Clinical Trial Details
— Status: Recruiting
Administrative data
NCT number |
NCT04048603 |
Other study ID # |
2018.641 |
Secondary ID |
|
Status |
Recruiting |
Phase |
|
First received |
|
Last updated |
|
Start date |
May 15, 2019 |
Est. completion date |
October 1, 2022 |
Study information
Verified date |
August 2021 |
Source |
Chinese University of Hong Kong |
Contact |
Jihui Zhang, PhD |
Phone |
(852)39197647 |
Email |
jihui.zhang[@]cuhk.edu.hk |
Is FDA regulated |
No |
Health authority |
|
Study type |
Observational
|
Clinical Trial Summary
This study is a prospective study with a mean of 7-year follow-up interval, aims to monitor
the progression of α-synucleinopathy neurodegeneration by the evolution of prodromal markers
and development of clinical disorders in patients with idiopathic REM Sleep Behavior Disorder
(iRBD) and healthy controls.
Description:
REM sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment behaviors
and REM sleep without muscle atonia (excessive EMG activity) during REM sleep.Increasing
studies revealed that iRBD eventually converts to α-synucleinopathy, such as Parkinson's
disease (PD), dementia with Lewy Bodies (DLB), and multiple system atrophy (MSA). Recent
studies reported that over 80% of patients with iRBD eventually developed neurodegeneration
at a mean interval of 14 years after iRBD onset or diagnosed. Thus, iRBD is regarded as a
precursor of α-synucleinopathies. In addition to iRBD, a large series of other non-motor
symptoms also present before the emergence of typical motor symptoms of PD, including
autonomic dysfunction, olfactory loss, color vision impairment, neurocognitive
impairment,neuroimaging of dopamine dysfunction, daytime sleepiness, and psychiatric
disorders. In recent years, several longitudinal studies have found that patients with iRBD
with a higher rate of these markers may have a faster progression of neurodegeneration. On
the other hand, a variety of external risk factors of PD including environmental toxic
exposure, lifestyle factors, and some medications have long been recognized, which affect
numerous fundamental cellular processes by interaction with genetic predisposition.
However, several knowledge gaps still need further studies to uncover. First, few studies
have explored the predictive value of dynamic change of biomarkers in prodromal stage of PD.
Second, few previous prospective studies also employed a control group to compare the change
of these prodromal markers between patients and healthy controls over time. Third, as some of
previous studies employed a retrospective study design, potential recall bias may contaminate
the results. Moreover, the sample sizes of most previous studies investigating biomarkers
were relative small (n < 80) and follow-up durations in most study are relatively short,
which may have limited the statistical power to detect the risk factors with mild to moderate
effect size. Finally, as previous reported longitudinal studies of iRBD mainly focused on
Caucasian or other ethnic groups, there is only limited data about neurodegenerative
biomarkers in Chinese iRBD. In conclusion, prospective longitudinal studies with larger
sample size, regular follow-up, and relative long follow-up duration are needed to better map
the progression of neurodegeneration.