For the sleep deprived, a new solution may be on the way

A new memory medication may aid future generations of sleep-starved Penn students.

A Penn-led international team of researchers published a study in Nature last month that suggests that certain drugs can counteract the memory-related effects of sleep deprivation.

The paper revealed that sleep deprivation increases activity of the enzyme phosphodiesterase-4 (PDE).

Increased levels of PDE degrade the protein cyclic AMP (cAMP) at higher rate in the hippocampus, a region of the brain that controls long-term memory.

Falling cAMP levels in the hippocampus can interfere with memory retrieval.

In the study, mice given PDE-inhibiting drugs saw higher cAMP levels and improved performance in long-term memory.

According to Ted Abel, one of the study’s co-authors and director of the Biological Basis of Behavior program, these breakthroughs have immediate implications in the world of human neurobiology.

“Millions of people regularly obtain insufficient sleep,” he said in a statement. “Our work has identified a treatment in mice that can reverse the cognitive impact of sleep deprivation.”

Future study of the proteins involved, Abel said, should “reveal novel therapeutic approaches” to treating sleep-related symptoms of sleep apnea, Alzheimer’s disease and schizophrenia.

Lead author Chris Vecsey, a postdoctoral student at Brandeis University and former neuroscience graduate student under Abel, said the genes controlling these mechanisms in mice are nearly identical to those in humans.

While specialized PDE-inhibiting drugs are already commercially available for humans, Vecsey said, further research will be necessary to prepare a drug that will restore memory to the sleep-deprived.

“That’s only one effect of sleep deprivation,” said Vecsey, who pointed to inattentiveness as another effect. “Your memory might improve, but you could still drive a car off a cliff.”

In addition, the PDE-inhibiting drugs used in the study were noted to cause severe nausea and vomiting in test mice.

FDA-approved medications derived from the group’s findings may be possible in the future, said Vecsey, but further research is necessary — such as looking into how to target specific PDE receptors.

“You can’t just block all PDE,” he said, since it has many other uses elsewhere in the body.

The study began as a project in Abel’s neuroscience lab, which specializes in biological memory storage. Experts from Glasgow, Scotland, and Toronto, Canada, were brought into the study after Nature’s editors suggested additional experiments.

The international researchers were very instrumental, according to Vecsey, and contributed “some of the strongest data.”

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