Tobias M. Boeckers

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

The paper shows that amphisomes formed at presynaptic boutons during sustained synaptic activity facilitate protein degradation and local replenishment through mRNA translation.

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

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

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.

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

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 uses functional ultrasound imaging to study memory recall in mice, finding changes in neural connectivity patterns during recent and remote fear memory retrieval.

This study identifies gene dysregulation and striosome-matrix imbalance in Shank3 mutant mice, linking these changes to behavioral abnormalities associated with autism.

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.

This study identifies SULT4A1 as a regulator of synaptic development and function by modulating dendritic morphology and NMDAR synaptic activity through its interaction with Pin1.

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.