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Bad sleep may predict Alzheimer’s,” the BBC has reported, saying that “problems sleeping may be an early sign of Alzheimer’s if a study in mice also applies to people”.

This news is based on research into the association between sleep patterns and accumulation of plaques in the brains of mice. These plaques, which are made up of clumps of small proteins in the brain, are a sign of Alzheimer’s disease. They are reported to start to form in the brain 10 to 15 years before symptoms such as memory problemsappear.

The researchers investigated whether the early stages of plaque development were associated with changes to the sleeping patterns of mice. They found that as plaques began to develop, the mice spent more time awake and less time asleep.

The researchers concluded that further research in humans is needed to determine whether or not this association is also seen in people with Alzheimer’s disease, and whether changes in sleep behaviour may be a sign of early Alzheimer’s.

If researchers confirm a similar association in humans, then the findings may provide an additional warning sign for early-stage Alzheimer’s. However, sleep problems in themselves are not evidence that a person is developing Alzheimer’s.

Many things can cause difficulty sleeping (insomnia), including normal ageing, stress, medications and physical or mental health conditions. Read more about the causes of insomnia.

Where did the story come from?

The study was carried out by researchers from Washington University School of Medicine in the USA and was funded by the American Academy of Neurology, the Ellison Medical Foundation and the Cure Alzheimer’s Fund.

The study was published in the peer-reviewed journal Science Translational Medicine.

The media coverage of this research was quite appropriate. The BBC emphasised that we will have to wait to see whether or not the results of this animal study apply to humans before concluding that sleep troubles are an early sign of Alzheimer’s.

What kind of research was this?

This was an animal study into the association between the accumulation of amyloid-β peptide and sleep patterns. The research used mice that had been bred with a genetic mutation similar to those seen in a mainly inherited form of the disease in humans.

In people, this particular mutation is associated with the early development of Alzheimer’s, often in young adulthood.

Previous research in both mice and healthy people has shown that amyloid-β levels vary naturally with the sleep–wake cycle, with levels increasing while people are awake, and dropping during sleep.

The early stages of Alzheimer’s (before symptoms such as memory and thinking problems are apparent) are marked by the accumulation of amyloid-β into clumps of proteins known as plaques. Given that higher amyloid-β levels are associated with wakefulness, the researchers thought that sleep patterns may be an early behavioural sign of plaque development.

Animal studies are often used in the early stages of clinical research, but it is not appropriate to assume that the results from such studies can be generalised to human disease. Studies using mouse models for Alzheimer’s can give us a general idea of the associations and causes that may underlie the illness. Further research in humans is required to be sure that the results are applicable to Alzheimer’s in humans.

What did the research involve?

The researchers used two groups of mice, one with a genetic mutation similar to that seen in some people with an inherited form of Alzheimer’s, and one without the mutation (the control mice). Within each group, they examined differences in the sleep–wake cycle before and after the development of amyloid-β plaques.

Before the plaques developed, they measured the amount of time the mice were awake each hour throughout the day, as well as the amount of sleep time spent in rapid eye movement (REM) sleep. REM sleep is a marker of the quality of sleep – people experience REM sleep when they are in deep sleep and, often, while dreaming. Once the plaques started forming, the researchers once again measured these two factors and determined whether or not any changes to sleep patterns had occurred.

What were the basic results?

The researchers found that before the plaques developed the mice with the genetic mutation spent an average of 30 minutes each hour awake during a 24-hour period. After three months, plaques began to form and the mice spent significantly more time awake, on average. After six months the mice were awake for an average of 40 minutes each hour. The control mice were spending approximately 30 minutes awake each hour after six months, similar to the amount of time seen before the development of plaques in the Alzheimer’s model mice.

The researchers also found that as the amount of time spent asleep decreased, the quality of the sleep deteriorated as well, with the mice spending fewer minutes each hour in REM sleep.

How did the researchers interpret the results?

The researchers concluded that the accumulation of amyloid-β plaques was associated with getting less, as well as poorer quality, sleep in mice.

Conclusion

This study suggests that, in mice, the amount and quality of sleep decreases as amyloid-β plaques accumulate. Further research in humans will be needed before we know whether this is also the case in people with Alzheimer’s.

The researchers say that the relationship between changes in the sleep cycle and amyloid-β accumulation is not well understood. They say that previous research has shown that “sleep disruption and disorders might be a risk factor for the development” of amyloid-β deposits and possibly Alzheimer’s. Yet their research found that the development of these plaques led to the disruption of sleep.

They suggest that this may not be a straightforward cause-and-effect relationship, but may represent a cycle in which an initial increase in the amount of time spent awake initiates the clumping of amyloid-β, which leads to further disruption of the sleep–wake cycle, which leads to further clumping of amyloid-β, and so on.

Several factors should be considered when interpreting this research. First, the mouse model used is intended to mirror only one type of Alzheimer’s that arises due to a specific genetic mutation, and often results in the development of the disease earlier in life. Thus, research will need to confirm whether the findings hold in people with this genetic mutation, and whether they can be further generalised to people who do not have this mutation and develop Alzheimer’s later in life.

If similar disruptions to sleep patterns are found in humans, the researchers suggest that changes in sleep patterns may be a useful indicator of the early stages of Alzheimer’s, or as a way to measure responsiveness to “new disease-modifying therapies as they become available”.

However, the usefulness of recognising changes in sleep patterns in terms of identifying people in the early stages of the disease may be limited, as difficulty sleeping is fairly common, especially as people age.

Getting less and poorer quality sleep may not be a specific enough sign to be clinically useful, as such problems may result from a number of factors.

At this stage, this study can serve as a useful addition to the body of knowledge surrounding Alzheimer’s, but does not offer a practical ‘early-warning sign’ for the disease.