The brain is the most sophisticated and important organ of the human body but little is known about normal brain function and how brain function is compromised in neurological and psychiatric disorders. Elucidation of the mechanisms responsible for the workings of the healthy brain is essential for genuine progress in treating its disorders. My vision is to identify cellular, molecular, circuit and behavioural defects associated with memory loss (dementia), a condition defined as “a chronic or persistent disorder of the mental processes caused by brain disease or injury and marked by memory disorders, personality changes, and impaired reasoning”. Dementia is a world-wide health problem; locally, tens of thousands of Singaporeans are afflicted and the prevalence of dementia is expected to quadruple by 2050 as the population ages. Dementia arises from a variety of causes, including normal aging, neurodegenerative disorders – such as Alzheimer’s, Parkinson’s, Huntington’s, and Down’s syndrome –as well as traumatic brain injury and posttraumatic stress disorder. The research in my lab is closely aligned with the category “neurological and sense disorders” which has been identified by the Ministry of Health (MOH) as one of the key areas of research focus based on factors such as disease impact, scientific excellence in Singapore and national needs according to Research, Innovation and Enterprise Council (RIEC) 2020 plans (RIE2020).

My lab has four integrated themes to investigate the following objectives:

(1) Synaptic mechanisms –defining synaptic mechanisms underlying memory and memory disorders under the frame works of synaptic tagging /capture and metaplasticity using rodents and non-human primates (NHP) models.

(2) Molecular mechanisms –defining cellular and molecular mechanisms underlying dementia-related circuit defects.

(3) Circuit analysis –characterizing hippocampal microcircuits using optogenetics in isolated brain tissue of normal mice and dementia mouse model.

(4) Behavioral causality – determining whether changes in synaptic mechanism cause long-term plasticity and memory deficits in rodents.