Last month, surgeons at Johns Hopkins implanted a pacemaker-like device into the brain of a patient with mild Alzheimer’s, the sixth patient in a multicenter trial of the experimental therapy. The hope is that the electrical stimulation delivered by the device could improve memory and slow cognitive decline in patients with the disease.
Deep-brain stimulation is already used to treat patients with Parkinson’s, epilepsy, and obsessive-compulsive disorder, and researchers are exploring its use in other conditions, including obesity. In each case, electrodes are inserted into different regions of the brain depending on the intended therapy. In the Alzheimer’s trial, the device is placed into a region of the brain involved in learning and memory.
The treatment has so far been tested in an already completed pilot study with six patients with Alzheimer’s. After a year of constant stimulation, the brains of these patients showed slightly increased glucose consumption in PET scans—a sign of increased neuron activity—in areas in the brain involved in learning and memory. Typically in Alzheimer’s patients, glucose metabolism decreases in the brain regions involved in memory, says Constantine Lyketsos, director of the Johns Hopkins Memory and Alzheimer’s Treatment Center and co-chair of the new trial.
Although the results are preliminary, with few options in sight for fighting the debilitating disease (see “The Dementia Plague”), even a small positive sign may be worth pursuing.
“Alternative treatment strategies need to be evaluated in Alzheimer’s disease due to the numerous recent failures of drug trials to halt or stave off cognitive decline in this population,” says Michele York, who is an assistant professor of neurology at Baylor College of Medicine in Houston. “The surgery could provide a new avenue for treatment for this debilitating and progressive disorder.”
The researchers are still recruiting patients into the new trial, which was initiated by Toronto-based Functional Neuromodulation. The trial will track Alzheimer’s patients who have a device that is either on or off for a year through physician observation and brain scans. The researchers hypothesize that the electrical shocks could stimulate critical neural networks that have been disrupted by Alzheimer’s. What sparks the disease is still an unsettled matter, but whatever the cause, the results are brain tissue atrophy and reduction of memory and thinking skills that increase over time.
The underlying brain changes and the associated behavioral difficulties can complicate treatment, says York. “The long-term use of this invasive intervention will require close scrutiny due to the progressive nature of the disease,” she writes.
Even if brain stimulation is proven to help patients, it probably won’t be a permanent fix. “It’s unlikely that deep-brain stimulation is going to reverse the pathological cascade in Alzheimer’s disease. It is very difficult to change that course,” says Mike R. Schoenberg, a licensed psychologist and neuroscientist at the University of South Florida Morsani College of Medicine. “The bigger issue at hand is one that we are grappling with in neuroscience in general: treatments may help with symptom relief and provide patients with some improvement over a period of time, but they aren’t curative.”
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