The development of non-invasive methods to detect early yet subtle changes in the brains of patients with Stroke and Alzheimer Disease (AD) would have considerable clinical value since therapy is most likely to be successful if intervention can occur before neurons are irreversibly damaged or lost. There is currently no such sensitive and specific biological marker for the post ischemic period of stroke or the pre-clinical stages of AD. Ideal biological-neuroimaging markers would be early, sensitive, and valid indicators of brain changes, or of a characterized and altered physiology. In AD, they must distinguish the effects of normal aging. Our research is aimed at identifying and evaluating such a set of potential markers using quantitative high field Magnetic Resonance Imaging (MRI).

In the case of AD, we use high-field MRI with high spatial resolution in a transgenic mouse model of extensive amyloidosis - one of the hallmark neuropathological features of AD. We attempt to exploit the exquisite sensitivity of quantitative measurements of MRI parameters to changes in the biophysical environment of water. Overall, it is expected that this work will provide us with a better understanding of the effects of amyloid burden on brain structure and brain function. We have recently begun to translate this early work to the application of high-field MRI assessment in human AD patients.

Our stroke research is aimed at investigating to what extent hemodynamic factors are involved in increased tissue damage associated with ischemia under conditions of hyperglycemia. We are interested in this since elevated systemic blood glucose concentrations have been implicated in poor neurological outcome following stroke in experimental animals and humans. This work will improve our understanding of the role of hyperglycemia in stroke and may help lead to new approaches for stroke management.