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Faculty Detail
Name
LINDY E HARRELL
Campus Address
SC 620F Zip 0017
Phone
(205) 934-3847
E-mail
lharrell@uab.edu
Other websites
Faculty Appointment(s)
Appointment Type
Department
Division
Rank
Primary
Neurology Chair Office
Neurology Chair Office
Professor Emeritus
Graduate Biomedical Sciences Affiliations
Neuroscience Graduate Program
Neurosciences
Waiting to be Seated
Biographical Sketch
Dr. Harrell received her Ph.D. in Physiological Psychology from the University of Massachusetts (1974) and an M.D. from the University of Miami (1977). She did her Medical Internship, Neurology Residence, and Geriatric Fellowship at Duke University. In 1983, she came to UAB and rose to the rank of Professor of Neurology with tenure in 1991.
Research/Clinical Interest
Title
Description
Dr. Harrell’s research investigates the effects of neuronal plasticity (sprouting of normal fibers after brain injury) in hippocampus, an area essential for normal learning/memory, and an area known to be injured early and to undergo neuronal plasticity in Alzheimer’s Disease (AD). In this model, cholinergic neurons, which are also essential for normal learning, are injured and replaced by sprouting noradrenergic fibers. Early behavioral studies found that noradrenergic fibers were detrimental to learning /memory. Biochemical studies, however, revealed that noradrenergic fibers seemed to “normalize” many brain physiological functions including cholinergic receptor number, second messenger systems, enzymes important in learning/memory, etc. Recent results have begun to explain these discrepancies. Treatment of normal animals with an alpha-adrenergic receptor blocker significant decreased hippocampal cholinergic receptors. In further studies, animals with sympathetic sprouting were also treated with either an alpha-adrenergic receptor blocker or excitor. Treatment with exciters reduced the enzyme important for activity in the cholinergic system and binding of cholingeric substances to cholingeric receptors. Treatment with alpha-adrenergic blockers increased binding of cholingeric substances to cholingeric receptors. These studies suggest that adrenergic fibers may affect the injured cholinergic system differently depending on the presence of different brain chemicals, which may explain the discrepancies between our behavioral and biochemical findings. More importantly, these results suggest that at least alpha-adrenergic medications, which are used clinically to treat a number of different illnesses, might either have a detrimental or beneficial effect on learning/memory in AD patients. These findings may provide a new approach to the treatment of AD patients, as well as patients with other neurodegenerative diseases, if verified by clinical trials.
