Computational modelling shows that innervation of vascular smooth muscle cells provides the motive force for IPAD, which has led us to hypothesize that 1) failure of elimination of Aβ along IPAD pathways could be a major factor in the pathogenesis of AD and 2) LC deafferentation of vascular smooth muscle cells (VSMCs) promotes IPAD failure in AD by impairing the motive force driving this clearance pathway.
Our lab is focused to studying the population of microglial cells from development to ageing, as well as chronic neurodegenerative disease such as Alzheimer’s. We have ongoing projects studying both rodent and human microglia, characterising it’s dynamics and phenotype with a range of techniques such as molecular phenotyping, scRNAseq, as well as modulating their activity via pharmacological or transgenic interventions. We are particularly interested in the role of proliferation and senescence in the specification of detrimental microglial phenotypes that can be targeted as a therapeutic approach in Dementia.
