Going Deep to Halt Alzheimer’s
Date: June 7, 2013
This past November, Johns Hopkins surgeons eased a fine electrode into the brain of a patient in early-stage Alzheimer’s disease, down to the fornix, a site hard-hit by the illness.
Far from being routine therapy, the operation was the first in this country to explore deep brain stimulation (DBS) for Alzheimer’s. At issue: Can the technique, long used in treating Parkinson’s disease, slow or even halt patients’ decline into dementia?
This new trial follows a preliminary study in Toronto, Canada, in which surgeons implanted the stimulating devices in six Alzheimer’s patients. The researchers found that under the pulsed mild current that DBS creates, those in the study—all in early stages of Alzheimer’s—showed increases in glucose metabolism that mark heightened activity in known memory circuits. The effect lasted over the 13-month test period. Most patients with Alzheimer’s would normally see decreases in that length of time.
Patients undergoing DBS carry a pacemaker-like stimulator implanted just under the skin. An electrode extends from it, painlessly, to the brain. The arrangement isn’t new: Well established in treating Parkinson’s, it’s currently under study for depression and chronic pain.
In this newest work, some 40 Alzheimer’s patients will receive DBS over the next year or so at Hopkins and four other North American medical centers—all part of the ADvance Study co-led by Johns Hopkins psychiatrist Constantine Lyketsos and neurologist Andres Lozano at the University of Toronto. Only those impaired mildly enough to still be able to make informed decisions can participate.
Interest in DBS as a potential therapy for Alzheimer’s is keen in part because researchers have had relatively little success in developing effective drugs to fight the disease, and because the number of sufferers is almost guaranteed to rise, thanks to simple demographics. According to the Alzheimer’s Association, 5.4 million Americans currently suffer from Alzheimer’s, and that number is expected to reach 16 million by the year 2050.
“Recent failures of the large trials of drugs that target beta-amyloid plaques, a prime AD suspect in the brain, have sharpened our need for alternative strategies,” says psychiatrist Paul Rosenberg, site director of the new work at Johns Hopkins. “Trying to enhance brain function by mechanical means is a whole new avenue to explore.” Marjorie Centofanti