Dementia describes clusters of symptoms associated with brain decline but the most common is Alzheimer’s disease. The symptoms develop gradually over many years and eventually become more severe. Memory loss is often the first visible sign and as the condition progresses, this may be accompanied by more severe symptoms such as personality changes and hallucinations. Unfortunately, there is currently no cure for Alzheimer’s disease so the focus has been on finding ways to reduce the risk.
This has led researchers to look at the risk factors associated with Alzheimer’s.
The logic is clear – if warning signs can be spotted early enough, lifestyle interventions may be taken to reduce the risk.
New research published in the journal Neurology advances this effort.
According to the research, supported by the UK Dementia Research Institute, the country’s largest dementia research initiative, sleeping patterns are associated with an increased risk of dementia in people with a higher genetic risk of the condition.
Dementia: Morning people may be a higher risk of Alzheimer’s if they carry the genetic risk
More specifically, the study found that people with twice the genetic risk for Alzheimer’s disease were one percent more likely to call themselves “morning people” compared to people at lower genetic risk.
What’s more, people with twice the genetic risk of Alzheimer’s had a one percent lower risk of insomnia.
Commenting on the findings, Dr Sara Imarisio, Head of Research at Alzheimer’s Research UK, said: “Many of us have experienced a bad night’s sleep and probably know that it can have an impact on our memory and thinking in the short term, but an intriguing question is whether sleep problems have a long-term effect on the brain.
“This research shows a small link between different sleep patterns and the risk of developing Alzheimer’s disease, but did not find any evidence for sleep disturbance causing the disease.”
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She continued: “A recent large-scale review of risk factors for dementia within our control to change found there have not been enough studies in this area for sleep to be included on the list.
“Dementia is not an inevitable part of ageing and more evidence on the complex topic of sleep is needed before we can make a judgement on its impact on dementia risk. We hope findings like this will act as a catalyst for further research.”
While the study did not attempt to unpick the relationship between sleep and Alzheimer’s, previous research has floated some convincing theories.
According to Alzheimer’s Research UK, a number of studies have shown that interrupted sleep may speed up the progression of Alzheimer’s in the brain.
Dementia sleep link: Animal studies show continued lack of sleep can increase levels of amyloid
But, as the health body points out, it’s difficult for researchers to tease apart cause and effect.
“They need to work out whether poor quality sleep might contribute to the development of the disease or vice-versa,” says the research body.
Research in mice has shown that continued lack of sleep can increase levels of amyloid – one of the hallmark proteins involved in Alzheimer’s.
Amyloid protein clumps together in Alzheimer’s disease and triggers damage to the brain.
Alzheimer’s disease: Those with an inherited gene are at a higher risk
Who carries a higher genetic risk of Alzheimer’s?
According to the Alzheimer’s Society (AS), in just over 600 families worldwide, studies reveal many close family members who are affected by Alzheimer’s disease across successive generations.
“This pattern of ‘familial clustering’ of Alzheimer’s disease suggests there is a mutation within a single gene that causes the disease,” explains the AS.
It adds: “In these cases, the mutation is being passed down in the DNA from parent to child, across several generations.”
If several of your family members have developed dementia over the generations, and particularly at a young age, you may want to seek genetic counselling for information and advice about your chances of developing Alzheimer’s disease when you’re older, advises the NHS.