What is the literature and recommendations for the use of sleep aids in patients with dementia?

Comment by InpharmD Researcher

Current guideline recommendations generally favor non-pharmacologic strategies as first-line management for sleep disturbances in patients with dementia or Alzheimer’s disease (AD), given the limited efficacy and potential safety concerns associated with sedative-hypnotic medications. The American Academy of Sleep Medicine and NICE recommend against melatonin for insomnia in elderly patients with dementia or AD because evidence of benefit is limited and inconsistent, although more recent analyses suggest melatonin may provide small improvements in total sleep time and cognition with generally good tolerability; however, these benefits may not be clinically meaningful. Non-pharmacologic interventions such as physical and social activity programs, caregiver-focused interventions, CPAP adherence, and multimodal behavioral approaches may offer modest benefit with minimal reported harms, though evidence remains low certainty overall. Among pharmacologic therapies, trazodone and dual orexin receptor antagonists (eg, suvorexant and lemborexant) have demonstrated the most consistent improvements in sleep measures without major short-term safety concerns, although long-term data remain limited and monitoring for adverse effects such as falls is warranted. Benzodiazepines and nonbenzodiazepine hypnotics are generally not recommended in elderly patients with dementia because of risks including oversedation, falls, parasomnias, and worsening cognitive impairment.

Background

The American Academy of Sleep Medicine (AASM) and the National Institute of Health and Clinical Excellence (NICE) guidelines recommend against using melatonin for managing insomnia for elderly patients with dementia and Alzheimer’s disease (AD). The AASM recommends against the use due to limited studies reporting detrimental effects on neurologic function without clear benefit, while NICE provides no further commentary. Furthermore, the AASM strongly recommends against using sleep-promoting medications for demented elderly patients with irregular sleep-wake rhythm disorder due to a lack of evidence for use and known increased risk of complications like falls in older adults. [1], [2]

A 2025 narrative review evaluated the management of sleep disturbances in AD and dementia by analyzing a range of completed clinical trials indexed in the ClinicalTrials.gov database. This extensive literature review included nine interventional trials involving 1,139 participants, conducted up to July 21, 2024, focusing on both pharmacological and non-pharmacological interventions. The trials assessed various approaches, including pharmacological agents like melatonin, lemborexant, and suvorexant, as well as behavioral and environmental modifications like continuous positive airway pressure (CPAP) and bright light therapy. Notably, three of the trials implemented non-pharmacological strategies, while the remaining six evaluated pharmacological treatments. The trials revealed mixed outcomes regarding the efficacy of the interventions. For instance, melatonin and suvorexant demonstrated significant improvements in sleep quality and cognitive performance in specific AD populations, whereas trials involving piromelatine and mibampator (not FDA approved) failed to show consistent benefits for managing sleep disturbances. Conversely, non-pharmacological interventions, such as the LOCK sleep intervention and CPAP adherence, indicated potential for enhancing sleep patterns and daytime functioning among patients. Although bright light therapy did not significantly benefit sleep quality among care recipients, it improved sleep and mood among caregivers. The review underscored the need for future research to tailor interventions to individual patient characteristics and to address the identified gaps, as effective management of sleep disturbances holds promise for improving the quality of life for AD patients and their caregivers. [3]

A comprehensive 2023 review evaluated various pharmacological and non-pharmacological therapies for managing sleep disturbances in patients with AD. The review synthesized evidence from multiple clinical studies, including 28 randomized controlled trials, to ascertain the efficacy and safety of different interventions targeting sleep disruptions, which are a common accompaniment of AD. It outlined that non-pharmacological interventions are generally recommended as the frontline treatment due to their favorable safety profile, but when these do not achieve desired outcomes, a variety of pharmacological therapies, such as trazodone and melatonin, can be considered as adjunctive treatments. The analysis highlighted the detrimental impact of sleep disturbances not only on the progression of AD symptoms but also on the patients' overall quality of life. The findings detailed that while agents like melatonin showed limited efficacy, they remain a popular choice due to their safety. Additionally, the examination of light therapy indicated potential improvements in circadian rhythm disruptions among AD patients. In more severe cases, drugs such as Z-drugs (zopiclone and zolpidem) have been utilized specifically for insomnia, despite the need for careful consideration of side effects. Ultimately, the review proposed a stepwise algorithm for managing sleep disturbances, suggesting a gradual escalation from non-pharmacological to pharmacological interventions, accommodating the intricate balance of efficacy, safety, and patient-specific factors in treatment planning. [4]

An updated 2020 Cochrane review aimed to evaluate the effects of pharmacologic treatment versus placebo for sleep disorders in dementia. This review examines nine RCTs investigating pharmacotherapies for sleep disturbances in patients with AD, focusing on melatonin, trazodone, ramelteon, and orexin antagonists. Five studies on melatonin included 222 participants, with only two suitable for meta-analysis on primary sleep outcomes. Melatonin showed low-certainty evidence of minimal impact on major sleep outcomes over 8 to 10 weeks, including total nocturnal sleep time (TNST) and the day-to-night sleep ratio without serious adverse effects. In a study of 30 participants with moderate-to-severe AD, trazodone 50 mg for two weeks showed low-certainty evidence of improvements in TNST and sleep efficiency, with no serious adverse effects. However, the impact on time awake after sleep onset was uncertain due to imprecision. A small phase 2 trial on ramelteon (74 participants) did not provide peer-reviewed evidence of significant effects on sleep outcomes, and the evidence certainty was considered low. Orexin antagonists, studied in 323 participants with mild-to-moderate AD, showed moderate-certainty evidence of increasing TNST and reducing time awake after sleep onset. They may also lead to a small increase in sleep efficiency without significant effects on sleep latency, the number of awakenings, or the mean duration of sleep bouts. Adverse events were likely comparable to placebo. Overall, the studies were perceived as having a low or unclear risk of bias, with the certainty of evidence varying across interventions. [5], [6]

A 2023 Cochrane review evaluated the efficacy and safety of non-pharmacologic interventions for sleep disturbances in people with dementia, analyzing 19 randomized controlled trials involving 1,335 participants across nursing home, community, inpatient, and mental health settings. Interventions studied included light therapy, physical and social activities, caregiver-focused interventions, daytime sleep restriction, slow-stroke back massage, transcranial electrostimulation, and multimodal behavioral approaches. Overall, the evidence was limited by methodological concerns and low certainty, with no intervention demonstrating consistently robust or conclusive benefit. Physical and social activity interventions showed modest improvements in nocturnal sleep time, sleep efficiency, and nighttime awakenings, while caregiver interventions and multimodal approaches demonstrated small improvements in sleep duration and nighttime wakefulness. In contrast, evidence for light therapy, daytime sleep restriction, massage therapy, and transcranial electrostimulation remained uncertain or suggested little to no meaningful benefit. Adverse events were infrequently reported and appeared minimal. The authors concluded that although some non-pharmacologic strategies demonstrated modest potential benefit, current evidence is insufficient to support widespread implementation of any single intervention, and further rigorously designed studies are needed to better define effective multimodal approaches for sleep disturbances in dementia. [7]

A 2025 review article assessed the efficacy and safety of Dual Orexin Receptor Antagonists (DORA), specifically suvorexant and lemborexant, for treating sleep disturbances in patients with Alzheimer’s disease. This comprehensive review synthesized findings from four relevant studies conducted between 2014 and 2024. The studies primarily focused on the ability of suvorexant to enhance total sleep time (TST), decrease wakefulness after sleep onset (WASO), and improve sleep efficiency (SE) in individuals with Alzheimer’s disease-related insomnia. Additionally, lemborexant was evaluated for its potential to enhance circadian rhythm parameters, particularly in patients suffering from irregular sleep-wake rhythm disorder (ISWRD). The review article revealed that suvorexant improved TST, WASO, and SE with a favorable safety profile, although mild to moderate adverse events were noted. The potential risk of falls highlighted the need for careful monitoring. The review underscored the promise of DORA medications in managing sleep disturbances in Alzheimer’s disease, but also pointed out limitations such as the constrained diversity of study populations and short study durations. The authors called for further clinical trials with broader inclusion criteria and extended durations to fully understand the sustained efficacy and safety of DORA interventions in this vulnerable population. [8]

A 2025 systematic review and meta-analysis encompassing 10 randomized controlled trials (RCTs), synthesized data from a pool of 516 older adults with cognitive impairment, including both mild cognitive impairment and dementia. This comprehensive analysis primarily sought to quantify melatonin's effects on total sleep time and global cognitive performance, while also examining secondary outcomes such as sleep efficiency, circadian markers, and neuropsychiatric symptoms. The results of the meta-analysis indicated that melatonin significantly increased total sleep time by a mean difference of 12.4 minutes and improved Mini-Mental State Examination (MMSE) scores by 1.8 points, both reaching statistical significance with P-values of <.001 and .002, respectively. Neuropsychiatric symptoms also showed a modest reduction, yet no significant improvements were observed in sleep efficiency, circadian markers, depression, or activities of daily living. Despite these statistically significant results, the clinical relevance remains minimal, as the improvements fall short of meeting clinically important benchmarks. The analysis reveals moderate heterogeneity, highlighted by an I2 of 65% for sleep outcomes, suggesting variability in the results. The authors concluded that while melatonin shows promise for improving sleep duration and cognitive function, larger, more rigorously designed RCTs with harmonized outcomes are essential to confirm the findings and establish clinically meaningful benefits for older adults with cognitive impairment. [9]

A 2021 review investigated the impact of pharmacotherapy on insomnia in patients with AD, providing a comprehensive overview of available options and their efficacy. Non-pharmacological options, as well as pharmacological therapy, were discussed. Melatonin has shown some efficacy in elderly patients for sleep disruption but has not been thoroughly investigated in AD. Mouse models have demonstrated some success; in humans, small, low-quality studies suggest some benefits, but these studies contain limitations such as lack of a control group, open-label design, and data derived from case studies. Several randomized placebo-controlled studies, however, failed to show significant benefits. In most studies, melatonin is reported to be well-tolerated, with minimal adverse events. One study did suggest a subjective increase in aggression and mood disturbance. [10]

Ramelteon, a melatonin receptor agonist with an affinity for MT1 and MT2 receptors, was not as successful in AD mice models, but randomized trials demonstrated significantly improved sleep onset latency and total sleep time (TST) in elderly patients without AD; data in AD patients are limited. Some case reports have stated subjective benefits from ramelteon in AD. Adverse event risk is reported to be similar to melatonin. [10]

Benzodiazepines and nonbenzodiazepine receptor site-specific γ-aminobutyric acid (GABA) agonists (e.g., zolpidem, zaleplon, zopiclone, and eszopiclone) are not recommended in elderly patients with AD due to risk of oversedation, falls, genesis of parasomnias, and altered cognitive function. Based on the American Geriatrics Society Beers criteria, both benzodiazepines and nonbenzodiazepine GABA receptor agonists are stated to be potentially inappropriate for use in elderly people. Additionally, efficacy data of these medications supported by randomized trials are lacking. [10]

Dual orexin receptor antagonists also have limited data for use in AD; however, a 2020 phase 3 trial (Table 1) showed improvement in TST with suvorexant compared to placebo in 285 patients with mild-to-moderate probable AD. Evidence from case series also demonstrates successful use of suvorexant on symptoms of nocturnal delirium in AD patients. Lemborexant also appears to have a promising outlook for use in relevant patient populations (Table 2), as well as daridorexant. No serious treatment-related adverse events have been reported for these agents, such as no worsening of cognitive function measured by the Mini-Mental State Examination and the Alzheimer’s Disease Assessment Scale-Cognitive Subscale. [10]

Antidepressants, suggesting some benefits for insomnia in the general population, have limited evidence in AD. Additionally, antidepressants, especially tricyclic antidepressants, may induce a cholinergic effect, potentially worsening accompanying AD symptoms. Antipsychotics and first-generation antihistamines possess sedating qualities; however, these are not recommended in elderly patients per the Beers criteria due to their adverse event profiles. Additional agents/classes of medications have been investigated for insomnia, including cannabidiol/tetrahydrocannabinol, tryptophan, and herbal/aroma therapies. However, there is a paucity of quality data supporting their use or describing their safety profiles in elderly AD patients. [10]

A 2020 Cochrane review examined pharmacotherapies for sleep disturbances in dementia which included nine eligible randomized controlled trials (RCTs) investigating: melatonin (5 studies, n= 222, five studies, but only two yielded data on our primary sleep outcomes), trazodone (1 study, n= 30), ramelteon (1 study, n= 74, no peer-reviewed publication), and orexin antagonists (suvorexant, lemborexant) (2 studies, n= 323). Most participants in trazodone and melatonin studies had moderate-to-severe AD, whereas ramelteon and orexin antagonists had majorly mild-to-moderate AD. The mean age of subjects ranged from 74.5 to 86.0 years old (standard deviation [SD] 5.8 to 8.9). Overall, there is a distinct lack of evidence for definite guidance on the therapeutic choice of agent in this population; some beneficial effects were exhibited on trazodone and orexin antagonists without significant harmful effects, whereas melatonin (up to 10 mg) or a melatonin receptor agonist demonstrated no evidence. Based on two studies that reported adverse effects in the insomnia subgroup, melatonin, and placebo groups did not differ in the number of adverse event reports per person (mean difference [MD] 0.20, 95% CI -0.72 to 1.12; 1 study, n= 151), in the severity of adverse events (3-point scale from 1 = mild to 3 = severe; MD 0.10, 95% CI -0.06 to 0.26; 1 study, n= 151), or in the likelihood of reporting any adverse event (74% melatonin vs. 69% placebo; relative risk 1.07, 95% CI 0.86 to 1.33; 1 study, n= 151). One other study merely commented that either melatonin or placebo was well-tolerated in all cases. No other safety aspects regarding interventions were discussed. [11]

References: [1] Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical Practice Guideline for the Treatment of Intrinsic Circadian Rhythm Sleep-Wake Disorders: Advanced Sleep-Wake Phase Disorder (ASWPD), Delayed Sleep-Wake Phase Disorder (DSWPD), Non-24-Hour Sleep-Wake Rhythm Disorder (N24SWD), and Irregular Sleep-Wake Rhythm Disorder (ISWRD). An Update for 2015: An American Academy of Sleep Medicine Clinical Practice Guideline. J Clin Sleep Med. 2015;11(10):1199-1236. Published 2015 Oct 15. doi:10.5664/jcsm.5100
[2] National Institute for Health and Clinical Excellence. Dementia: assessment, management and support for people living with dementia and their carers. Available at https://www.nice.org.uk/guidance/ng97. Accessed May 20, 2026.
[3] Aldurdunji MM. Management of sleep disturbance related to Alzheimer disease and dementia: An updated review of ClinicalTrials.gov. Medicine (Baltimore). 2025;104(32):e43725. doi:10.1097/MD.0000000000043725
[4] Javed B, Javed A, Kow CS, Hasan SS. Pharmacological and non-pharmacological treatment options for sleep disturbances in Alzheimer's disease. Expert Rev Neurother. 2023;23(6):501-514. doi:10.1080/14737175.2023.2214316
[5] McCleery J, Cohen DA, Sharpley AL. Pharmacotherapies for sleep disturbances in dementia. Cochrane Database Syst Rev. 2016;11(11):CD009178. Published 2016 Nov 16. doi:10.1002/14651858.CD009178.pub3
[6] McCleery J, Sharpley AL. Pharmacotherapies for sleep disturbances in dementia. Cochrane Database Syst Rev. 2020;11(11):CD009178. Published 2020 Nov 15. doi:10.1002/14651858.CD009178.pub4
[7] ​​Wilfling D, Calo S, Dichter MN, Meyer G, Möhler R, Köpke S. Non-pharmacological interventions for sleep disturbances in people with dementia. Cochrane Database Syst Rev. 2023;1(1):CD011881. Published 2023 Jan 3. doi:10.1002/14651858.CD011881.pub2
[8] Alshiban A, Hasoglu T, Oster J. Efficacy And Safety of Dual Orexin Receptor Antagonist (DORA) For Sleep Disturbance in Patients With Alzheimer's Disease Dementia. A Review Article. Am J Geriatr Psychiatry. 2025;33(2):209-218. doi:10.1016/j.jagp.2024.09.016
[9] Mdluli NT, Banda KJ, Chang YC. Melatonin for sleep and cognitive outcomes in older adults with cognitive impairment: a meta-analysis of randomised controlled trials. Age Ageing. 2025;54(11):afaf333. doi:10.1093/ageing/afaf333
[10] Roland JP, Bliwise DL. Impact of Pharmacotherapy on Insomnia in Patients with Alzheimer's Disease. Drugs Aging. 2021;38(11):951-966. doi:10.1007/s40266-021-00891-1
[11] McCleery J, Sharpley AL. Pharmacotherapies for sleep disturbances in dementia. Cochrane Database Syst Rev. 2020 Nov 15;11(11):CD009178. doi:10.1002/14651858.CD009178.pub4. PMID: 33189083; PMCID: PMC8094738.
Literature Review

A search of the published medical literature revealed 3 studies investigating the researchable question:

What is the literature and recommendations for the use of sleep aids in patients with dementia?

Level of evidence

C - Multiple studies with limitations or conflicting results  Read more→



Please see Tables 1-3 for your response.


 

Polysomnographic assessment of suvorexant in patients with probable Alzheimer’s disease dementia and insomnia: a randomized trial

Design

Randomized, double-blinded trial 

N= 285

Objective

To evaluate the clinical profile of the orexin receptor antagonist suvorexant for treating insomnia in patients with mild-to-moderate probable Alzheimer’s disease (AD) dementia

Study Groups

Suvorexant (n= 142)

Placebo (n= 143)

Inclusion Criteria

Between 50 and 90 years of age, met National Institute on Aging-Alzheimer’s Association and Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) clinical criteria for probable AD dementia, as well as DSM-5 criteria for insomnia, a score of 12 to 26 on the Mini-Mental State Exam (MMSE, range 0–30, lower indicating worse performance), a mean total sleep time (TST) of < 6 hours over screening and baseline sleep laboratory polysomnography (PSG) visits, with neither night >6.5 hours, a competent trial partner who resided with the patient overnight, taking stable doses of acetylcholinesterase inhibitor and/or memantine

Exclusion Criteria

Lived in a nursing home or had evidence of significant neurological, psychiatric, or other sleep disorders that might have confounded the diagnosis of AD dementia or insomnia, PSG evidence of significant/severe sleep-related breathing disorder (defined in this trial as >30 apnea/hypopnea episodes per hour) or periodic limb movement disorder (defined in this trial as >30 periodic leg movements associated with an arousal per hour)

Methods

After a baseline overnight PSG assessment at the patient's habitual bedtime, eligible patients were randomly assigned (1:1) to receive nightly oral suvorexant or a matching placebo, given 30 mins prior to bedtime. Patients initiated suvorexant at a dose of 10 mg during week 1, and at the week 2 visit, the dose may be up-titrated to the maximum recommended dose of 20 mg in those who did not achieve sufficient response based on tolerability at the investigator's discretion. 

Use of sedating medications was prohibited before and during the trial, and there were restrictions on the use of alcohol, caffeine, and tobacco. 

Duration

3-week screening, 2-week single-blind placebo run-in, 4-week treatment period 

Outcome Measures

Primary: change from baseline to week 4 in TST over the 8-hour PSG recording period, measured in minutes (higher score corresponds to improved sleep)

Secondary: wake after persistent sleep onset (WASO) measured in minutes, defined as the total wake time over the PSG recording period after the first period of continuous sleep lasting at least 10 minutes (lower score corresponds to improved sleep) 

Safety: adverse event reports, laboratory analyses, electrocardiography, and physical examinations

Baseline Characteristics

 

Suvorexant (n= 142)

Placebo (n= 143)

 

Age, years

≥ 65 years

69.6

72.5%

69.1

69.2%

 

Female

64.1% 66.4%  

White 

Black

60.6%

16.9%

55.9%

15.4%

 

MMSE

Mild (21–26)

Moderate (12 to 12)

22.5

79.6%

20.4%

22.3

79%

21%

 

PSG measures

TST, min

WASO, min

Apnea/Hypopnea Index (AHI) 

Periodic Leg Movement Arousal Index (PLMAI) 

 

277.7 ± 76.9

134.3 ± 59.5

10.1

2.2 

 

274.1 ± 84.3

142.3 ± 61.3

8.8

2.1

 

Taking AD medication

Donepezil 

Memantine 

Rivastigmine 

 

33.1%

16.2%

4.2%

 

35.7%

13.3%

2.8%

 

Taking selective serotonin reuptake inhibitor/serotonin and norepinephrine reuptake inhibitor

16.2%

17.5%

 

Results

Endpoint

Suvorexant (n= 142)

Placebo (n= 143)

Difference in least squares mean suvorexant vs. placebo (95% confidence interval [CI]); p-value

TST at week 4, min

349.4 ± 71.9 321.0 ± 85.2 28.2 (11.1 to 45.2); 0.001

WASO at week 4, min 

92.5 ± 55.5 109.8 ± 55.1 -15.7 (-28.1 to -3.3); 0.014

General categories of events

≥ 1 Adverse event

≥ 1 Drug-related adverse event

≥ 1 Serious adverse event

≥ 1 Serious drug-related adverse event

 

32 (22.5%)

15 (10.6%)

1 (0.7%)

0

 

23 (16.1%)

11 (7.7%)

0

0

 

Specific events ≥ 2% in any group 

Somnolence

Headache

Fall

Dry mouth

Diarrhea

 

6 (4.2%)

5 (3.5%)

3 (2.1%)

3 (2.1%)

0

 

2 (1.4%)

6 (4.2%)

0

1 (0.7%)

4 (2.8%)

 

Pre-specified events of clinical interest

Events indicative of abuse potential

Hypnagogic/hypnopompic hallucination

Somnolence resulting in dose reduction

Falls/ataxia/worsening of balance 

 

2 (1.4%)

1 (0.7%)

1 (0.7%)

3 (2.1%)

 

1 (0.7%)

0

0

0

 

No significant differences were noted between suvorexant and placebo groups in pre-defined exploratory outcomes, such as latency to persistent sleep and latency to rapid eye movement sleep, except for sleep efficiency (% of time in bed spent asleep), which favored suvorexant-recipients (difference in LS mean 5.7, 95% CI 2.2 to 9.3; p= 0.002). 

Suvorexant-induced somnolence was not severe and did not lead to discontinuation of trial medication. Suvorexant did not appear to impair next-day cognitive or psychomotor performance as assessed by objective tests, although these assessments do not constitute a comprehensive assessment of cognition. 

Adverse Events

See results 

Study Author Conclusions

Results suggest that functional orexin signaling is sufficiently retained in patients with (predominantly mild) probable AD dementia, as suvorexant was able to competitively antagonize the action of endogenous orexin neuropeptides at orexin receptors to improve sleep in this population.

InpharmD Researcher Critique

As the study enrolled most patients (79%) with probable AD dementia of mild severity, the generalizability of study results to those with moderate-severity AD remained uncertain. Further trials are also required to confirm long-term safety and efficacy data in this particular patient population. 



References:
[1] [1] Herring WJ, Ceesay P, Snyder E, et al. Polysomnographic assessment of suvorexant in patients with probable Alzheimer's disease dementia and insomnia: a randomized trial. Alzheimers Dement. 2020;16(3):541-551. doi:10.1002/alz.12035

 

Safety and Efficacy of Lemborexant in Patients With Irregular Sleep-Wake Rhythm Disorder and Alzheimer’s Disease Dementia: Results From a Phase 2 Randomized Clinical Trial

Design

Multicenter, randomized, double-blind, placebo-controlled, parallel-group study

N= 62

Objective

To evaluate the effects of lemborexant compared with placebo on circadian rhythm parameters, nighttime sleep, daytime wakefulness, and other clinical measures of irregular sleep-wake rhythm disorder (ISWRD), in individuals with ISWRD and mild to moderate Alzheimer’s disease dementia (AD-D)

Study Groups

Placebo (n= 12)

Lemborexant 2.5 mg (LEM 2.5, n= 12)

Lemborexant 5 mg (LEM 5, n= 13)

Lemborexant 10 mg (LEM 10, n= 13)

Lemborexant 15 mg (LEM 15, n = 12)

Inclusion Criteria

Men and women 60 to 90 years of age with documentation of diagnosis with AD-D and Mini-Mental State Exam (MMSE) score 10 to 26

Exclusion Criteria

Individuals with dementia other than AD-D and sleep disorders other than ISWRD

Methods

During the screening period, eligible subjects were given an actigraph to wear continuously for at least the first 14 days. These subjects underwent a polysomnogram to rule out moderate to severe sleep apnea (≥ 15 events per hour of sleep). After at least 2 weeks of actigraphy, subjects were randomized (1:1:1:1:1) to receive either a placebo or one of four lemborexant treatment arms once nightly within 5 minutes of bedtime. 

Duration

Screening: 2 weeks

Treatment: 4 weeks

Outcome Measures

Least active 5 hours (L5), the relative amplitude of the rest-activity rhythm (RA), mean duration of sleep bouts, and changes in cognitive function

Baseline Characteristics

 

Placebo (n =12)

LEM 2.5 mg (n= 12)

LEM 5 mg (n= 13)

LEM 10 mg (n= 13) LEM 15 mg (n= 12)

Age, years

75.3 ± 6.2 76.5 ± 6.3 76.9 ± 8.0 71.8 ± 7.1 71.9 ± 6.1

Female

58.3% 50.0% 61.5% 46.2% 83.3%

White

66.7% 75.0%  61.5% 69.2% 75.0% 

Body mass index, kg/m2

29.3 26.1 24.7 26.3 30.5

Results

Endpoint

Placebo (n= 12)

LEM 2.5 mg (n= 12)

LEM 5 mg (n= 13) LEM 10 mg (n= 13)

LEM 15 mg (n= 12)

L5, activity counts

Baseline

11,635 ± 373.3 1,266.4 ± 678.1  1,163.2 ± 591.8  1,257.1 ± 836.6 1,490.4 ± 963.1

Week 4

1,493.4 ± 750.6 1,017.0 ± 603.5 997.8 ± 621.6 1,463.6 ± 827.9 1,272.4 ± 907.3

Least square (LS) mean estimate (95% CI) 

155.6 (−235.5 to 546.8) −234.2 (−626.6 to 158.2) −247.4 (−583.9 to 89.2) 14.6 (−373.9 to 403.1) −212.2 (−606.6 to 182.2)

LS mean difference versus placebo (95% CI)

- −389.9 (−739.2 to −40.6) −403.0 (−751.7 to  −54.3) −141.0 (−489.8 to 207.8) −367.8 (−717.9 to −17.8)

p-value

- 0.029 0.024 0.421 0.040

Relative amplitude of the rest-activity rhythm     

Baseline 0.73 ± 0.14 0.79 ± 0.14 0.82 ± 0.09 0.77 ± 0.17 0.76 ± 0.15
Week 4 0.73 ± 0.14 0.78 ± 0.15 0.83 ± 0.10 0.72 ± 0.13 0.79 ± 0.17
LS mean estimate (95% CI) −0.030 (−0.090 to 0.031) −0.010 (−0.070 to 0.050) 0.030 (−0.022 to 0.082) −0.027 (−0.087 to 0.033) 0.027 (−0.033 to 0.087)
LS mean difference vs placebo (95% CI) - 0.020 (−0.034 to 0.074) 0.060 (0.005 to 0.115) 0.003 (−0.051 to 0.056) 0.057 (0.004 to 0.110)
p-value - 0.464 0.032 0.914 0.036

Sleep efficiency, %

Baseline 76.34 ± 6.56 77.64 ± 7.88 78.45 ± 6.84 76.38 ± 8.04 77.35 ± 8.62
Week 4 75.09 ± 7.69 79.85 ± 6.89 78.19 ± 7.92 74.32 ± 9.26 76.54 ± 9.65
LS mean estimate (95% CI) −1.25 (−5.67 to 3.18) 1.93 (−2.47 to 6.33) 1.56 (−2.17 to 5.28) −2.21 (−6.55 to 2.14) −0.53 (−4.92 to 3.85)
LS mean difference vs placebo (95% CI) - 3.18 (−0.74 to 7.10) 2.80 (−1.12 to 6.72) −0.96 (−4.78 to 2.86) 0.71 (−3.16 to 4.59)
p-value - 0.110 0.158 0.616 0.714

Total sleep time during the night, minutes     

Baseline 413.74 ± 79.21 415.49 ± 116.93 408.71 ± 88.96 413.33 ± 76.36 399.13 ± 59.33
Week 4 421.76 ± 57.18 395.56 ± 67.27 419.26 ± 83.45 412.75 ± 89.53 412.50 ± 64.24
LS mean estimate (95% CI) −4.98 (−40.89 to 30.93) −5.56 (−41.65 to 30.52) 5.75 (−25.00 to 36.49) −6.23 (−41.40 to 28.93) 11.48 (−24.46 to 47.42)
LS mean difference vs placebo (95% CI - −0.59 (−32.92 to 31.74) 10.73 (−21.41 to 42.86) −1.25 (−32.86 to 30.35) 16.46 (−15.65 to 48.57)
p-value - 0.971 0.506 0.937 0.309

Number of wake bouts during nighttime

Baseline 2.31 ± 0.76 2.67 ± 2.01 2.09 ± 1.23 2.38 ± 1.54 2.35 ± 1.37
Week 4 2.99 ± 1.37 1.90 ± 1.20 1.97 ± 1.37 2.29 ± 1.70 2.46 ± 1.63
LS mean estimate (95% CI) 0.61 (−0.13 to 1.35) −0.26 (−1.01 to 0.49) −0.16 (−0.78 to 0.47) 0.28 (−0.45 to 1.00) 0.30 (−0.44 to 1.04)
LS mean difference vs PBO (95% CI) - −0.87 (−1.53 to −0.21) −0.77 (−1.42 to −0.11) −0.33 (−0.98 to 0.31) −0.31 (−0.96 to 0.34)
p-value - 0.011 0.023 0.308 0.346

Summary of treatment-emergent adverse events

Any treatment-emergent adverse events (TEAE) 4 (33.3%) 3 (25.0%) 3 (23.1%) 4 (30.8%) 6 (50.0%)
Treatment-related TEAEs 0 0 1 (7.7%) 3 (23.1) 4 (33.3)

TEAEs by severity

Mild

Moderate 

Severe

 

3 (25.0%)

1 (8.3%)

0

 

2 (16.7%)

1 (8.3%)

0

 

3 (23.1%)

0

0

 

4 (30.8%)

0

0

 

3 (25.0%)

2 (16.7%)

1 (8.3%)

TEAEs occurring in ≥ 2 subjects in any group

Constipation

Somnolence

Arthralgia

Headache

Nightmare

 

0

0

0

0

0

 

0

0

0

0

0

 

0

0

0

0

0

 

1 (7.7%)

1 (7.7%)

0

0

2 (15.4%)

 

2 (16.7%)

2 (16.7%)

2 (16.7%

2 (16.7%)

0

Adverse Events

Common Adverse Events: See Results

Serious Adverse Events: None

Percentage that Discontinued due to Adverse Events: None

Study Author Conclusions

This study provides preliminary evidence of the potential utility of lemborexant as a treatment to address both nighttime and daytime symptoms in patients with ISWRD and AD-D.

InpharmD Researcher Critique

The result of this study should be interpreted with caution due to its exploratory nature of phase 2 study, small sample size, and the short duration of treatment interventions. 



References:
[1] [1] Moline M, Thein S, Bsharat M, et al. Safety and Efficacy of Lemborexant in Patients With Irregular Sleep-Wake Rhythm Disorder and Alzheimer's Disease Dementia: Results From a Phase 2 Randomized Clinical Trial. J Prev Alzheimers Dis. 2021;8(1):7-18. doi:10.14283/jpad.2020.69

 

Effect of bright light and melatonin on cognitive and noncognitive function in elderly residents of group care facilities: a randomized controlled trial

Design

Randomized, double-blind, placebo-controlled trial

N= 189

Objective

To determine whether the progression of cognitive and noncognitive symptoms may be ameliorated by individual or combined long-term application of the two major synchronizers of the circadian timing system: bright light and melatonin

Study Groups

Light only (n= 49)

Melatonin only (n= 46)

Melatonin and light (n= 49)

Double placebo (n= 45)

Inclusion Criteria

Residents of assisted care facilities

Exclusion Criteria

Use of monoamine oxidase inhibitors, long-term use of nonsteroid antiinflammatory drugs, severe liver or kidney dysfunction, and aphakia

Methods

Enrolled patients were randomized in a 2x2 factorial design to either whole-day bright light or dim light and melatonin 2.5 mg or placebo given one hour before bedtime.

Clinical diagnosis of dementia was made according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for dementia and dementia subtypes. Clinical diagnosis of Alzheimer's disease was made based on criteria from the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer's Disease and Related Disorders Association (ADRDA). 

One hundred and twenty patients met the NINCDS criteria for probable Alzheimer's disease, 20 met the DSM-IV criteria for vascular dementia, and 24 met the criteria for other dementia subtypes. Seventeen patients did not meet the criteria for dementia, and eight did not have enough data in their medical history to determine the clinical diagnosis.

Duration

Maximum follow-up: 3.5 years

Outcome Measures

Standardized scale measurements of cognitive and noncognitive symptoms, limitations of activities of daily living, actigraphic sleep estimates, and adverse effects assessed every 6 months

Baseline Characteristics

 

Light only (n= 49)

Melatonin only
(n= 46)
Melatonin and light (n= 49) Double placebo (n= 45)

Female

45/170 (26%)  38/170 (22%) 47/170 (28%) 40/170 (24%)

Diagnosis

Alzheimer's disease

Other

 

37/120 (31%)

12/69 (17%)

 

28/120 (23%)

18/69 (26%)

 

33/120 (28%)

16/69 (23%)

 

22/120 (18%)

23/69 (33%)

Age, years

85 86 87  85

TESS score

101 104 102 104

Medication use at inclusion

Antipsychotics

Anxiolytics

Hypnotics

Antidepressants

 

37%

6%

22%

10%

 

26%

11%

14%

17%

 

27%

16%

27%

20%

 

24%

16%

22%

24%

TESS, Therapeutic Environment Screening Scale

Results

Endpoint

Light only
(n= 49)

Melatonin only
(n= 46)
Melatonin and light
(n= 49)
Double placebo (n= 45)
 

Cognitive Scale

Mini-Mental State Examination

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.87 (0.04 to 1.71)

0.04

 

-0.01 (-0.79 to 0.76)

-0.23

 

-0.23 (-1.38 to 0.93)

0.70

 

--

--

 

Mood Scales

Cornell Scale for Depression in Dementia

Effect estimate (95% CI) up to 3.5 years

p-value

 

-1.47 (-2.70 to -0.24)

0.02

 

-0.82 (-1.87 to 0.23)

0.12

 

-0.94 (-2.48 to 0.61)

0.24

 

--

--

Philadelphia Geriatric Center Affect Rating Scale positive

Effect estimate (95% CI) up to 3.5 years

p-value

 

-0.17 (-0.81 to 0.48)

0.61

 

-0.55 (-1.00 to -0.10)

0.02 

 

0.60 (-0.28 to 1.49)

0.18

 

--

-- 

Philadelphia Geriatric Center Affect Rating Scale negative

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.50 (-0.07 to 1.07)

0.08

 

0.82 (0.20 to 1.44)

0.01

 

-1.00 (-1.82 to -0.17)

0.02 

 

--

-- 

Philadelphia Geriatric Center Morale Scale

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.35 (-0.28 to 0.98)

0.18

 

0.21 (-0.38 to 0.80)

0.36

 

0.07 (-0.71 to 0.85)

0.28

 

--

-- 

 

Behavioral Scales

Multi Observation Scale for Elderly Subjects

Effect estimate (95% CI) up to 3.5 years

p-value

 

-0.51 (-1.55 to 0.53)

0.34

 

1.02 (0.18 to 1.86)

0.02

 

-0.74 (-2.35 to 0.87)

0.37 

 

--

-- 

Neuropsychiatric Inventory questionnaire format on severity

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.23 (-0.73 to 1.19)

0.41

 

-0.41 (-1.21 to 0.39)

0.52 

 

-0.36 (-1.42 to 0.70)

0.77 

 

--

-- 

Neuropsychiatric Inventory questionnaire format on distress

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.25 (-0.87 to 1.37)

0.18

 

-0.68 (-1.64 to 0.28)

0.32

 

-0.56 (-1.81 to 0.69)

0.80 

 

--

-- 

Cohen-Mansfield Agitation Index

Effect estimate (95% CI) up to 3.5 years

p-value

 

-1.61 (-4.82 to 1.60)

0.33

 

1.28 (-1.99 to 4.55)

0.44 

 

-3.90 (-6.92 to -0.88)

0.01

 

--

-- 

Nurse-informant activities of daily living scale

Effect estimate (95% CI) up to 3.5 years

p-value

 

-1.77/y (-2.92 to -0.61)

0.003

 

-0.92 (-2.33 to 0.49)

0.20 

 

-1.25 (-3.13 to 0.63)

0.19

 

--

-- 

 

Actigraphic Sleep Estimates

Sleep efficiency, %

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.83 (-1.89 to 3.55)

0.55

 

1.50 (-1.40 to 4.40)

0.31

 

3.46 (0.84 to 6.09)

0.01 

 

--

-- 

Sleep onset latency, min

Effect estimate (95% CI) up to 3.5 years

p-value

 

-3.61 (-11.23 to 4.01)

0.35 

 

-8.23 (-15.38 to -1.08)

0.02

 

-1.71 (-14.3 to 10.8)

0.79

 

--

-- 

Total sleep duration, min

Effect estimate (95% CI) up to 3.5 years

p-value

 

10.14/y (0.38 to 19.90)

0.04 

 

27.48 (8.55 to 46.41)

0.004

 

8.46 (-27.6 to 44.6)

0.65 

 

--

--

Nocturnal restlessness, min/h

Effect estimate (95% CI) up to 3.5 years

p-value

 

-0.25 (-1.47 to 0.97)

0.69

 

-0.48 (-1.62 to 0.66)

0.41 

 

-1.00 (-1.78 to -0.26)

0.01

 

--

-- 

Duration of awakenings, min

Effect estimate (95% CI) up to 3.5 years

p-value

 

-0.50 (-1.04 to 0.04)

0.07

 

-0.05 (−0.52 to 0.41)

0.83

 

-0.53/y (-0.85 to -0.21)

0.01

 

--

-- 

Duration of uninterrupted sleep epochs, min

Effect estimate (95% CI) up to 3.5 years

p-value

 

0.05 (-4.93 to 5.03)

0.98 

 

5.83 (1.05 to 10.61)

0.02

 

-0.15 (-8.30 to 8.00)

0.97

 

--

-- 

Adverse Events

Common Adverse Events: drowsiness and irritability had the highest overall adverse effect ratings. On the contrary, light treatment significantly reduced the ratings of irritability, dizziness, headache, constipation, and inability to sleep, while melatonin reduced the ratings of constipation. 

Serious Adverse Events: no severe adverse events were reported by the patients' physicians

Discontinued due to Adverse Events: one patient in the double placebo group discontinued the study. The patient's daughter suspected her increase in restlessness and falls were related to the study treatment. 

Study Author Conclusions

In conclusion, the simple measure of increasing the illumination level in group care facilities ameliorated symptoms of disturbed cognition, mood, behavior, functional abilities, and sleep. Melatonin improved sleep, but its long-term use by elderly individuals can only be recommended in combination with light to suppress adverse effects on mood. The long-term application of whole-day bright light did not have adverse effects, on the contrary, and could be considered for use in care facilities for elderly individuals with dementia.

InpharmD Researcher Critique

While the long-term safety profile of melatonin appeared to be well-tolerated, it is recommended only in combination with light to counteract its adverse effect on mood. Inclusion of patients without dementia may further affect the generalizability of the findings to patients with Alzheimer's Disease. 



References:
[1] [1] Riemersma-van der Lek RF, Swaab DF, Twisk J, Hol EM, Hoogendijk WJ, Van Someren EJ. Effect of bright light and melatonin on cognitive and noncognitive function in elderly residents of group care facilities: a randomized controlled trial. JAMA. 2008;299(22):2642-2655. doi:10.1001/jama.299.22.2642