Penn professor of biology Ted Abel led the study to uncover more information about the role of the nucleoside adenosine
in the hippocampus
, the section of the brain linked to memory functions.
Their research, funded by the National Institutes of Health, has been published in The Journal of Neuroscience
In this study, two experiments on sleep-deprived mice demonstrated the key role adenosine plays in the neurochemical pathway underlying sleep deprivation symptoms, by disrupting this molecular activity.
One group of mice were genetically engineered to lack glial transmitters, the chemicals in glia
(brain cells) that produce adenosine. The second group of mice were pharmacologically altered with surgically grafted pumps that dosed the hippocampus regions of their brains with a drug known to block adenosine-receptors.
With the adenosine connection blocked, both groups of mice performed normally on object recognition tests, showing no signs of sleep deprivation, demonstrating that cognitive impairments caused by lack of sleep can be reversed.
In previous projects, Abel studied other molecular mechanisms linked to the cognitive consequences
of sleep deprivation, revealing other possibilities for developing future treatments for humans suffering from any of the diverse health diminishing effects of sleep loss.
In humans, sleep deficit effects relate to many acute or chronic problems, disorders and diseases, from clumsiness to loss of creativity to major physical and mental illnesses, according to Bryn Mawr's Serendip
According to the Franklin Institute
, most neuroscientists agree sound sleep aids brain development and helps process waking experiences into memory, and many psychological and medical problems and ailments are related to sleeping troubles: schizophrenia, depression, dementia, stroke, injuries, stress, poor mental and physical performance and more.
In a prepared statement
, Abel said of his ongoing research at Penn:
“Millions of people regularly obtain insufficient sleep. Our work has identified a treatment in mice that can reverse the cognitive impact of sleep deprivation. Further, our work identifies specific molecular changes in neurons caused by sleep deprivation, and future work on this target protein promises to reveal novel therapeutic approaches to treat the cognitive deficits that accompany sleep disturbances seen in sleep apnea, Alzheimer’s disease and schizophrenia.”