Visit Dr. Woodruff-Pak's personal page at http://astro.temple.edu/~pak.
Diana S. Woodruff-Pak has a primary appointment as Professor of Psychology at Temple University and secondary appointments at Temple University School of Medicine in Neurology and Radiology. To date, she has written or edited 8 books and authored over 150 publications and won a number of research awards. Her research program uses the model system of eyeblink classical conditioning to investigate neurobiological mechanisms in learning, memory, and aging in three species: humans, rabbits, and mice. Her initial work in this area demonstrated the significant role of aging in the cerebellum for impairments of learning and memory in rabbits and humans. She and her lab group demonstrated that the neural circuitry involved in eyeblink conditioning in non-human mammals (rabbits, rats, mice, cats, monkeys) is the same in humans. For example, they reported the striking parallels between this neural circuitry for learning and memory using patients with brain lesions and neurodegenerative diseases (cerebellar unilateral and bilateral lesions, Huntington's disease, Parkinson's disease) and normal adults tested in dual-task performance tasks or with anatomical or functional MRI.
Data from the animal model led to the hypothesis that patients with probable Alzheimer's disease (AD) would be severely impaired in eyeblink conditioning. Four separate studies supporting this hypothesis were carried out; the result was replicated independently in other labs. In longitudinal studies her research group demonstrated that eyeblink conditioning detects AD early, before other clinical symptoms such as memory loss are apparent. Grants from the Alzheimer's Association continue to support this work.
The clear parallels between eyeblink conditioning in rabbits and humans give this test of associative learning utility in preclinical studies of cognition-enhancing drugs. Drugs targeted for AD have been tested in her lab supported by pharmaceutical companies in Asia, Europe, and the United States. Her research on galantamine contributed to the data submitted to the FDA leading to approval of the drug (Reminyl™, renamed Razadyne™) for the treatment of dementia in AD. This work continues to receive support from pharmaceutical companies and from a 5-year NIH (NIA) grant entitled, “Aging and sites of action of cognition-enhancing drugs.” Most recently her group is working with a rabbit model of AD.
Motivated by the mapping of the mouse genome, the availability of transgenic and knockout mouse models of neurodegenerative diseases related to aging, and the short life span of mice, she added mouse eyeblink conditioning studies. She received support from NIH and the Albert Einstein Society for research on normal aging in C57BL/6 mice. Transgenic mouse models of AD and knockout mouse models missing selected nicotinic acetylcholine receptors were tested. Additional research with mouse models is supported by a 5-year NIH (NIA) grant entitled, “Mechanisms of associative learning and aging: Mouse models,” in collaboration with Richard F. Thompson, Ph.D. at the University of Southern California.