Neurological complications and stroke mechanisms in sickle cell disease
Chronically low arterial oxygen content caused by hemolytic anemia in sickle cell disease leads the heart and brain to engage several compensatory mechanisms which lead to elevation in cerebral oxygen delivery to meet cerebral metabolic demands. We are examining how global and regional cerebral hemodynamics and oxygen metabolism provide patient and tissue specificity for predicting risk for cerebral ischemic injury and cognitive impairment in pediatric and adult sickle cell disease. Using both old and new imaging techniques, we are investigating the interaction of hypoxia-ischemia with endothelial and blood-brain barrier disruption on progressive cerebral injury and cognitive decline. We are linking our imaging and cognitive findings to genomic and proteomic pathways across a population with varying levels of disease severity to help understand which pathways are protective and which are harmful.
Natural history of inherited small vessel diseases: RVCL-S and CADASIL
Our lab is investigating the influence of oxygen metabolic stress with respect to ischemic vulnerability in patients with active cSVD who have or are at risk for vascular contributions to cognitive impairment and dementia (VCID). One inherited cSVD of particular interest is retinal vasculopathy with cerebral leukoencephalopathy (RVCL-S) which rapidly progresses over 10-15 years in mid adulthood. We follow an observational RVCL-S cohort with sequential MRI and cognitive testing which may serve as an accelerated model of cSVD, allowing us to gain a greater understanding of imaging biomarkers of risk as well as imaging.
Sporadic cerebral small vessel disease and vascular contributions to dementia
As the 2nd leading cause of dementia after Alzheimer’s Disease, the Ford lab, in collaboration with Hongyu An’s and Jin-Moo Lee’s Lab, prioritizes the investigation of vascular contributions to cognitive impairment and dementia, also known as VCID. Shown is a MRI of brain showing how hypertension and other systemic vascular insults wreak havoc and structurally injure various brain regions, leading to fragile brain health and lowering the threshold for dementia.