Disruption to sleep patterns is traditionally seen as a downstream symptom of Alzheimer’s disease.
Recent evidence, however, has sparked a debate of whether circadian dysfunction may actually lead to the development of Alzheimer’s disease by causing the accumulation of one of its main pathogens, amyloid-beta (Aβ) in the brain.
Converging research in both animal and human studies has found that the circadian cycle regulates levels of Aβ in the brain, and that acute suppression of sleep increases these levels. The principal hormone of the circadian system, melatonin, which is protective in cells exposed to toxic Aβ, is also seen to be dysregulated in Alzheimer’s disease. This raises the possibility that insomnia in humans could cause toxic Aβ accumulation over time, leading to the development of Alzheimer’s disease.
The debate arises in that although acute sleep loss may raise Aβ levels, it is not known if chronic suppression has the same effect. It is also argued that subject selection and methodologies used in existing research may account for this conclusion, and a call for prospective studies to decipher whether circadian dysfunction is a cause, or a result of, amyloid accumulation, is prevalent.
See the full debate
In the launch of a new “Debate” article type in BioMed Central’s Alzheimer’s Research & Therapy, Tracy Bedrosian and Randy Nelson (Ohio State University) approach this topic from a pro viewpoint: “Pro: Alzheimer’s disease and circadian dysfunction: chicken or egg?”
In counterpoint, Abhay Moghekar and Richard O’Brien (John Hopkins University) highlight the problems and holes of current research: “Con: Alzheimer’s disease and circadian dysfunction: chicken or egg?”
If you would like to continue this debate, or suggest a new debate topic to be covered in the journal, please contact the Alzheimer’s Research & Therapy Editorial Office at firstname.lastname@example.org.