BOSTON: In the late 1990s, Donna Wilcock was exploring electrical activity in the epileptic brain as part of her undergraduate study in England, but her focus took an interesting turn as her studies into brain function deepened.
“I began to wonder what, exactly, was going wrong in the brain as people developed dementia? What made them forget things?” said Wilcock. And that question bloomed into a career path focused on the triggers for a disease process that affects millions of people worldwide.
After stints in several university laboratories in the U.S., Wilcock was recruited to the University of Kentucky Sanders-Brown Centre on Aging in 2011 and is now associate professor and the Sweeney-Nelms Professor in Alzheimer’s Disease Research.
Wilcock’s early graduate work in Alzheimer’s disease immunotherapy stimulated her interest in inflammation and vascular cognitive impairment. “I’m most curious about the role inflammation plays in the development of dementia, and about the vascular contribution to cognitive impairment,” Wilcock said.
Her work in both areas has led to an interesting “triple play” that will help inform dementia research worldwide.
“It is a common misconception that dementia and Alzheimer’s disease are synonymous, however, just over half of all dementia (cases) are a result of Alzheimer’s disease. The second most common cause of dementia is vascular dementia,” Wilcock explained. “Moreover, it is rare that we see pure Alzheimer’s disease without other issues.”
Cerebrovascular disease and vascular dementia can be caused by anything from strokes and transient ischemic attacks (TIAs) to the more exotic sounding — but more common — white matter infarcts or chronic cerebral hypoperfusion. Wilcock shares the view of many of her colleagues that this mix of vascular dementia and Alzheimer’s disease might explain why many promising drugs to combat AD have failed in clinical trials.
“If you are testing a drug against a single disease, but a person has more than one disease with similar symptoms, the drug may appear to fail,” she says. “It’s the prevailing view that, for this reason, the best chance for beating AD and other dementias will be a cocktail of drugs.”
But the research community’s work has been hampered by the lack of a reliable animal model that mimicked co-morbid AD and vascular dementia.