Brain Amyloid beta is elevated in patients with sporadic Alzheimer’s disease and is the main component of amyloid plaques. Similar plaques appear in some variants of Lewy body dementia and in inclusion body myositis, while Amyloid beta can also form the aggregates that coat cerebral blood vessels in cerebral amyloid angiopathy. The plaques are composed of a tangle of regularly ordered fibrillar aggregates called amyloid fibers, a protein fold shared by other peptides such as the prions associated with protein misfolding diseases.

The mechanism by which Amyloid beta may damage and kill neurons is by generating reactive oxygen species during the process of its self-aggregation. It has been reported that amyloid beta production follows a circadian rhythm, rising when an animal or a person is awake and falling during sleep. The wakefulness-promoting neuroprotein orexin has been shown to be necessary for the circadian rhythm of amyloid beta production. This is consistent with recent findings that chronic sleep deprivation is associated with early onset Alzheimer’s disease.