Sleep Apnea, Neurocognitive Decline and Brain Imaging in Patients With Subjective or Mild Cognitive Impairment
Trial statusRecruiting
Trial phaseNot listed
Trial typeObservational
Biological sexAll
Age50-80
SponsorThe University of Hong Kong
About this trial
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).
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
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
Disqualifiers
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 population
Patients will be recruit in the Memory clinic or Sleep clinic, Queen Mary Hospital
Trial design
Design model
Cohort
Time perspective
Prospective
Treatments tested in this trial
Continuous Positive Airway Pressure or other management for OSA per clinical indications.
DevicePAP therapy or other management will be advised for subjects with OSA per usual clinical criteria
Treatment groups
180 Participants
are divided into 1 treatment groupGroup A: Subjective or mild cognitive impairment patients1 intervention
Trial outcomes
Primary outcomes
1
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.
Time frame
Baseline, 6 months, 1 year, 2 year, 3 year2
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.
Time frame
BaselineSecondary outcomes
1
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.
Time frame
Baseline, 6 months, 1 year, 2 year, 3 year2
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.
Time frame
Baseline, 6 months, 1 year, 2 year, 3 year3
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
Time frame
Baseline, 6 months, 1 year, 2 year, 3 year4
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.
Time frame
Baseline, 6 months, 1 year, 2 year, 3 yearSponsors and contacts
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Source ClinicalTrials.gov