Clinical Trial Details
— Status: Enrolling by invitation
Administrative data
NCT number |
NCT05433883 |
Other study ID # |
Hsueh-Yu Li |
Secondary ID |
|
Status |
Enrolling by invitation |
Phase |
N/A
|
First received |
|
Last updated |
|
Start date |
November 3, 2020 |
Est. completion date |
October 2022 |
Study information
Verified date |
March 2022 |
Source |
Chang Gung Memorial Hospital |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Interventional
|
Clinical Trial Summary
The research plan to enroll 15 simple snoring patients (apnea/hypopnea <5, control group), 30
severe OSA patients (apnea/hypopnea >30, treatment group), and 15 mild cognitive impairment
patients (comparative group). All patients complete Mini-Mental State Examination, peripheral
blood sample for plasma Aβ42, Aβ40, Aβ42/Aβ40, Tau, NfL; amyloid deposit in18F-florbetapir
PET; and Taiwan smell identification test. Thirty severe OSA patients (AHI>30, treatment
group) receive comprehensive upper airway surgery with/without bariatric surgery and repeat
postoperative assessment in polysomnography and aforementioned examinations 1 year later.
Description:
Obstructive sleep apnea and Alzheimer's disease are both highly prevalent and age-related
chronic disease with significant impacts on global public health. The link between OSA and AD
showed an inter-dependent relationship. Our genetic study showed the expressions of
AD-associated genes (CCL2, IL6, CXCL8, HLA-A, IL1RN) in severe OSA patients. Our
epidemiological study revealed OSA patients were significantly associated with a higher
incidence of AD (adjusted hazard ratio: 2.12) in comparison to non-OSA subjects and treated
OSA patients exhibited a significantly reduced risk of AD (incidence rate ratio: 0.23)
compared with non-treated OSA patients. Possible mechanisms of OSA in contributing to AD are
sleep fragmentation, intermittent hypoxia, intrathoracic swings, and olfactory dysfunction.
The cognitive decline in AD seems progressive and irreversible, by contrast, OSA sharing
similar cognitive impairment is treatable. The purposes of this study are (1) to explore the
relationship and mechanism between OSA and AD, and establish an alarm system as early stage
of AD in OSA patients, (2) to testify the improvement of OSA can feedback to ameliorate
cognitive impairment and modify the process of AD.
The research plan to enroll 15 simple snoring patients (apnea/hypopnea <5, control group), 30
severe OSA patients (apnea/hypopnea >30, treatment group), and 15 mild cognitive impairment
patients (comparative group). All patients complete Mini-Mental State Examination, peripheral
blood sample for plasma Aβ42, Aβ40, Aβ42/Aβ40, Tau, NfL; amyloid deposit in18F-florbetapir
PET; and Taiwan smell identification test. Thirty severe OSA patients (AHI>30, treatment
group) receive comprehensive upper airway surgery with/without bariatric surgery and repeat
postoperative assessment in polysomnography and aforementioned examinations 1 year later.
The data from the study can be used to explore the association between polysomnography and
AD-related examinations, to compare the perioperative changes in polysomnography and
AD-related examinations, to correlate the perioperative changes between polysomnography and
AD-related examinations. The contributions of the study are to clarify the hypothesis: severe
OSA is early stage and one of the etiology contributing to the development of AD, and sleep
surgery improves OSA and consequently modify the process of AD, early detection of cognition
and olfactory function in OSA patients can contribute to diagnosis of early stage AD and
consequently early treatment to modify the development of AD.