Introduction:
In this multicenter study on subjective cognitive decline (SCD) in community-based and memory clinic settings, we assessed the (1) incidence of Alzheimer’s disease (AD) and non-AD dementia and (2) determinants of progression to dementia.
Methods:
Eleven cohorts provided 2978 participants with SCD and 1391 controls. We estimated dementia incidence and identified risk factors using Cox proportional hazards models.
Results:
In SCD, incidence of dementia was 17.7 (95% Poisson confidence interval 15.2–20.3)/1000 person-years (AD: 11.5 [9.6–13.7], non-AD: 6.1 [4.7–7.7]), compared with 14.2 (11.3–17.6) in controls (AD: 10.1 [7.7–13.0], non-AD: 4.1 [2.6–6.0]). The risk of dementia was strongly increased in SCD in a memory clinic setting but less so in a community-based setting. In addition, higher age (hazard ratio 1.1 [95% confidence interval 1.1–1.1]), lower Mini-Mental State Examination (0.7 [0.66–0.8]), and apolipoprotein E ε4 (1.8 [1.3–2.5]) increased the risk of dementia.
Discussion:
SCD can precede both AD and non-AD dementia. Despite their younger age, individuals with SCD in a memory clinic setting have a higher risk of dementia than those in community-based cohorts.
Our findings suggest that cognitively intact older men compared with women have higher resilience to pathophysiological processes of Alzheimer's disease.
Study Objectives
Sleep changes have been associated with increased risks of developing cognitive disturbances and Alzheimer’s disease (AD). A bidirectional relation is underlined between amyloid-beta (Aß) and sleep disruptions. The sleep profile in participants at risk to develop AD is not fully deciphered. We aim to investigate sleep–wake changes with objective sleep measurements in elderly participants without cognitive impairment depending on their brain amyloid status, positive (Aß+) or negative (Aß−) based on standard absorption ratios (SUVr) positron emission tomography-florbetapir imaging.
Methods
Sixty-eight participants without cognitive impairment who have accepted to be involved in the sleep ancillary study from the InveStIGation of Alzheimer’s Predictors in Subjective Memory Complainers (INSIGHT-pre AD) cohort, aiming to record sleep profile based on the analyses of an ambulatory accelerometer-based assessment (seven consecutive 24-hour periods). Neuropsychological tests were performed and sleep parameters have been individualized by actigraph. Participants also underwent a magnetic resonance imaging scan to assess their hippocampal volume. Based on SUVr PET-florbetapir imaging, two groups Aß+ and Aß− were compared.
Results
Participants were divided into two groups: Aß+ (n = 24) and Aß− (n = 44). Except for the SUVr, the two subgroups were comparable. When looking to sleep parameters, increased sleep latency, sleep fragmentation (wake after sleep onset [WASO] score and awakenings) and worst sleep efficiency were associated with cortical brain amyloid load.
Conclusion
Actigraphic sleep parameters were associated with cortical brain amyloid load in participants at risk to develop AD. The detection of sleep abnormalities in those participants may be of interest to propose some preventive strategies.
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