Francesco Roselli

This study shows that loss of C3 and CD14 reduces neuroinflammation in a murine polytrauma model, with differential effects across brain regions.

The paper investigates synapto-nuclear signaling defects in mSOD1 mice and shows that restoring cAMP/PKA signaling mitigates pathology in motoneurons.

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 basophil recruitment to the spleen following TBI and shows their activation of B cells and dendritic cells via IL-13 signaling, enhancing protein translation through NORAD.

This study identifies a mechanosensitive astrocyte signaling pathway linking intracranial pressure to neuroinflammation via Piezo1-dependent EGFR activation.

The paper investigates how spinal microcircuits adapt in a mouse model of motoneuron degeneration, finding specific multiphasic homeostatic compensations that preserve force output.

This study shows that FGFR inhibition with Rogaratinib reduces microglia reactivity and synaptic loss in TBI by dampening neuroimmunological responses.

The paper introduces hCLARITY, a clearing method that improves the sensitivity and specificity of fluorescence immunostaining in archived human brain tissue for high-resolution imaging.

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.