Welcome to the AD/PD™ 2021 Interactive Program
The congress will officially run on Central European Time (CET) - Barcelona Time
To convert the congress times to your local time Click Here
Icons Legend: ![]()
- Live Session | 
- On Demand Session | 
- On Demand with Live Q&A
The viewing of sessions, cannot be accessed from this conference calendar. All sessions are accessible via the Main Lobby.
FOLLOWING THE LIVE DISCUSSION, THE RECORDING WILL BE AVAILABLE IN THE ON-DEMAND SECTION OF THE AUDITORIUM.
CAN SLEEP/WAKE CYCLE PATTERNS CAUSE ND?
Abstract
Aims
Sleep/wake cycle alterations are common in Parkinson’s disease (PD) and Alzheimer’s disease (AD). Traditionally, they have been described as early manifestations in PD and AD. However, observational studies suggest that they could also be causal risk factors for these neurodegenerative diseases. Our aim was to determine whether there is a causal relationship between sleep/wake cycle patterns and age at onset (AAO) of PD and AD using two-sample Mendelian Randomization (MR).
Methods
We selected 12 sleep traits (exposure) with available Genome-Wide Association Study (GWAS) data to evaluate their causal relationship with the risk of PD and AD (considered the outcome variables) through Inverse-Variance Weighted regression. We selected the genome-wide significant polymorphisms from the exposure and extracted them in the largest GWAS with available summary-statistics selected as outcomes: PD AAO (N=17,996) and AD (N=21,235). Sensitivity analyses were performed to confirm the results.
Results
MR results suggested a causal effect of morning chronotype, based on subjective and objective measures, on later PD AAO (95%CI: 1.20-2.43, p=8.47x10-09 and 95% CI:-7.28 to -4.44, p=5.87x10-16, respectively). Sleep efficiency was causally related with a lower risk of AD (95% CI:-20.408 to -0.66, p=0.04). These results were confirmed after sensitivity analyses.
Conclusions
This study suggest a potential causal effect of morning chronotype in PD AAO and sleep efficiency with a lower risk of AD. Given that sleep/wake patterns may be modifiable risk factors, they could be investigated further in order to potentially reduce the PD and AD risk.
THE POTENTIAL ROLE OF SLEEP IN PREDICTING THE COGNITIVE EVOLUTION OF MILD-MODERATE ALZHEIMER’S DISEASE PATIENTS
Abstract
Aims
To investigate the association between sleep and the cognitive evolution of mild-moderate Alzheimer’s disease patients.
Methods
Observational, prospective, single-center study, including consecutive patients diagnosed with mild-moderate Alzheimer’s disease (NCT02814045). The individuals were submitted to overnight polysomnography, followed by neuropsychological evaluations at baseline and after 12 months of follow-up. Principal component analysis characterized the sleep architecture of the cohort into two main types: individuals with a propensity to deepen their sleep (deep sleepers) and individuals who spent most of the time in the lighter sleep stage (light sleepers).
Results
The cohort included 125 subjects with a median [IQR] of 75.0 [72.0;80.0] years. The mean difference (95% CI) in the Mini-mental state examination score at 12 months between deep and light sleepers was -1.51 (95% CI: -2.47 to -0.54; p-value = 0.002). Accordingly, sleep depth and cognitive evolution presented a dose-response relationship (p-for-trend = 0.02). Regarding the specific cognitive subdomains, we observed differences related to the processing speed, demonstrated by the Stroop words test (-1.48; 95% CI: -2.58 to -0.38; p-value = 0.009), and to the executive function, demonstrated by the Verbal fluency test (-1.70; 95% CI: -2.85 to -0.55; p-value = 0.004).
Conclusions
Considering that light sleepers presented an increased cognitive decline, the sleep profile may have a predictive role in the cognitive evolution of mild-moderate Alzheimer’s disease patients. The modifiable nature of sleep sets this behavior as a possible useful intervention for the improvement of cognitive evolution.
GAIT AND TURNING ALTERATIONS IN IDIOPATHIC REM SLEEP BEHAVIORAL DISORDER AND EARLY PARKINSON’S DISEASE: A CROSS-SECTIONAL STUDY WITH MOBILE HEALTH TECHNOLOGY.
Abstract
Aims
The aim of the study was investigate the differences in performances of gait and turning under supervised conditions in healthy controls (HC), idiopathic REM sleep behavior disorders (RBD) and patients with Parkinson’s disease (PD).
Methods
Each participant underwent a supervised mobile health technology-instrumented assessment including the timed up and go test (TUG), and one minute walking tasks with turns in normal and dual task conditions (cognitive task, motor task).
Results
Sixty-eight PD patients (26 drug naïve and 42 under treatment, mean UPDRS-III 15±9), 18 RBD (mean UPDRS-III 1±1) and 33 age-matched controls entered the study. Compared to controls, PD patients (both naive and under treatment) needed more time to perform the TUG. During straight walking, the showed higher stride time, higher double limb support variability and a higher asymmetry index. Moreover, they turned slower than controls. Compared to controls, RBD subjects showed a higher swing time and turned slower.
Conclusions
This study suggests that RBD patients have a gait pattern that is distinguishable from controls and show features comparable to early PD patients. These results partly support results from a recent study investigating RBD gait in free-living conditions, and build a bridge between the control and PD state. Future studies using mobile health technology are needed to evaluate the predictive capacity of the method, to define RBD subjects that are in prodromal PD phases.
PUPILLOMETRY FINDINGS IN ISOLATED REM SLEEP BEHAVIOR DISORDER
Abstract
Aims
The impairment of melanopsin retinal ganglion cell (mRGCs)-mediated pupillary light reflex (PLR) and mRGC loss in post-mortem retinas have been demonstrated in PD and we recently described reduction of the rod-transient PLR in AD suggesting a possible mRGC-dendropathy.
Idiopathic/isolated REM sleep Behavior Disorder (iRBD) represents the strongest prodromal risk factor for α-synucleinopathies.
Methods
We evaluated with chromatic pupillometry PLR in 16 iRBD patients and 21 age-matched controls. iRBD and controls underwent ophthalmological evaluation including optical coherence tomography (OCT) and cognitive tests. In controls, the absence of sleep disorders was confirmed by sleep questionnaires and actigraphy (including I<O index). For iRBD, PLR metrics were correlated to clinical variables including REM atonia index (RAI) and the presence of α-synuclein deposition in skin biopsy.
Pupillometry data were analyzed by custom MATLAB scripts. Chi-square, independent-t and ANOVA tests were used to compare variables among groups. ANCOVA analysis with age as covariate was used for comparisons between groups for pupil metrics. For OCT data we evaluated eyes tested by pupillometry.
Results
In iRBD we documented higher baseline pupil diameter and decreased rod-transient PLR amplitude (p=0.007), whereas the mRGC-sustained response did not differ between groups. We found significant correlation between RAI and rod-transient PLR amplitude. Moreover, the difference in pupil metrics compared to controls was evident only in the iRBD group with α-synuclein deposition. OCT findings did not differ between iRBD and controls.
Conclusions
These findings envisage a parasympathetic dysfunction combined with mRGC-mediated PLR dysfunction in iRBD. PLR can be proposed as a potential biomarker for this sleep disorder.