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The overarching aims of my research are the following:

Normal brain function is predicated upon continuous adjustments in focal hemodynamics to meet local energy demands, a mechanism that is essential to brain function. It is also likely to experience impediments during the cognitive decline associated with aging as well as neurological disorders. Despite previous research efforts, the causes of many illnesses such as dementia remain unclear, and the key to preventative treatment elusive. My primary research will involve the following topics.

1. Vascular and Structural Aspects of Functional Connectivity

One intriguing aspect of functional connectivity is the spatially selective synchrony in BOLD signal fluctuations, which is assumed to be neuronal in origin. However, being an indirect measure of neuronal activity, the BOLD signal has significant cerebral blood flow (CBF) and volume (CBV) contributions, which fundamentally modulate the resting-state fluctuations. Without these latter measurements, the functional connectivity remains incompletely understood, and prone to misinterpretation in altered cerebrovascular health, such as seen in aging and neurodegenerative illnesses. We will utilize structural measures (e.g. diffusion-tensor and diffusion-kurtosis imaging) as well as vascular measurements (e.g. arterial-spin labeling) to investigate the origins of BOLD-based functional connectivity. We will also integrate these methods to furnish a novel approach to examining brain connectivity, involving the use of FreeSurfer structural and functional mapping tools.

2. Cerebral Vascular Reactivity, Oxygen Extraction and Links to Neurodegeneration

Cognitive deficits characterize normal aging as well as a myriad of neurodegenerative diseases, and have been linked to cortical and subcortical tissue atrophy in a large array of populations. In abnormal conditions, it remains unclear whether an impaired capacity for blood oxygen extraction engenders in corresponding neuronal degeneration, or pre-existing neuronal damage propagates into reduced oxygen metabolism. In addition, age-associated increases in cerebrovascular risks factors, such as hypertension, have recently been shown to promote white-matter lesions and cerebral atrophy as well as cerebral microbleeds. The extent of vascular reactivity changes in normal aging have yet to be experimentally shown, as well as how such changes affect neuronal health. However, the paucity of knowledge regarding the effect of cerebrovascular status on cognitive function engenders significant impediments in the diagnosis of neurological disorders. We will develop MR methodologies for measuring hemodynamic and metabolic variables of brain function, such as vascular reactivity and oxygen extraction. These MR methodologies will also be refined for clinical use.

3. Indices of Neurovascular Coupling in Health and Disease

Neurovascular coupling, is central to the ability of fMRI techniques such as BOLD to map neuronal activity. As mentioned earlier, hemodynamic contributions can dominate the BOLD signal, implying that knowledge regarding neurovascular coupling is critical to the utility of BOLD fMRI. It is unclear whether neurovascular coupling becomes altered in older adults, although these have been observed in Alzheimer's patients. While the development of such methods as pCASL and VERVE for measuring CBF and CBV specific to the BOLD effect are paving the way for the in vivo estimation of cerebral metabolism at high spatial resolution, we will focus on investigating the feasibility of novel contrast mechanisms based on the phase and/or magnitude of the MR signal have been shown to provide BOLD-indepdent measures of oxygen utilization, and may represent a compelling attempt to estimate quantitative cerebral oxygen metabolism and hemodynamic variables simultaneously and in a spatially resolved manner.

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