Mechanisms that maintain the functional and structural integrity of neurons and their disruption in aging and disease. Our brains enable us to laugh, dance, love, and create. Brains are made up of networks of neuronal cells, which process and store huge amount of information. The vast majority of neurons that operate your brain last a lifetime and are not replaced and loss of neurons causes neurodegenerative diseases such as Alzheimer's disease. How can we keep our brain functions during aging and reduce the risk of age-associated neurodegenerative diseases?
We tackle these questions with focuses on mitochondrial distribution in neurons and microtubule-binding protein tau, both of which play key roles in the pathogenesis of Alzheimer's disease and other neurodegenerative diseases.

Our current research projects include (1) How tau gain toxicity in disease pathogenesis, (2) mechanisms underlying depletion of axonal mitochondria increase neuronal vulnerability, (3) age-dependent changes in local energy metabolism in neurons and risks of neurodegenerative diseases.
As experimental approaches, we use Drosophila models, molecular biology, biochemistry, behavioral analysis, gene expression analysis, and imaging.

We hope discoveries from this research enhance understanding of disease pathogenesis and contribute to increasing our healthspan.

Current topics includes:
-Alzheimer's disease and related tauopathies
-Mitochondria in neurons in physiology and diseases
-Brain aging and energy metabolism