Gut–Brain Axis and Translational Psychiatry

Our research in Gut–Brain Axis and Translational Psychiatry focuses on understanding the biological mechanisms that determine individual variability in response to stress and shape vulnerability or resilience to psychiatric disorders, including depression, anxiety, and substance abuse. By integrating findings from animal models and human studies, we aim to bridge fundamental biological discoveries with clinically relevant applications, advancing the development of personalized approaches to mental health.

A central component of our work is the investigation of the gut–brain axis, a complex bidirectional communication network linking the gastrointestinal system and the brain through neural, endocrine, immune, and microbial pathways. We examine how interactions between the gut microbiome, immune signaling, hormonal regulation, and brain function influence behavior, emotional responses, and susceptibility to stress-related psychopathology.

Using our unique mouse models of dominance and submissiveness, which represent opposite stress-response phenotypes, we identify biological signatures associated with behavioral resilience and vulnerability. Our studies combine microbiome profiling with molecular, genetic, and hormonal analyses to uncover biomarkers and pathways that distinguish stress-resilient from stress-vulnerable individuals. Particular attention is given to mechanisms involving the gut microbiome, the hypothalamic–pituitary–adrenal (HPA) axis, dopaminergic signaling, inflammatory processes, and genes regulating synaptic plasticity.

By exploring how gut–brain communication interacts with genetic and neurobiological factors, we seek to identify individual risk profiles and novel biomarkers that can support early diagnosis, prognosis, and targeted interventions. Ultimately, our goal is to translate mechanistic insights into innovative and personalized therapeutic strategies for stress-related behavioral and affective disorders.

Gut microbiome composition influences brain function and behavior via neural, endocrine, and immune pathways. Using dominance and submissiveness mouse models, we show microbiome differences drive depressive-like behavior, supporting targeted microbiome modulation as a potential therapeutic strategy for behavioral disorders.
This study investigates how stress and personality traits influence vulnerability to drug addiction. Using a mouse model of dominance and submissiveness, we identify genomic and hormonal signatures underlying differential responses to drugs, aiming to develop personalized prognostic tools for addiction risk.
This study explores the biological mechanisms underlying depression and anxiety through animal models and human research. By comparing stress-resilient and vulnerable mouse strains, we identify biomarkers and assess their relevance to human psychiatric disorders, including MDD and bipolar disorder.
Exploring how stress, depression, and personality traits contribute to age-related cognitive decline, this research uses stress-resilient and vulnerable mouse models to identify underlying molecular mechanisms and genes, aiming to support early diagnosis and prevention of cognitive impairment in humans.
This research investigates molecular and functional mechanisms underlying learning, memory formation, and cognitive decline. Focusing on synaptic plasticity, signaling networks, and aging-related impairments, the study aims to identify key molecular regulators involved in memory deterioration, neurodegeneration, and depressive-like behavior.
Prenatal stress shapes lifelong vulnerability to behavioral disorders. Using mouse models of stress resilience and susceptibility, we show that offspring of stressed, vulnerable mothers exhibit heightened stress responses and depressive traits, and identify placental glucocorticoid receptor pathways as targets for early diagnosis.