07 Jul Structural Brain Changes in Sleep Apnea Linked to Cognitive Decline
MedicalResearch.com Interview with:
Nathan E. Cross PhD, first author
School of Psychology.
Sharon L. Naismith, PhD, senior author
Leonard P Ullman Chair in Psychology
Brain and Mind Centre
Neurosleep, NHMRC Centre of Research Excellence
The University of Sydney, Australia
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Between 30 to 50% of the risk for dementia is due to modifiable risk factors such depression, hypertension, physical inactivity, obesity, diabetes and smoking.
In recent years, multiple longitudinal cohort studies have observed a link between sleep apnoea and a greater risk (1.85 to 2.6 times more likely) of developing cognitive decline and dementia. Furthermore, one study in over 8000 people also indicated that the presence of obstructive sleep apnoea (OSA) in older adults was associated with an earlier age of cognitive decline, and that treatment of OSA may delay the onset of cognitive impairment.
This study reveals important insights into how sleep disorders such as OSA may impact the brain in older adults, as it is associated with widespread structural alterations in diverse brain regions. We found that reduced blood oxygen levels during sleep are related to reduced thickness of the brain’s cortex in both the left and right temporal areas – regions that are important in memory and are early sites of injury in Alzheimer’s disease. Indeed, reduced thickness in these regions was associated with poorer ability to learn new information, thereby being the first to link this structural change to memory decline.MedicalResearch.com: What should readers take away from your report?
Response: While in this study, we did not specifically examine biomarkers for Alzheimer’s disease, it is interesting to note that the temporal lobe is affected early in the progression of Alzheimer’s disease. This brain region is also particularly susceptible to hypoxia (reduction of blood oxygen), such as experienced with obstructive sleep apnea. Therefore, OSA may contribute to injury in this region, a notion that would be aligned with the robust association between OSA and dementia/memory decline across older clinical OSA samples. The increased thickness in the other brain regions may be linked with maladaptive mechanisms in response to OSA (e.g. inflammation, edema). Therefore a specific time course of events may occur in older adults with OSA, displaying an increase in some regions followed by a reduction in others. Given the clinical importance of this sample of at-risk older adults, we need to be screening older adults for sleep-disordered breathing.
MedicalResearch.com: What recommendations do you have for future research as a result of this work?
Response: Given we have gold-standard treatments for sleep-disordered breathing, we have a real opportunity to prevent cognitive decline caused by OSA before it’s too late. Future research should look at the long term effects of obstructive sleep apnea on brain health and whether treatment of OSA has any effect on this relationship. We are now analysing data pertaining to the connectivity of the brain and we are conducting a study examining how CPAP treatment may prevent cognitive decline in people with Mild Cognitive Impairment, a syndrome whereby 50% convert to dementia within 5 years. We are interested to see how CPAP may produce changes in brain neurometabolites and how it may improve functional connectivity. We will also examine the precise mechanisms by which OSA may contribute to the formation of beta-amyloid in the brain of older adults, and how treatment may alleviate the build up of beta-amyloid and tau, the key proteins implicated in the pathogenesis of Alzheimer’s disease.
Disclosures: This work was funded by an NHMRC fellowship awarded to Professor Naismith. Drs Cross and Duffy were funded by the Neurosleep Centre of Research Excellence.
Cross NE, Memarian N, Duffy SL, et al. Structural brain correlates of obstructive sleep apnoea in older adults at risk for dementia. Eur Respir J 2018; 52: 1800740 .
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