Stephen E.P. Smith

This study shows that SORL1 deficiency in neurons alters synaptic protein interactions, causes hyperexcitability, and impairs synaptic plasticity, linking endosomal recycling defects to Alzheimer's disease pathogenesis.

This study shows that reactivating SynGAP1 in adult mice restores disrupted synaptic protein interactions and normalizes network dynamics, even after critical developmental periods.

This study shows that Shank3 mutations alter how mTOR signaling networks dissociate in response to neuronal activation, affecting synaptic plasticity.

CAR T cell therapy causes cytokine release, leading to increased endothelial-leukocyte interactions and brain capillary plugging, which correlates with neurotoxicity.

The paper investigates how FMRP deficiency disrupts synaptic protein interaction networks in Fragile X syndrome and finds that SFK inhibition rescues behavioral phenotypes but not network dynamics.

The paper analyzes the mTOR protein interaction network to reveal its modular organization and how it responds to kinase inhibitors.

The paper identifies stimulus-specific and brain-region-specific synaptic protein interaction network dynamics during learning tasks.

This study shows that Shank3 mutations disrupt the association between NMDARs and connexin36, impairing electrical synaptic transmission and synchrony in mouse inferior olive.

The paper identifies PI3K and AKT inhibition as effective in suppressing PIK3CA-driven epileptiform activity in a mouse model, offering a potential therapeutic strategy for drug-resistant epilepsy.

The paper investigates how homeostatic plasticity alters synaptic protein interactions, showing that Homer1 and Shank3B are critical for structural rearrangements during synaptic scaling.

The paper examines how different detergents affect activity-dependent synaptic protein interactions and finds that while detergent solubility varies, activity-dependent changes in protein complexes are consistent across detergents.