Alzheimer’s disease (AD) is the most common form of dementia, an age-related neurodegenerative condition affecting 46.8 million people worldwide.

Treatment for the disease is purely symptomatic due to a lack of understanding of its causes. However, research from Washington University has found a link between getting a good night’s sleep and a reduction in the AD-associated proteins amyloid-β and tau.

Blocking up the brain

AD is known for its amyloid plaques and tau tangles, which form in the brain and can block neuronal activity and cause inflammation.

This neuronal degradation leads to the symptoms of AD, including memory loss, mood swings and problems with language.

The power of sleep

Work by neurologists in the US has found that the quality of sleep, rather than the quantity, is responsible for the modulation of amyloid-β levels.

Deep sleep, or slow-wave sleep, is important in preventing the formation of amyloid plaques. These are associated with lower levels of neuronal activity, meaning less amyloid is released into the brain and a reduced risk of aggregation.

One night of poor-quality sleep was enough to raise amyloid-β levels markedly in volunteers, while chronic poor sleep over a number of days increased levels of tau.

Prevention, not cure

While the results are interesting, their impact is focused more on the prevention of AD, rather than a cure.

By better understanding the early stages of AD, more steps can be put in place to target the populations most at risk of disease development, such as those with sleep disorders.