Abstract
Suboptimal sleep causes cognitive decline and probably accelerates Alzheimer's Disease (AD) progression. Several sleep interventions have been tested in established AD dementia cases. However early intervention is needed in the course of AD at Mild Cognitive Impairment (MCI) or mild dementia stages to help prevent decline and maintain good quality of life. This systematic review aims to summarize evidence on sleep interventions in MCI and mild AD dementia. Seven databases were systematically searched for interventional studies where ≥ 75% of participants met diagnostic criteria for MCI/mild AD dementia, with a control group and validated sleep outcome measures. Studies with a majority of participants diagnosed with Moderate to Severe AD were excluded. After removal of duplicates, 22,133 references were returned in two separate searches (August 2019 and September 2020). 325 full papers were reviewed with 18 retained. Included papers reported 16 separate studies, total sample (n = 1,056), mean age 73.5 years. 13 interventions were represented: Cognitive Behavioural Therapy – Insomnia (CBT‐I), A Multi‐Component Group Based Therapy, A Structured Limbs Exercise Programme, Aromatherapy, Phase Locked Loop Acoustic Stimulation, Transcranial Stimulation, Suvorexant, Melatonin, Donepezil, Galantamine, Rivastigmine, Tetrahydroaminoacridine and Continuous Positive Airway Pressure (CPAP). Psychotherapeutic approaches utilising adapted CBT‐I and a Structured Limbs Exercise Programme each achieved statistically significant improvements in the Pittsburgh Sleep Quality Index with one study reporting co‐existent improved actigraphy variables. Suvorexant significantly increased Total Sleep Time and Sleep Efficiency whilst reducing Wake After Sleep Onset time. Transcranial Stimulation enhanced cortical slow oscillations and spindle power during daytime naps. Melatonin significantly reduced sleep latency in two small studies and sleep to wakefulness transitions in a small sample. CPAP demonstrated efficacy in participants with Obstructive Sleep Apnoea. Evidence to support other interventions was limited. Whilst new evidence is emerging, there remains a paucity of evidence for sleep interventions in MCI and mild AD highlighting a pressing need for high quality experimental studies exploring alternative sleep interventions.
Highlights
The association between Alzheimer's Disease [AD] and sleep disturbance is well established (Mander, 2013; Tranah et al, 2011)
The traditional view has been that AD causes sleep impairment and the extent of symptomatic sleep disturbance correlates with the severity of dementia (Benca et al, 1992; Montplaisir et al, 1995; Pat-Horenczyk et al, 1998; Prinz et al, 1982; Weldemichael & Grossberg, 2010)
A standard Cognitive Behavioural Therapy – Insomnia (CBT-I) protocol over 6 weeks was adapted for participants with Mild Cognitive Impairment (MCI) through a reduction in content covered, inclusion of brief, focused rationales for treatment, time allowed for review and repetition of content as well as reminder/ troubleshooting calls between intervention sessions
Summary
The association between Alzheimer's Disease [AD] and sleep disturbance is well established (Mander, 2013; Tranah et al, 2011). A recent prominent theory postulates a bidirectional relationship between poor sleep and AD (Mander et al, 2016) – as well as AD causing sleep disturbance, sleep disturbance may lead directly to pathological accumulation of proteins that cause neurodegeneration (Fultz et al, 2019; Hahn et al, 2014). Chronic sleep deprivation accelerates accumulation of soluble beta amyloid into insoluble amyloid plaques in two mouse models (Kang et al, 2009). A cascade is envisaged in which poor sleep disrupts the clearance of soluble amyloid, leading to plaque deposition. This precipitates further plaque formation through recognised positive feedback loops (Mandrekar-Colucci et al, 2012). Regardless of whether sleep disturbance arises directly from accumulation of AD pathology or through an independent problem such as sleep apnoea (Ancoli-Israel, 2000; Bliwise, 1999; Van Cauter et al, 2000), poor sleep might be a significant contributory factor in the eventual onset and progression of AD
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