ENERGY METABOLISM AND BRAIN CHANGES WITH AGE AND ALZHEIMER'S DISEASE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The candidate is a geriatric neurologist with postdoctoral training in dementia and Alzheimer's disease (AD) who will use the K23 to develop expertise in clinical research methodology, advanced neuroimaging techniques, and metabolism. The proposal combines the candidate's experience in the clinical evaluation of dementia, neuroimaging research on structural brain changes, and a new focus on metabolism. The academic environment will support the training and research experience through the Hoglund Brain Imaging Center, the Energy Balance Laboratory, the Biostatistics and Bioinformatics Center, and an NIH-sponsored K30 curriculum training program. Career Development: The candidate will obtain a Master's in Clinical Research, training in the assessment of metabolism and body composition, and training and formal coursework in advanced neuroimaging techniques. Research Program: Research into caloric restriction and insulin metabolism have led to seminal advances in our understanding of aging processes and have implicated energy metabolism as an underlying etiology for age-related disease such as AD. The overall goal of the research program is examine the hypothesis that peripheral energy metabolism influences brain aging. Using well-established clinical and neuroimaging methods from the candidate's postdoctoral training program, standard methods to clinically characterize and neuroimage older adults with and without memory problems will be developed, piloted, and implemented (aim 1). The relationship of brain structure with insulin-mediated glucose disposal (aim 2) and resting metabolic rate (aim 3) will be cross-sectionally examined in a cohort of nondemented (n = 32) and early-stage AD participants (n = 32). Improved understanding of the physiologic mediators of structural brain changes may lead to new therapeutic targets for promoting brain health arid preventing age-related brain disease. K23 support will allow the candidate to build a research and educational foundation to develop and launch an independent patient-oriented career using neuroimaging to study the pathophysiology of age-related structural brain changes and brain disease such as AD.