Obstructive Sleep ApneaNCT06150352
Sleep Apnea, Neurocognitive Decline and Brain Imaging in Patients With Subjective or Mild Cognitive Impairment
An observational study of Obstructive Sleep Apnea and Mild Cognitive Impairment, run by The University of Hong Kong at 1 site in Hong Kong.
Trial summary
Obstructive sleep apnea (OSA) is recurrent episodes of partial or complete obstruction of the upper airway during sleep that causes intermittent hypoxia and sleep fragmentation and potentially lead to cardiometabolic and neurocognitive sequelae. Read more about this study
- Who is it for?
- Ages 50 to 80 years
- Conditions the study is for
- Obstructive Sleep Apnea, Mild Cognitive Impairment, Subjective Cognitive Impairment
- What is being tested?
- Continuous Positive Airway Pressure or other management for OSA per clinical indications.
- Type of treatment
- Medical device
- How many people
- 180 participants
- Where
- 1 siteHong Kong
- Study dates
- 26 Sep 2023to 31 Mar 2027
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 50 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients will be recruit in the Memory clinic or Sleep clinic, Queen Mary Hospital
Who may be able to join
- Aged 50 - 80 years
- Diagnosis of mild cognitive impairment based on Peterson's criteria.
- Diagnosis of subjective cognitive impairment, based on the subjective complaint of cognitive impairment, but with an unremarkable assessment of the Hong Kong version of Montreal cognitive Assessment scores
- Able to speak and read Chinese
- Adequate visual and auditory to perform a cognitive test
- Subjects with moderate-severe OSA or No OSA (diagnosis based on sleep study) would be invited for baseline PET-MRI brain scan
Who cannot join
- Diagnosed psychiatric illness with or without medication, e.g. major depressive disorder.
- Other clear organic causes of cognitive impairment, e.g. vascular cognitive impairment, brain tumour, dementia with Lewy body, mild cognitive impairment with Lewy body, Parkinson's disease, normal pressure hydrocephalus, neurosyphilis, autoimmune encephalitis, substance abuse, history of alcohol abuse.
- Diagnosis of cancer on active treatment
- Contraindications to PET-CT or MRI brain scan (excluded for neuroimaging studies)
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
Yuen Kwan Agnes Lai, PhD contact
Hong Kong1 site, 1 recruiting
- Recruiting
Queen Mary Hospital
Hong Kong
Sau Man Mary Ip, MD, 2255 5885, msmip@hku.hk
Yuen Kwan Agnes Lai, PhD, ayklai@hkmu.edu.hk
About this study
Official title: Exploring the Association Between Cognitive Function, Obstructive Sleep Apnea and Brain Imaging, and the Determinants of Neurocognitive Decline in Subjects With Subjective or Mild Cognitive Impairment
Obstructive sleep apnea (OSA) is recurrent episodes of partial or complete obstruction of the upper airway during sleep that causes intermittent hypoxia and sleep fragmentation and potentially lead to cardiometabolic and neurocognitive sequelae. Chronic intermittent hypoxia, sleep fragmentation of OSA, and insufficient sleep have been significantly associated with higher risks of neurocognitive impairment, including mild cognitive impairment (MCI) and Alzheimer's disease. Thus, sleep and sleep apnea might be modifiable factors to neurocognitive impairment.
Positive airway pressure (PAP) is the first line of treatment to maintain open airways for patients with OSA. Improving sleep, sleep apnea and circadian function could be a high-value intervention target to alleviate cognitive impairment and decline in subjects with mild neurocognitive impairment.
Read more
Amyloid accumulation in brain tissue is a distinct feature of Alzheimers' disease, which is associated with potential impairment of neurocognition clinically. It predicts memory decline in initially cognitively unimpaired individuals.
The study explores the associations between sleep apnea, cognitive function and cerebral imaging and the role of PAP therapy on neurocognitive trajectory in these patients with subjective cognitive impairment /mild cognitive impairment (SCI/MCI).
Read the detailed description
Obstructive sleep apnea (OSA) is recurrent episodes of partial or complete obstruction of the upper airway during sleep . Chronic intermittent hypoxia, sleep fragmentation of OSA, and insufficient sleep have been significantly associated with higher risks of neurocognitive impairment, including mild MCI and Alzheimer's disease. Thus, sleep and sleep apnea might be modifiable factors contributing towards neurocognitive impairment . Improving sleep and sleep apnea could be a high-value intervention to alleviate cognitive impairment and decline in subjects with mild neurocognitive impairment.
Amyloid accumulation in brain tissue is a distinct feature of Alzheimer's disease, which is associated with potential impairment of neurocognition clinically. It predicts memory decline in initially cognitively unimpaired individuals. Research suggested that cerebrospinal fluid amyloid-β42 levels showed significant differences in subjects with moderate/severe OSA compared with healthy control.
Investigators hypothesize that (i) OSA is a determinant of neurocognitive decline, and regular PAP therapy for OSA could reduce this decline in subjects presenting with subjective cognitive impairment (SCI) or MCI; (ii) OSA may contribute to cerebral amyloid burden in these subjects with clinical diagnosis of SCI/MCI.
This study (i) assesses the role of obstructive sleep apnea as a potential determinant of neurocognitive status and the impact of OSA therapy (CPAP or other interventions) on neurocognitive decline (ii) evaluates if OSA increases cerebral amyloid deposition using PET imaging.
Subjects are recruited from Memory clinic and who have undergone a study with sleep questionnaires, neurocognitive tests and home sleep apnea test (HSAT). Subjects with OSA (identified on HSAT) will be referred for management of OSA per usual clinical criteria. Sleep questionnaires and cognitive assessment tests will be reassessed at six months, one year, two year and 3 year, and determinants to neurocognitive changes will be analyzed.
Amyloid PET-MRI brain will also be done at baseline. Owing to resource constraints, investigators can only provide PET-MRI investigation for 90 subjects ( 60 subjects with moderate/severe OSA to be compared with 30 subjects with no/mild OSA) .
- Being tested
- Continuous Positive Airway Pressure or other management for OSA per clinical indications.
- Keywords
- Obstructive sleep apnea, Neurocognitive function, CPAP
- Medical subject headings
- Sleep Apnea, Obstructive, Cognitive Dysfunction
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Continuous Positive Airway Pressure or other management for OSA per clinical indications.Device
PAP therapy or other management will be advised for subjects with OSA per usual clinical criteria
| Study group | Role | What they receive |
|---|---|---|
| Subjective or mild cognitive impairment patients | Subjective or mild cognitive impairment patients with or without CPAP treatment Receives: Device: Continuous Positive Airway Pressure or other management for OSA per clinical indications. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in neurocognitive function (ADAS Cog)
Measured by ADAS-Cog. The scores range from 0 to 70, "0" is the best possible score and "70" is the worst possible score.
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Cerebral amyloid update in moderate to severe OSA and no to mild OSA
The brain images for each subject will consist of fused MRI (3D MPRAGE) and 18F-Flutemetamol PET images. The scans were visually interpreted as positive (abnormal) or negative (normal) by a trained neuroradiologist based on uptake of 18F-Flutemetamol.
Measured: Baseline
Secondary outcomes (8)
Change in ability to inhibit cognitive interference
Measured by Stroop Colour and Word Test (SCWT). Scored by time and error. A longer time indicates a worst score, while a shorter time indicates a better score.
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in neurocognitive function (MoCA)
Measured by Montreal Cognitive Assessment (MoCA) score. The scores range from 0 to 30, "0" is the worst possible score and "30" is the best possible score.
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in sleep profile and quality
Measured by Severe Insomnia Index. Each item asks the individual to rate the severity of his or her symptoms with a 4-point Likert scale. The total score ranges from 0 to 28. The higher the scores the greater the severity of insomnia
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in sleep apnea symptoms
Measured by Pittsburgh Sleep Quality Index. Each of the sleep components yields a score ranging from 0 to 3, with 3 indicating the greatest dysfunction. The sleep component scores are summed to yield a total score ranging from 0 to 21, with the higher total score indicating worse sleep quality.
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in daytime sleepiness
Measured by Epworth Sleepiness Scale. Each item asks the individual to rate their daytime sleepiness. The total score ranges from 0 to 24. The higher the scores, the greater the severity of daytime sleepiness
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in insomnia symptoms
Measured by Severe Insomnia Index. Each item asks the individual to rate the severity of his or her symptoms with a 4-point Likert scale. The total score ranges from 0 to 28. The higher the scores, the greater the severity of insomnia
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Change in depression symptoms
Measured by Geriatric Depression Scale - short form. The score ranges from 0 to 15. The higher the scores the more severe of depression.
Measured: Baseline, 6 months, 1 year, 2 year, 3 year
Neuroimaging outcomes between two groups of subjects with moderate-severe OSA or no-mild OSA
- Cerebral amyloid burden as measured by SUVR global and regional scores on 18F-Flutemetamol PET-CT imaging:
Normalized for injected dose and body weight of each subject, standardized uptake values (SUVs) are calculated in 16 Alzheimer's disease signature brain regions by Cortex-ID softward (General Electric Healthcare Ltd., USA). The composite SUVR representing the global amyloid burden is the average SUVR value of the area-weighted mean for the 16 cortical ROIs;
- Cortical brain volumes based on brain segmentation using 3D T1-MPRAGE images by Freesurfer software, including total, deep gray and hippocampal volumes; temporal, parietal, frontal and occipital cortical volumes; and Alzheimer's signature regional volumes
Measured: Baseline
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted29 Nov 2023
- Study start26 Sep 2023
- Primary completion30 Dec 2026 (estimated)
- Study completion31 Mar 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Obstructive Sleep ApneaStudies of the same condition, open and under way.
- More trials run by The University of Hong KongThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 180 participants (estimated)
Sponsor and investigators
- Lead sponsor
- The University of Hong Kong
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Professor Mary Ip Sau-man, The University of Hong Kong
- Investigators
- Mary SM Ip, MD, Principal investigator, School of Clinical Medicine, The University of Hong Kong
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06150352
- Sponsor's protocol ID
- UW 23-291
- Status last verified
- Mar 2025
- First submitted
- 12 Oct 2023
- Last updated
- 2 Apr 2025
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Bao YW, Chau ACM, Chiu PK, Shea YF, Kwan JSK, Chan FHW, Mak HK. Heterogeneity of Amyloid Binding in Cognitively Impaired Patients Consecutively Recruited from a Memory Clinic: Evaluating the Utility of Quantitative 18F-Flutemetamol PET-CT in Discrimination of Mild Cognitive Impairment from Alzheimer's Disease and Other Dementias. J Alzheimers Dis. 2021;79(2):819-832. doi: 10.3233/JAD-200890.
PubMed 33361593Collij LE, Mastenbroek SE, Salvado G, Wink AM, Visser PJ, Barkhof F, van Berckel BNM, Lopes Alves I. Regional amyloid accumulation predicts memory decline in initially cognitively unimpaired individuals. Alzheimers Dement (Amst). 2021 Aug 2;13(1):e12216. doi: 10.1002/dad2.12216. eCollection 2021.
PubMed 34368416Cui W, Duan Z, Li Z, Feng J. Assessment of Alzheimer's disease-related biomarkers in patients with obstructive sleep apnea: A systematic review and meta-analysis. Front Aging Neurosci. 2022 Oct 13;14:902408. doi: 10.3389/fnagi.2022.902408. eCollection 2022.
PubMed 36313031Emamian F, Khazaie H, Tahmasian M, Leschziner GD, Morrell MJ, Hsiung GY, Rosenzweig I, Sepehry AA. The Association Between Obstructive Sleep Apnea and Alzheimer's Disease: A Meta-Analysis Perspective. Front Aging Neurosci. 2016 Apr 12;8:78. doi: 10.3389/fnagi.2016.00078. eCollection 2016.
PubMed 27148046Jackson ML, Cavuoto M, Schembri R, Dore V, Villemagne VL, Barnes M, O'Donoghue FJ, Rowe CC, Robinson SR. Severe Obstructive Sleep Apnea Is Associated with Higher Brain Amyloid Burden: A Preliminary PET Imaging Study. J Alzheimers Dis. 2020;78(2):611-617. doi: 10.3233/JAD-200571.
PubMed 33016907Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of Sleep-Disordered Breathing With Cognitive Function and Risk of Cognitive Impairment: A Systematic Review and Meta-analysis. JAMA Neurol. 2017 Oct 1;74(10):1237-1245. doi: 10.1001/jamaneurol.2017.2180.
PubMed 28846764Lutsey PL, Norby FL, Gottesman RF, Mosley T, MacLehose RF, Punjabi NM, Shahar E, Jack CR Jr, Alonso A. Sleep Apnea, Sleep Duration and Brain MRI Markers of Cerebral Vascular Disease and Alzheimer's Disease: The Atherosclerosis Risk in Communities Study (ARIC). PLoS One. 2016 Jul 14;11(7):e0158758. doi: 10.1371/journal.pone.0158758. eCollection 2016.
PubMed 27415826Buckley CJ, Sherwin PF, Smith AP, Wolber J, Weick SM, Brooks DJ. Validation of an electronic image reader training programme for interpretation of [18F]flutemetamol beta-amyloid PET brain images. Nucl Med Commun. 2017 Mar;38(3):234-241. doi: 10.1097/MNM.0000000000000633.
PubMed 27984539
Study at a glance
From the registry record, last updated by the sponsor on 2 Apr 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Exploring the Association Between Cognitive Function, Obstructive Sleep Apnea and Brain Imaging, and the Determinants of Neurocognitive Decline in Subjects With Subjective or Mild Cognitive Impairment
- ClinicalTrials.gov ID
- NCT06150352
- Acronym / sponsor ID
- UW 23-291
- Keywords
- Obstructive sleep apnea, Neurocognitive function, CPAP
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 180 participants (estimated)
- Lead sponsor
- The University of Hong KongUniversity, hospital or other
- Study start
- 26 Sep 2023 (actual)
- Primary completion
- 30 Dec 2026 (estimated)
- Study completion
- 31 Mar 2027 (estimated)
- First posted
- 29 Nov 2023 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Obstructive sleep apnea (OSA) is recurrent episodes of partial or complete obstruction of the upper airway during sleep that causes intermittent hypoxia and sleep fragmentation and potentially lead to cardiometabolic and neurocognitive sequelae. Chronic intermittent hypoxia, sleep fragmentation of OSA, and insufficient sleep have been significantly associated with higher risks of neurocognitive impairment, including mild cognitive impairment (MCI) and Alzheimer's disease. Thus, sleep and sleep apnea might be modifiable factors to neurocognitive impairment.
Positive airway pressure (PAP) is the first line of treatment to maintain open airways for patients with OSA. Improving sleep, sleep apnea and circadian function could be a high-value intervention target to alleviate cognitive impairment and decline in subjects with mild neurocognitive impairment.
Amyloid accumulation in brain tissue is a distinct feature of Alzheimers' disease, which is associated with potential impairment of neurocognition clinically. It predicts memory decline in initially cognitively unimpaired individuals.
The study explores the associations between sleep apnea, cognitive function and cerebral imaging and the role of PAP therapy on neurocognitive trajectory in these patients with subjective cognitive impairment /mild cognitive impairment (SCI/MCI).
Detailed description
Obstructive sleep apnea (OSA) is recurrent episodes of partial or complete obstruction of the upper airway during sleep . Chronic intermittent hypoxia, sleep fragmentation of OSA, and insufficient sleep have been significantly associated with higher risks of neurocognitive impairment, including mild MCI and Alzheimer's disease. Thus, sleep and sleep apnea might be modifiable factors contributing towards neurocognitive impairment . Improving sleep and sleep apnea could be a high-value intervention to alleviate cognitive impairment and decline in subjects with mild neurocognitive impairment.
Amyloid accumulation in brain tissue is a distinct feature of Alzheimer's disease, which is associated with potential impairment of neurocognition clinically. It predicts memory decline in initially cognitively unimpaired individuals. Research suggested that cerebrospinal fluid amyloid-β42 levels showed significant differences in subjects with moderate/severe OSA compared with healthy control.
Investigators hypothesize that (i) OSA is a determinant of neurocognitive decline, and regular PAP therapy for OSA could reduce this decline in subjects presenting with subjective cognitive impairment (SCI) or MCI; (ii) OSA may contribute to cerebral amyloid burden in these subjects with clinical diagnosis of SCI/MCI.
This study (i) assesses the role of obstructive sleep apnea as a potential determinant of neurocognitive status and the impact of OSA therapy (CPAP or other interventions) on neurocognitive decline (ii) evaluates if OSA increases cerebral amyloid deposition using PET imaging.
Subjects are recruited from Memory clinic and who have undergone a study with sleep questionnaires, neurocognitive tests and home sleep apnea test (HSAT). Subjects with OSA (identified on HSAT) will be referred for management of OSA per usual clinical criteria. Sleep questionnaires and cognitive assessment tests will be reassessed at six months, one year, two year and 3 year, and determinants to neurocognitive changes will be analyzed.
Amyloid PET-MRI brain will also be done at baseline. Owing to resource constraints, investigators can only provide PET-MRI investigation for 90 subjects ( 60 subjects with moderate/severe OSA to be compared with 30 subjects with no/mild OSA) .
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Subjective or mild cognitive impairment patients | – | Device: Continuous Positive Airway Pressure or other management for OSA per clinical indications.Subjective or mild cognitive impairment patients with or without CPAP treatment |
Who may qualify
- Ages
- 50 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients will be recruit in the Memory clinic or Sleep clinic, Queen Mary Hospital
Key inclusion criteria (6 listed)
- Aged 50 - 80 years
- Diagnosis of mild cognitive impairment based on Peterson's criteria.
- Diagnosis of subjective cognitive impairment, based on the subjective complaint of cognitive impairment, but with an unremarkable assessment of the Hong Kong version of Montreal cognitive Assessment scores
- Able to speak and read Chinese
- Adequate visual and auditory to perform a cognitive test
Key exclusion criteria (4 listed)
- Diagnosed psychiatric illness with or without medication, e.g. major depressive disorder.
- Other clear organic causes of cognitive impairment, e.g. vascular cognitive impairment, brain tumour, dementia with Lewy body, mild cognitive impairment with Lewy body, Parkinson's disease, normal pressure hydrocephalus, neurosyphilis, autoimmune encephalitis, substance abuse, history of alcohol abuse.
- Diagnosis of cancer on active treatment
- Contraindications to PET-CT or MRI brain scan (excluded for neuroimaging studies)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Continuous Positive Airway Pressure or other management for OSA per clinical indications.PAP therapy or other management will be advised for subjects with OSA per usual clinical criteria | Device | Subjective or mild cognitive impairment patients |
Primary outcome
Change in neurocognitive function (ADAS Cog)
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Measured by ADAS-Cog. The scores range from 0 to 70, "0" is the best possible score and "70" is the worst possible score.
Cerebral amyloid update in moderate to severe OSA and no to mild OSA
Time frame: Baseline
The brain images for each subject will consist of fused MRI (3D MPRAGE) and 18F-Flutemetamol PET images. The scans were visually interpreted as positive (abnormal) or negative (normal) by a trained neuroradiologist based on uptake of 18F-Flutemetamol.
8 secondary outcomes
Change in ability to inhibit cognitive interference
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in neurocognitive function (MoCA)
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in sleep profile and quality
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in sleep apnea symptoms
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in daytime sleepiness
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in insomnia symptoms
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Change in depression symptoms
Time frame: Baseline, 6 months, 1 year, 2 year, 3 year
Neuroimaging outcomes between two groups of subjects with moderate-severe OSA or no-mild OSA
Time frame: Baseline
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 2 Apr 2025.
- Background: PubMed 33361593Bao YW, Chau ACM, Chiu PK, Shea YF, Kwan JSK, Chan FHW, Mak HK. Heterogeneity of Amyloid Binding in Cognitively Impaired Patients Consecutively Recruited from a Memory Clinic: Evaluating the Utility of Quantitative 18F-Flutemetamol PET-CT in Discrimination of Mild Cognitive Impairment from Alzheimer's Disease and Other Dementias. J Alzheimers Dis. 2021;79(2):819-832. doi: 10.3233/JAD-200890.
- Background: PubMed 34368416Collij LE, Mastenbroek SE, Salvado G, Wink AM, Visser PJ, Barkhof F, van Berckel BNM, Lopes Alves I. Regional amyloid accumulation predicts memory decline in initially cognitively unimpaired individuals. Alzheimers Dement (Amst). 2021 Aug 2;13(1):e12216. doi: 10.1002/dad2.12216. eCollection 2021.
- Background: PubMed 36313031Cui W, Duan Z, Li Z, Feng J. Assessment of Alzheimer's disease-related biomarkers in patients with obstructive sleep apnea: A systematic review and meta-analysis. Front Aging Neurosci. 2022 Oct 13;14:902408. doi: 10.3389/fnagi.2022.902408. eCollection 2022.
- Background: PubMed 27148046Emamian F, Khazaie H, Tahmasian M, Leschziner GD, Morrell MJ, Hsiung GY, Rosenzweig I, Sepehry AA. The Association Between Obstructive Sleep Apnea and Alzheimer's Disease: A Meta-Analysis Perspective. Front Aging Neurosci. 2016 Apr 12;8:78. doi: 10.3389/fnagi.2016.00078. eCollection 2016.
- Background: PubMed 33016907Jackson ML, Cavuoto M, Schembri R, Dore V, Villemagne VL, Barnes M, O'Donoghue FJ, Rowe CC, Robinson SR. Severe Obstructive Sleep Apnea Is Associated with Higher Brain Amyloid Burden: A Preliminary PET Imaging Study. J Alzheimers Dis. 2020;78(2):611-617. doi: 10.3233/JAD-200571.
- Background: PubMed 28846764Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of Sleep-Disordered Breathing With Cognitive Function and Risk of Cognitive Impairment: A Systematic Review and Meta-analysis. JAMA Neurol. 2017 Oct 1;74(10):1237-1245. doi: 10.1001/jamaneurol.2017.2180.
- Background: PubMed 27415826Lutsey PL, Norby FL, Gottesman RF, Mosley T, MacLehose RF, Punjabi NM, Shahar E, Jack CR Jr, Alonso A. Sleep Apnea, Sleep Duration and Brain MRI Markers of Cerebral Vascular Disease and Alzheimer's Disease: The Atherosclerosis Risk in Communities Study (ARIC). PLoS One. 2016 Jul 14;11(7):e0158758. doi: 10.1371/journal.pone.0158758. eCollection 2016.
- Background: PubMed 27984539Buckley CJ, Sherwin PF, Smith AP, Wolber J, Weick SM, Brooks DJ. Validation of an electronic image reader training programme for interpretation of [18F]flutemetamol beta-amyloid PET brain images. Nucl Med Commun. 2017 Mar;38(3):234-241. doi: 10.1097/MNM.0000000000000633.
- Individual participant dataSharing planned: Undecided
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Yuen Kwan Agnes Lai, PhD contact
Mary SM Ip, MD principal investigator
School of Clinical Medicine, The University of Hong Kong
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Obstructive Sleep Apnea and Mild Cognitive Impairment, run by The University of Hong Kong at 1 site in Hong Kong.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 6 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 2 Apr 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Hong Kong. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Sau Man Mary Ip, MD (2255 5885, msmip@hku.hk), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change in neurocognitive function (ADAS Cog) (time frame: Baseline, 6 months, 1 year, 2 year, 3 year). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT06150352, which also lists 8 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 2 Apr 2025.