At the core of my research is the question of why neurons fail.

Using models of neurodegenerative disease, I investigate:

• Mitochondrial dysfunction and ATP depletion

• Oxidative stress and redox imbalance

• Glial regulation of neuronal survival

My work on the MBLAC1/SWIP-10 pathway explores how disruptions in copper homeostasis impair mitochondrial function, elevate oxidative stress, and ultimately drive neuronal degeneration.

Copper is essential for life, yet toxic when dysregulated.

I study how copper cycling between Cu(I) and Cu(II):

• supports mitochondrial respiration

• regulates oxidative stress

• contributes to neurodegenerative pathology when disrupted

This work connects metal biology to broader questions of energy metabolism and neuronal vulnerability.

Neurons rely on tightly regulated excitatory signaling.

I investigate how:

• excess glutamate signaling

• calcium dysregulation

• impaired glial buffering

lead to excitotoxic damage and progressive neuron loss, particularly in dopamine systems.

The brain is deeply connected to the immune system.

My research examines:

• microglial activation

• cytokine signaling

• peripheral-to-central immune communication

and how chronic inflammation contributes to both neurodegeneration and psychiatric conditions.

Experience shapes biology across time.

Using models of environmental stress, including maternal separation, I study how early-life conditions:

• alter stress-response systems

• reshape immune tone

• influence long-term brain function and behavior

These changes can increase vulnerability to depression, cognitive decline, and neurodegenerative disease.

Rather than viewing depression as a simple neurotransmitter imbalance, I approach it as a systems-level condition.

This includes:

• immune activation

• metabolic disruption

• altered neural signaling

In this framework, depression can be understood as a sickness phenotype, emerging from the interaction of stress, inflammation, and energy dysregulation.

Using established models of Alzheimer’s disease, I study:

• amyloid pathology

• neuroinflammation

• synaptic dysfunction

• behavioral decline

while focusing on how these features emerge from deeper disruptions in metabolism, immune signaling, and cellular stress.

The brain retains the capacity to change.

I explore how adult neurogenesis and neural plasticity are influenced by:

• stress

• environment

• behavior

and how these processes may be leveraged for resilience and recovery.