Frequent sleep disruptions may increase amyloid deposits down the road
Daily sleep disturbances could be a precursor to amyloid deposits in the brain, potentially increasing the risk of developing Alzheimer’s disease (AD), new research suggests.
In a study of more than 300 adults, researchers observed higher amyloid-β burden among adults who reported frequent disruptions to their sleep. This finding was consistent even among participants who did not display any Alzheimer’s pathology at baseline, indicating that sleep disturbances could contribute to the development of the neurological condition, authors of the study suggest.
“Sleep disturbances are common among older adults and have been associated with the development of Alzheimer disease, such as amyloid-β (Aβ) pathology,” corresponding author Julia Neitzel, PhD, from the department of radiology and nuclear medicine at Erasmus University Medical Center in the Netherlands, and co-authors write. “For effective AD prevention, it is essential to pinpoint the specific disturbances in sleep and the underlying 24-hour activity rhythms that confer the highest risk of Aβ deposition.”
Experts used participants' baseline PET imaging completed between 2004 and 2006 and from 2012 to 2014, and additional scans conducted between September 2018 and November 2021. The participants also had baseline seven-day actigraphy sleep activity data available that dated back an average of 7.8 years. None of the patients had been diagnosed with dementia or reported any dementia-related symptoms.
The finding of higher daily sleep disturbances at baseline being linked to amyloid deposits on later follow-up imaging was especially prevalent in carriers of the apolipoprotein E ε4 (APOE4) genotype—a significant genetic risk factor for AD. What’s more, the impact of fragmented sleep was consistent even after adjusting for things like the use of sleep medication, education, possible sleep apnea, body mass index, hypertension, diabetes, smoking, physical activity, depressive symptoms and more.
Given that sleep disturbances are a modifiable risk factor, the authors suggest that future longitudinal studies should focus on how reducing such disruptions might impact amyloid deposition.
“As further evidence for this association accumulates, intervention trials will be needed to investigate whether reducing fragmentation of the rest-activity rhythms can prevent or slow AD progression.”
The study abstract is available in JAMA Neurology.