Several new research analyses found significant associations between sleep disordered breathing (SDB) and the accumulation of biomarkers for Alzheimer’s disease.
Peter Sayer, Alison Bloomer, and Eve Batt report from the Alzheimer’s Association International Conference 2017 (AAIC).
These findings highlight the idea that SDB is a modifiable factor that may help lower the risk of dementia and possibly slow the progression of dementia where it already exists.
Sleep disordered breathing is characterised by repeated episodes of hypopnea (under breathing) and apnoea during sleep. The predominant form of apnoea, obstructive sleep apnoea, occurs when an individual’s upper airway closes partially or fully, but efforts to breath continue. OSA occurs in an estimated three in 10 men and one in five women.
Research reported at AAIC 2017 found:
- SDB accelerated the accumulation of brain β-amyloid both in cognitively normal individuals and individuals with mild cognitive impairment (data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI)).
- Obstructive sleep apnea (OSA) was associated with increased brain β-amyloid deposition, decreased cerebrospinal fluid (CSF) levels of β-amyloid and increased tau protein levels.
Dean M Hartley, PhD, Alzheimer’s Association Director of Science Initiatives, said: “The Centers for Disease Control and Prevention says more than one third of American adults do not get enough sleep on a regular basis. Clearly this is not good for brain health or overall health. Sleep disordered breathing is treatable in many cases. Through early diagnosis and effective treatment of these sleep disorders, there is the potential to improve cognition and possibly reduce dementia risk. But first we need to know more about the connections between these medical conditions.”
Three analyses reported by investigative teams at Wheaton College in Wheaton, Illinois, at AAIC 2017 examined sleep patterns among participants in ADNI to characterise potential effects of SDB and OSA on brain changes associated with mild cognitive impairment and Alzheimer’s disease.
Amanda Shim and colleagues examined brain β-amyloid-42 accumulation in a cohort of 516 cognitively normal subjects and found that those with SDB had higher levels in CSF at baseline and more rapid accumulation over time. They found no interactive effect between OSA and the Alzheimer’s risk gene APOE- e4. This suggests that OSA may be independently associated with brain amyloid burden.
Megan Hogan and colleagues performed similar analyses to assess the effects of OSA in 798 subjects with mild cognitive impairment (MCI). As with the cognitively normal cohort, both baseline β-amyloid-42 levels and the rate of accumulation were higher in subjects with OSA. While MCI does not always lead to dementia, a person with MCI is at an increased risk of developing Alzheimer’s or another dementia. These results suggest that SDB may be an independent risk factor for Alzheimer’s and raises the possibility that interventions aimed at treating SDB may also reduce Alzheimer’s risk.
A combined analysis of the cognitively normal and mild cognitive impairment populations, plus a third group with Alzheimer’s disease (n=325), evaluated the effects of OSA on levels of several Alzheimer’s disease biomarkers in cerebrospinal fluid (CSF) and brain β-amyloid burden measured by positron emission tomography. Analyses showed:
- Significant OSA associations were observed with [brain] Aβ42 levels in CN and MCI participants.
- OSA subjects experienced faster increase in [brain] Aβ42 over time in the CN and MCI groups.
- OSA participants experienced a faster decrease in CSF Aβ42 and increases in TAU and PTAU volumes over time in both the CN and MCI groups.
According to research team leader, Omonigho Bubu, MD, MPH, these results “highlight the importance of checking for and accurately diagnosing sleep disordered breathing, especially in people at risk for dementia, and more importantly in people diagnosed with MCI, so that it can be addressed and treated.
“If OSA accelerates deposition of beta amyloid in the brain, then it becomes a possible target for therapeutic intervention. More research is needed to confirm these findings,” Bubu said.