Modulating the Blood-Brain Barrier (BBB) to enable delivery of drugs and development of therapeutics
The blood–brain barrier (BBB) helps maintain a constant, optimal environment for neuronal function through a combination of barriers and selective transport systems that regulate the passage of wanted and unwanted molecules. While important for brain functionality, the BBB presents a formidable challenge to medicine because it stops most drugs from passing from the bloodstream to the brain. Importantly, BBB compromise has been associated with several neurological disorders including multiple sclerosis and Alzheimer’s disease. Work published in Nature in 2014 and Neuron in 2017 by the Gu lab identified a mechanism responsible for BBB maintenance, involving the suppression of vesicle-mediated transfer of blood-plasma constituents to the brain (transcytosis). This suppression was shown to depend on a transmembrane protein, Mfsd2a, specific to the endothelial cells that line blood vessels in the brain.
Current work in the Gu lab is focused on characterization of a potential drug candidate - Mfsd2a blocking antibody. We are looking for collaborators interested in delivery drugs to the brain using this antibody.
Another line of work in the Gu lab is dedicated to further elucidation of the role of BBB in neurodegeneration and identification of potential novel therapeutic targets. To advance this research, we would like to work with collaborators interested in discovery of BBB integrity enhancers.
The blood–brain barrier (BBB) helps maintain a constant, optimal environment for neuronal function through a combination of barriers and selective transport systems that regulate the passage of wanted and unwanted molecules. While important for brain functionality, the BBB presents a formidable challenge to medicine because it stops most drugs from passing from the bloodstream to the brain. Importantly, BBB compromise has been associated with several neurological disorders including multiple sclerosis and Alzheimer’s disease. Work published in Nature in 2014 and Neuron in 2017 by the Gu lab identified a mechanism responsible for BBB maintenance, involving the suppression of vesicle-mediated transfer of blood-plasma constituents to the brain (transcytosis). This suppression was shown to depend on a transmembrane protein, Mfsd2a, specific to the endothelial cells that line blood vessels in the brain.
Current work in the Gu lab is focused on characterization of a potential drug candidate - Mfsd2a blocking antibody. We are looking for collaborators interested in delivery drugs to the brain using this antibody.
Another line of work in the Gu lab is dedicated to further elucidation of the role of BBB in neurodegeneration and identification of potential novel therapeutic targets. To advance this research, we would like to work with collaborators interested in discovery of BBB integrity enhancers.
Intellectual Property Status: Patent(s) Pending