Sleep Deprivation – Mechanism for Cognitive Impairment

As reported in Nature scientists have uncovered (in mice) a molecular mechanism by which brief sleep deprivation alters hippocampal function, involving the impairment of (cyclic-AMP- and protein-kinase-A-dependent) forms of synaptic plasticity.

Ted Abel, principal investigator and professor of biology, and his team showed that mice deprived of sleep had increased levels of the enzyme PDE4 and reduced levels of the molecule cAMP, the latter of which is crucial in forming new synaptic connections in the hippocampus, a physiological hallmark of learning.

PDE inhibitors mitigated the sleep deprivation-induced deficits in cAMP signaling, synaptic plasticity, and hippocampus dependent memory and helped to reverse deficits in synaptic connections in the hippocampus and therefore counteract some of the memory consequences of sleep deprivation.

“Millions of people regularly obtain insufficient sleep,” Abel says. “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.”

Researchers from the University of Glasgow and the University of Toronto contributed to the study, which was supported by the National Institutes of Health, the Human Frontier Science Program, the Netherlands Organization for Scientific Research, a Medical Research Council (U.K.) grant, a European Union grant, the Fondation Leducq, and a U.K. Engineering and Physical Sciences Research Council training grant.

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