Cerebral amyloid deposition correlates with objectively measured sleep dysfunction: Human neuropathology/amyloid. (7th December 2020)

• Record Type: Journal Article
• Authors: Tissot, Cécile; Blais, Hélène; Thompson, Cynthia; Benedet, Andréa Lessa; Pascoal, Tharick A.; Therriault, Joseph; Chamoun, Mira; Lussier, Firoza Z.; Savard, Melissa; Rahmouni, Nesrine; Stevenson, Jenna; Gauthier, Serge; Gosselin, Nadia; Rosa‐Neto, Pedro
• Is Part Of: Alzheimer's & dementia. Volume 16(2020)Supplement 2
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-12-07
• Subjects: Alzheimer's disease -- Periodicals; Alzheimer Disease -- Periodicals; Dementia -- Periodicals; Démence; Maladie d'Alzheimer; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.83
• DOI: 10.1002/alz.045395
• Languages: English
• ISSNs: 1552-5260

Abstract

Abstract: Background: Sleep and circadian problems are known to be common along the Alzheimer's disease (AD) spectrum. Previous research correlated an increase in CSF Aβ with poor sleep quality through self‐reported questionnaires in cognitively unimpaired (CU) individuals. Research on AD patients however showed an increase in tau‐PET. Today, there is increasing evidence that sleep disturbances are an early marker for AD pathology and marker of future risk of cognitive impairment. Our main objective was to study the relationship between sleep efficiency as assessed with polysomnography and amyloid, tau and neuroinflammation. Method: 28 individuals (21 CU and 7 mild cognitive impairment (MCI)) underwent a [ 18 F]AZD4694 amyloid‐PET scan, [ 18 F]MK6240 tau‐PET scan, [ 11 C]PBR28 neuroinflammation‐PET scan, an MRI a full neuropsychological evaluation as well as a polysomnography. [ 18 F]AZD4694, [ 18 F]MK6240 and [ 11 C]PBR28 standardized uptake value ratios (SUVRs) used the cerebellum grey matter as the reference region and were calculated between 40‐70 min, 90‐110 min and 0‐90 min post‐injection respectively. A voxel based regression model evaluated the relationship between the different pathophysiologies of AD, amyloid, tau and neuroinflammation, and sleep efficiency. The model's covariates were age and diagnosis. Result: We found a negative correlation between sleep efficiency as measured with a polysomnography and amyloid. The most impacted regions were the temporal poles, the inferior parietal cortex and subcortical regions such as the thalamus. However, we did not find a correlation with [ 18 F]MK6240 and [ 11 C]PBR28. When we corrected for apnea‐hypopnea index, sex and years of education, results were similar. Conclusion: These preliminary results show that poor sleep quality correlates with amyloid deposition in the brain of CU and MCI individuals. The regions impacted have been related to sleep regulation, such as the thalamus. They are also known to be vulnerable to AD pathophysiology, for example, temporal and inferior parietal cortices. Our study adds to previous research by identifying anatomical correlates, and also using objective assessment of sleep quality. It also corroborates with the idea that sleep deprivation promote Aβ deposition.