Tomohiro Nakamura

The paper identifies S-nitrosylation of STING as a redox modification driving aberrant cGAS-STING signaling in Alzheimer's disease, contributing to neuroinflammation and synaptic loss.

This study shows that S-nitrosylation of CRTC1 impairs CREB-dependent gene expression in Alzheimer's disease models, leading to synaptic dysfunction and suggesting a therapeutic target.

This study identifies phage genes that inactivate bacterial immune systems by testing gene deletions in a phage library against bacterial defense systems.

This study identifies a metabolic block in the TCA cycle in Alzheimer's disease neurons and shows that dimethyl succinate treatment rescues mitochondrial function and synapse loss.

The paper shows that manipulating the UPR pathway can restore brain function and reduce aging-related deficits.