The focus of the study was “excess brain activity” commonly associated with conditions that cause mild cognitive decline and memory loss, and are linked to an increased risk of Alzheimer’s, according to lead author Michela Gallagher, Ph.D., a professor of psychological and brain sciences in the Johns Hopkins University’s Krieger School of Arts and Sciences.
Previously, it had been thought that this hyperactivity in the hippocampus was the brain’s attempt to compensate for a weakness in forming new memories, she said. Instead, the researchers found that this excess activity contributes to conditions such as amnestic mild cognitive impairment (aMCI), in which patients’ memories are worse than would be expected in healthy people the same age.
“In the case of aMCI, it has been suggested that the increased hippocampal activation may serve a beneficial function by recruiting additional neural ‘resources’ to compensate for those that are lost,” she said. “However, animal studies have raised the alternative view that this excess activation may be contributing to memory impairment.”
To test how a reduction in that hippocampal activity would affect patients with aMCI, Gallagher’s team administered a low dose of a drug used to treat epilepsy. The goal was to reduce the test subjects’ activity to levels that were similar to those of healthy subjects in a control group.
The researchers used functional magnetic resonance imaging to determine the levels of excess activity, and how much the drug reduced that activity.
The research team found that the subjects who had been treated with an effective dose of the drug did better on a memory task.
According to Gallagher, the increased hippocampal activity observed in conditions that precede Alzheimer’s may be one of the underlying mechanisms contributing to neurodegeneration and memory loss.
Studies have found that if patients with aMCI are followed for a number of years, those with the greatest excess activation have the greatest decline in memory, and are more likely to receive a diagnosis of Alzheimer’s over the next four to six years, she said.
“Apart from a direct role in memory impairment, there is concern that elevated activity in vulnerable neural networks could be causing additional damage and possibly promoting the widespread disease-related degeneration that underlies cognitive decline and the conversion to Alzheimer’s Disease,” Gallagher said.
“Therefore, reducing the elevated activity in the hippocampus may help to restore memory and protect the brain. It will require a carefully monitored, lengthier clinical trial to determine if that is the case.”
The research was published in the May 10 issue of the journal Neuron.
Source: Johns Hopkins University