Orexin, a protein developed in the brain by the hypothalamus, is responsible for helping to wake the brain from a sleep state. It stimulates wakefulness, acting like a switch to wake the sleeping brain up. Researchers looking at this protein have learned that its presence in mice is a contributing factor to the development of brain plaques, mostly consisting of amyloid beta, which have been linked to memory loss, disorientation, personality changes, and dementia, all symptoms of Alzheimer’s disease. Brain plaques are always present before the onset of these conditions, and they increase in accumulation on the brain throughout their duration. Because of these known correlations, researchers are now looking at brain plaques, and at the orexin protein, for possible methods of preventing Alzheimer’s. By preventing the buildup of these plaques, researchers hope to slow, and possibly avoid, the onset of Alzheimer’s and other brain-related diseases.

Researchers out of Washington University School of Medicine looked at lab rats that were genetically manipulated to develop brain plaques more rapidly than normal. These rats developed symptoms of memory loss and dementia. They were then bred with rats that had a deficiency in the orexin protein. The result was as the researchers had hoped: the rats with less orexin slept an average of an entire hour more – over a 12 hour cycle – than rats with normal levels of the protein. The other result that researchers were hoping for also occurred; the rats that slept more (with deficient levels of the orexin protein) developed brain plaques at half the rate of those who had more orexin protein and slept less each day. Now that researchers are beginning to understand the link between sleep disorders and the development of Alzheimer’s, they are hopeful that the orexin protein could be a major factor in future Alzheimer’s prevention. One possible setback they learned from the study, though, is that decreasing the levels of orexin without changing the amount of sleep the rats got each night did not change the rate of brain plaque development. This means that in order for the elimination of the orexin protein to make any difference in slowing or stopping the onset of Alzheimer’s, there has to be a change in sleep patterns as well, which could be difficult to control on a large scale. Regardless, researchers are hopeful that this new understanding will help us get closer to eliminating Alzheimer’s disease in the future.