Toshifumi Tomoda

This study links the FREM3 gene to brain and cognitive aging using cross-species evidence from mice and humans, showing reduced brain volume and cognitive performance in Frem3 knockout mice and lower FREM3-GReX associated with reduced brain surface area and cognitive performance in humans.

This paper presents a novel monkey model with impaired DISC1 gene to study adolescent prodromal phenotypes of psychiatric disorders, finding altered social behavior and disrupted brain connectivity.

This study investigates the role of IFN-γ receptor signaling in SST interneurons, showing it supports normal behavior and molecular homeostasis while mediating inflammation-induced deficits.

This study identifies progressive molecular differences in depression across clinical stages using RNA-seq data, revealing shared and distinct pathways and cell-type-specific changes associated with symptom dimensions and therapeutic targets.

This study identifies ribosomal dysregulation as a conserved mechanism in human depression and mouse chronic stress, linking stress-induced changes in ribosomal proteins and pseudogenes to synaptic dysfunction.

This study characterizes olfactory neuronal cells from nasal biopsies using single-cell and bulk RNA sequencing, showing their neuronal similarity and utility in brain disorder research.

The paper identifies that somatostatin processing is a vulnerability factor in SST+ neurons under ER stress, linking chronic stress to behavioral deficits.

This study shows that high-sucrose diets in Glo1-deficient mice cause brain angiopathy, impaired glucose uptake, and psychosis-related behaviors, with aspirin offering protection.

The paper integrates transcriptomic data with in-silico analyses to identify cellular, molecular, and causal pathways in trait and state depression.

This study shows that chronic treatment with a 5-GABA-A receptor PAM increases dendritic length, spine count, and density in mice, suggesting potential for reversing age-related cognitive decline.

This study shows that reduced BDNF leads to increased p62 and decreased GABAAR surface expression, contributing to behavioral deficits in mice, and suggests similar changes in human depression.

This study shows that the cortico-striatal circuit regulates sensorimotor gating through Disc1/Huntingtin-mediated Bdnf transport, with lithium restoring deficits in Disc1-LI mice.