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Sleep quality tied to Alzheimer’s pathology

Tristan Manalac
09 Aug 2017
Fatal familial insomnia is a rare brain disease that causes sufferers to be unable to fall into deep sleep

Self-reported poor sleep is significantly associated with Alzheimer’s disease (AD)-related pathology measured by cerebrospinal fluid (CSF) biomarkers, a new study has shown.

“Self-report of less adequate sleep, greater daytime sleepiness and more sleep problems were associated with CSF biomarkers of amyloid deposition in combination with tau pathology, axonal degeneration and neuroinflammation,” said researchers.

In the study sample of 101 cognitively normal adults (mean age 62.9±6.2 years; 65.3 percent female) with parental histories of AD, lower sleep adequacy was significantly correlated with a lower ratio of amyloid β (Aβ) 42 to Aβ40 (Aβ42/Aβ40; p=0.010), suggesting worse amyloid pathology. [Neurology 2017;89:445-453]

In contrast, Aβ42/Aβ40 was not significantly associated with Epworth Sleepiness Scale (ESS), sleep problems index or somnolence.

A higher ratio of neurofilament light (NFL) to Aβ42 (NFL/Aβ42) was significantly correlated with somnolence (p=0.015) but not with ESS, sleep problems or sleep adequacy.

The t-tau to Aβ42 ratio (t-tau/Aβ42) showed significant positive correlations with sleep adequacy (p=0.003), somnolence (p=0.017) and sleep problems index (p=0.021). Similarly, p-tau/Aβ42 was also significantly positively correlated to these measures of sleep quality (p=0.007, p=0.038 and p=0.033, respectively). Neither tau marker was correlated with ESS.

Because AD is a progressive disease that involves several contributing factors, “CSF biomarker ratios indexing multiple pathologies capture the temporal relationship between pathologies, which is a better indicator of disease stage than absolute levels of individual pathologies,” researchers said.

“We did not find a relationship between CSF biomarkers and symptoms of obstructive sleep apnoea (OSA). This lack of relationship is surprising, given consistent findings that OSA is a risk factor for dementia, possibly promoting AD pathogenesis,” they added.

Participants were recruited from the Wisconsin Registry for Alzheimer’s Prevention programme. Only those who had complete CSF samples and analyses, complete sleep questionnaire responses, and were cognitively normal were included.

Sleep quality was measured using the Medical Outcomes Study Sleep Scale and the ESS. Analysis focused on sleep adequacy, somnolence and sleep problems index because they had been previously linked to amyloid burden. Sleep-disordered breathing was considered in a secondary analysis.

The cross-sectional design and the self-reported nature of sleep quality measures are both important limitations of the study as “[t]here is evidence of bidirectional relationships between sleep and amyloid that cannot be disentangled by this cross-sectional study design,” said researchers. [JAMA Neurol 2014;71:971-977; Sci Transl Med 2012;4:150ra122]

Regardless, the present study was still able to link sleep quality in late midlife with the neuropathology of AD even in the absence of cognitive impairment.

Future studies that examine the longitudinal trends of these relationships and objective measures of sleep qualities (ie, actigraphy and polysomnography) will be important to more accurately identify the role of sleep in AD development, according to researchers.

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