Insomnia memory loss may be reversible
27 Oct 2009, 1601 Hrs

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London, Oct 27 The loss of memory from insomnia (lack of sleep) may be reversible, according to researchers.

It is known that sleep deprivation can have cognitive consequences, including learning and memory deficits, but the mechanisms by which sleep deprivation affects brain function remain unknown.

Also, a particular challenge has been to develop approaches to reverse the impact of sleep deprivation on cognitive function.

Now, scientists have found a molecular pathway in the brain that is the cause of cognitive impairment due to sleep deprivation.

They have identified a molecular mechanism by which brief sleep deprivation alters hippocampal function in mice, involving the impairment of cyclic-AMP- and protein-kinase-A-dependent forms of synaptic plasticity, or readiness for cognitive function.

An international team of researchers, led by Ted Abel, principal investigator and professor of biology in the School of Arts and Sciences at the University of Pennsylvania, found that sleep deprivation in mice affects an important molecular pathway in the hippocampus, a region of the brain known to be important for memory and learning.

The study 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.

Researchers then treated the mice with PDE inhibitors, which rescued the sleep deprivation-induced deficits in cAMP signaling, synaptic plasticity and hippocampus dependent memory.

This reversal also helped to rescue 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. 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," Abel said.

The findings have been reported in this week's issue of the journal Nature. (ANI)

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