ALS.

The paper introduces a method to compress genetic data using autoencoders that leverage linkage disequilibrium structure, achieving high reconstruction accuracy while reducing data size.

This study identifies cMet/HGFR as a modulator of early neuroinflammation in TBI, showing that its inhibition reduces microglial reactivity and improves recovery.

This study shows that reducing neuronal nuclear calcium signaling after TBI increases microglial reactivity and synaptic loss, mediated by osteoprotegerin.

The paper identifies IL-13 and its receptor as neuronal synaptic proteins that enhance synaptic activity and neuroprotection in response to injury.

The paper identifies NUP50 gene variants and reduced expression as risk factors for ALS through transcriptome-wide association and functional studies.

The paper identifies disrupted orbitofrontal-hypothalamic projections in hypermetabolic ALS mouse models and human patients, linking them to hypermetabolism.

This study shows that cytoplasmic FUS mislocalization in mice causes behavioral changes and inhibitory synaptic defects without widespread neuronal loss.

The paper identifies a subpopulation of glycinergic interneurons in the spinal cord regulated by Shank2, whose dysfunction contributes to pain hypersensitivity in ASD mouse models.