Alzheimer's doesn't just cause sleep problems. It may begin with them.

Neurologists studying mice that had been engineered to develop the condition found that those in which they induced chronic insomnia also developed tell-tale brain plaques faster. They also concluded that an independent protein which regulates the sleep pattern may play a large role in causing the disease.

The implications for the treatment of sleep disorders could be huge. The fact that a growing sleep deficit speeds the development of neurodegenerative disorders only re-emphasizes the importance of treating chronic insomnia as soon as it appears, especially among aging patients. By measuring the amount of amyloid protein (the substance that forms plaques on affected brains) in these mice, researchers found that sleep played a significant role in amyloid buildup. 

Regularly depriving the mice of sleep for three weeks led to a 25% increase in amyloid beta levels while those that slept regularly simply had less of the substance and were therefore less likely to develop brain plaques. Cognitive changes in the Alzheimer's mice were not caused by the fatigue of sleep deprivation but by the overpresence of this amyloid protein, which is produced largely while they are awake because their neurological systems, being fully active, require more of the protein. A separate study of human spinal fluid samples found that our amyloid levels follow the same sleep-related pattern.

The study also considered a separate protein called orexin that plays a key role in sleep regulation: mutations in a related gene have been linked to narcolepsy and other sleep disorders. When researchers added more of the protein to the rats' brains, they slept less and developed higher levels of amyloid proteins. When they added a drug that blocks the receptors for orexin, the rats slept longer and their amyloid levels returned to normal. The overproduction of orexin could initiate the development of Alzheimer's in many cases, and the great promise of this research is that it may help speed the development of related treatments to prevent or delay plaque buildup in humans.

As the sleep cycles of older adults break down they grow more likely to display Alzheimer's symptoms. As their symptoms increase they have more sleep problems. It's a destructive circle of influence, and early treatment in the form of protein regulation may be the best response.