The focus of the Harrison lab is the role of vitamin C and its transporters (SVCT1 & SVCT2) in brain function during development and in neurodegenerative diseases.
Current projects :
Vitamin C in the brain in Alzheimer's disease. We use transgenic mice that carry human mutant genes for APP and PSEN1 which cause Alzheimer's disease and cross these with mice that have additional or only half of the normal copies of the SVCT2. With these models we can study the effects of a lifetime of low, normal and high levels of vitamin C in the brain on Alzheimer's disease neuropathology and cognitive deficits.
Vitamin C in the brain during development. We use a number of different mouse models including mice that express high or low levels of the SVCT2, mice that lack the SVCT1, and mice that cannot synthesize their own vitamin C and are supplemented with different amounts of it in their diet. Low vitamin C can cause scurvy in utero leading to death before or shortly after birth, and in less severe cases can causes permanent damage to brain function leading to permanent behavioral deficits. We aim to isolate the role of vitamin C in development and the mechanisms behind deficiency-induced damage.
Behavioral changes in a mouse model of Smith Lemli Opitz Syndrome. SLOS is a developmental disorder resulting from mutations in the Dhcr7 gene, that leads to severe deficits in cholesterol production in the brain. Many children face severe behavioral problems, including autistic syndrome disorders. In collaboration with the Korade lab we are investigating behavioral changes in SLOS mice as young as 7 days of age, all the way through adulthood to 12 months of age.