research @ THE TAN LAB

The hippocampus is a vital brain region that plays key roles in learning, memory, spatial navigation, and mood regulation. It’s also one of the first areas affected in several neurological disorders, including epilepsy and Alzheimer’s disease. In our lab, we use the hippocampus as a model system to explore how different types of brain cells are generated, maintained, eliminated, and wired into functional circuits. By uncovering how these processes go awry, we aim to deepen our understanding of disease mechanisms and contribute to the development of more effective therapies for neurological conditions.

Unlike many other cortical regions where neurogenesis is largely complete by birth, the dentate gyrus of the hippocampus continues to develop well into the postnatal period. This extended developmental window raises several exciting questions: 

How is early postnatal neurogenesis regulated?

What guides the migration of progenitors and newborn neurons?

Which factors ensure the precise wiring of these newly generated neurons into existing circuits?

While most neurons in the brain are generated during embryonic development and around birth, the mammalian brain remarkably retains the ability to produce new neurons well into adulthood. One of the few regions where this occurs is the dentate gyrus of the hippocampus—a brain area crucial for learning, memory, and mood regulation. 

Our lab is particularly interested in how new neurons mature during adult hippocampal neurogenesis, with a focus on the transition from neuroblasts to immature neurons. We’re working to answer key questions such as:

What regulates the initiation and termination of neuronal migration?

How is the intricate dendritic architecture of newborn granule neurons formed?

What factors make these developing neurons vulnerable to cell death?

By uncovering the answers, we hope to gain deeper insight into how the adult brain remains plastic—and how disruptions to this process may contribute to disease.

In the developing brain, 20–40% of newly born neurons undergo programmed cell death—a striking phenomenon that raises an important question: why does the brain eliminate so many neurons, and what is the functional significance of this loss?

Cajal-Retzius (CR) cells, a population of pioneer neurons present during early brain development but largely eliminated postnatally, offer a powerful system to explore this question. Interestingly, incomplete removal of CR cells has been observed in human neurological disorders such as epilepsy, suggesting that their timely death may be critical for healthy brain maturation.

Our lab investigates the role of CR cell death in shaping the cerebral cortex and hippocampus. We ask:

What regulates the developmental cell death of Cajal-Retzius cells?

Do residual CR cells serve a purpose in the adult hippocampus?

Could disruptions in CR cell removal contribute to epilepsy?

By exploring these questions, we aim to uncover how early developmental processes lay the groundwork for lifelong brain function—and what happens when those processes go awry.