Areas of Excellence (AoE)

Cellular Mechanisms of Synaptic Functions and Plasticity in Health and Neurodegenerative Diseases


Synaptic plasticity, the phenomenon by which the strength of a neuronal synapse is changed, is tightly regulated by various biochemical pathways.

Deciphering these mechanisms holds the key to understand how the brain learn and memorize, and why deregulation of these pathways cause synaptic dysfunctions and neurodegenerative diseases.

The goal of this project is to elucidate the cellular mechanisms that underlie synaptic plasticity, and to identify and characterize the relevant and crucial molecular players.

Project Summary

Neuronal synapses are critical for brain function. Modulation of their strength, termed synaptic plasticity, is essential for connecting and maintaining the neural network, and is the fundamental mechanism underlying learning and memory. Loss of synapses and their dysfunction are linked to neurodegenerative diseases such as Alzheimer’s disease (AD).

Synaptic plasticity is tightly regulated by various biochemical pathways. To unravel the mechanisms underlying synaptic plasticity, we will examine the precise signaling and cellular mechanisms governing neuron-neuron and glial-neuron communication. In particular, the cell population source of the receptor ligands within the neural circuit and the anatomical organization of these signaling pathways in the brain will be examined. We will also investigate how their deregulation contributes to the pathogenesis of neurodegenerative diseases, with a specific focus on AD.

Successful completion of the project will greatly facilitate development of new therapies to tackle these incurable diseases. The project will also enhance Hong Kong’s growing reputation as a center of excellence for neuroscience and will highlight the territory’s excellent scientific research capabilities, infrastructure, and highly skilled work force.


To elucidate intercellular signaling between neuron-neuron and neuron-glial cell communications by mapping the signals and circuitry of biochemical pathways.

To investigate the deregulation of signaling pathways in the hippocampus during synaptic dysfunctions in AD.


To determine whether manipulation of these pathways can reverse synaptic dysfunctions, neural network impairments, and cognitive deficits.

To identify additional molecular pathways that modulate synaptic strength during learning and memory, and synaptic dysfunctions during AD progression.