The Mechanisms of Reversing Working Memory Decline in Monkeys
The Technology Review looks at the work of researchers attempting to restore youthful function in brain cells associated with memory: "By delivering a certain chemical to the brain, researchers could make neurons in old monkeys behave like those in young monkeys. Clinical trials of a generic drug that mimics this effect are already underway. The findings support the idea that some of the brain changes that occur with aging are very specific - rather than being caused by a general decay throughout the brain - and can potentially be prevented. [Researchers] recorded electrical activity from neurons in a part of the brain called the prefrontal cortex, a region especially vulnerable to aging in both humans and [other] primates. It is vital for our most high-level cognitive functions, such as working memory and the ability to multitask and inhibit distractions. ... neural circuits in this region are organized to create a sustained level of activity that is crucial for working memory. ... By analyzing activity recorded from young, middle-aged, and old monkeys, the researchers found that the firing rate of the neurons in this area declines with age. They found that other neurons, such as those that respond to cues in the environment, still fired normally even as the monkeys aged. ... The researchers were able to rein in the problem by treating the cells with a drug that blocks the potassium channels. After treatment, brain cells in old monkeys fired more rapidly - just like those in their younger counterparts. The researchers already knew that giving monkeys this drug systemically, rather than delivering it directly into the brain, could reverse age-related deficits in working memory. A clinical trial of the compound, a generic drug called guanfacine, originally used to treat hypertension, is underway."