As a part of a new multicenter trial funded by the National Institute on Aging and Functional Neuromodulation, the ADvance Study, Johns Hopkins University neurosurgeons recently implanted the first device into a patient with mild Alzheimer's disease. Through two implanted ultrathin wires, the device delivers 4- to 8-V electrical charges directly to the fornix on both sides of the brain. The fornix is one of the first brain regions to be destroyed by Alzheimer's disease. Researchers hope that the procedure will boost memory and reverse cognitive decline.
"Recent failures in Alzheimer's disease trials using drugs such as those designed to reduce the buildup of beta amyloid plaques in the brain have sharpened the need for alternative strategies," said Paul B. Rosenberg, MD, an Associate Professor of Psychiatry and Behavioral Sciences at Johns Hopkins University School of Medicine in Baltimore and a site director of the trial's Johns Hopkins location. "This is a very different approach, whereby we are trying to enhance the function of the brain mechanically."
About 40 patients are expected to receive the deep brain stimulation implant during the next year or so at Johns Hopkins; the University of Toronto; the University of Pennsylvania, Philadelphia; the University of Florida, Gainesville; and Banner Health System in Phoenix.
The ADvance Study is led by Constantine G. Lyketsos, MD, MHS, a Professor of Psychiatry and Behavioral Sciences at the Johns Hopkins School of Medicine, and Andres Lozano, MD, PhD, Chairman of the Neurology Department at the University of Toronto.
Half of the patients in the study will have the devices activated two weeks after surgery, while the others will have the device turned on after one year. All study participants will be regularly assessed for at least 18 months to measure their rate of Alzheimer’s progression.
As part of a preliminary safety study in 2010, the devices were implanted in six patients with Alzheimer’s disease at the University of Toronto. Researchers observed that patients with mild forms of the disorder showed sustained increases in glucose metabolism, an indicator of neuronal activity, during a 13-month period. In contrast, most patients with Alzheimer’s disease show decreases in glucose metabolism over the same period.