Dr. Jeanne Wei is the Jackson T. Stephens Professor and Chair of the Donald W. Reynolds Department of Geriatrics and Executive Director of the Reynolds Institute on Aging at UAMS, and has been providing patient care in the Thomas and Lyon Longevity Clinic at the Reynolds Institute.
Jeanne is an experienced academic leader, clinician, scientist, teacher, and administrator. Recognized nationally and internationally for her work in the field of aging, Jeanne has many years of experience in caring for patients, training future geriatricians, conducting geriatric and gerontological research, mentoring geriatric fellows and junior faculty members, as well as developing academic programs and initiatives.
Dr. Wei has dedicated herself to collaborating with others on research to define cardiovascular aging, unraveling the mechanisms, and finding new treatments. She and her group found that seniors are more vulnerable than younger adults to ischemic &/or hypoxic, as well as doxorubicin-toxic insult to the heart and brain. In addition, the group found that the brain is much more vulnerable than the heart. The elderly sustain greater inflammation, tissue damage & cognitive impairment. To date, however, few medications have protected older patients from the impaired cognitive and cardiac function following ischemic, hypoxic, or chemotherapy–induced injury to normal tissue. The group’s research also noted that the omega-3 fatty acid (FA), docosahexaenoic acid (DHA), was able to reduce ER/SR inflammation and protected cells from toxic stress. Other similar research has noted that due to this ischemic and/or hypoxic insult, that age-related diastolic dysfunction (HFPEF), more common in older women than older men, can be partly reversed by exercise. To date, few medications have protected older patients from HFPEF, especially those with low physical function. Similarly, the research also noted that the omega-3 fatty acid (FA) reduced ER/SR inflammation and protected cells from stress. Older hearts also have impaired mitochondrial function, including increased ATP depletion and decreased ATP repletion following hypoxic injury, as well as reduced fatty acid metabolism. Current efforts are underway to delay and/or reverse these changes.