Research published this month in The Journal of Neuroscience has revealed some of the chemical triggers that mediate memory loss related to sleep deprivation. The researchers looked at the role of the nucleoside adenosine in the hippocampus, the center of the brain that directs the function of memory.
Sleep deprivation has long been known to cause an increase in adenosine, an effect common in all animals from arthropods to vertebrates, including humans. Now there is growing evidence that this nucleoside is the source of memory deficits that result from sleep deprivation.
Researchers tested the role of adenosine using two parallel experiments on sleep-deprived mice. In one experiment they used genetically engineered mice that were altered so they could not produce adenosine. In another experiment, researchers used a chemical pump that blocked an adenosine receptor in the hippocampus. Both of these experiments were designed to test whether adenosine was the key factor in sleep deprivation-related memory defects.
In both cases, the mice did not show memory deficits following sleep deprivation. The mice were able to recognize that a box had been moved in their environment, as opposed to the mice without adenosine blocking, who were all unable to identify what part of their environment had been changed from the prior day. These mice also stood up to an electrical measurement of their memory-forming synapses, showing objectively that they were unaffected by the loss of sleep.
In the future it is possible that this research will lead to us blocking the cognitive effects of sleep deprivation, but it is unlikely that it will help prevent some of the physiologic dangers of sleep apnea, such as coronary artery disease (CAD). Avoiding these consequences will still depend on successful sleep apnea treatment.
To learn more about your sleep apnea treatment options, please contact a local sleep dentist today.