Science
Research Mission
Dementia is a devastating disease that affects patients, their families, and society by impairing the ability to form new memories and gradually eroding existing ones. Nearly 1 million people in the UK are affected, and the problem is worsening as populations age. There are no robust or cost-effective treatments for common dementias like Alzheimer’s disease (AD), and diagnosis is challenging. Research efforts are focused on understanding the genetic, cellular, and molecular mechanisms by which the immune system controls cognitive function during normal and pathological brain ageing, including AD and vascular dementia.
About us
Our research group is dedicated to investigating the interplay between the immune system and cognitive function in the ageing brain focusing on neurodegenerative diseases like Alzheimer's disease. We study genetic variations and their effects on neurodegenerative diseases using techniques such as GWAS, transcriptomics, and epigenetics. Based at the University College London (UCL) branch of the UK Dementia Research Institute, we benefit from a robust neuroscience community. Our interdisciplinary approach integrates molecular biology, biochemistry, cell biology, and advanced genomic methods to advance our understanding and treatment of dementia. Our team is committed to translating our research findings into practical applications. By integrating GWAS data with transcriptomic and epigenetic analyses from human and model systems, we aim to identify new risk genes and pathways involved in dementia and ageing. Through our efforts, we strive to develop new therapeutic approaches and diagnostic tools. Ultimately to counteract cognitive decline and improve the quality of life for individuals affected by neurodegenerative diseases.
Our Findings
We have identified novel risk genes such as OAS1, LAPTM5, ITGAM, and ANKH associated with Alzheimer's disease (AD), unhealthy ageing, and severe COVID-19. Our research shows that OAS1 links AD risk with severe COVID-19. By integrating GWAS data with RNA sequencing and co-expression networks, our results suggest that OAS1 suppresses the pro-inflammatory response of microglia. We also found gene variants associated with human longevity and their links to immune function and AD risk. Our data suggest that the balance between homeostatic and activated immune cells contributes to brain health in ageing and AD.
