Samuel J. Pleasure

AEGIS identifies epitope- and clone-specific autoimmunity in ROHHAD by linking immune repertoires to self-epitopes, revealing convergence on ZSCAN1 epitopes in the CNS.

Paired CSF and blood scRNA/TCR-seq in treatment-naive MS shows a small set of expanded, cytotoxic CSF-enriched CD8+ clonotypes, two of which recognize EBV epitopes.

This paper designs a targeted autoantibody degrader to treat neurologic diseases by specifically clearing pathogenic autoantibodies while preserving the immune system.

This study shows that exposure to anti-GluN1 mAb during development causes long-term sensory-motor deficits and callosal axon changes in mice.

This study shows that Shh from mossy cells supports NSC pool maintenance after seizures and in aging by promoting neurogenesis and NSC self-renewal.

This study shows that neuronal activity influences OPC activation, synapse formation onto OPCs, and the balance of excitatory and inhibitory synapses.

This study identifies that CaMKII autophosphorylation and binding to GluN2B are necessary for synaptic memory, while kinase activity is not required.

This study identifies FGF5 signaling as a key driver in SHH subgroup infantile medulloblastoma, showing its upregulation and therapeutic potential through FGFR inhibition.

The paper shows that SHH signaling modulates FGF15 expression to maintain neocortical progenitor specification during corticogenesis.

This study shows that NMDA receptors, specifically NR2B-containing ones, control callosal axonal projections in the primary somatosensory cortex through interactions with EPHRIN-B/EPHB, independent of ion channel function.

This study shows that Sufu regulates Shh signaling to control the expansion and quiescence of neural stem cells in the developing dentate gyrus.

This study shows that Sufu deletion in neural progenitors causes increased proliferation and reduced survival of stem/precursor cells in the dorsal V-SVZ via a Gli3-dependent mechanism.