Four‐Year <scp>Follow‐up</scp> of [<sup>18</sup>F]Fluorodeoxyglucose Positron Emission Tomography–Based Parkinson's Disease–Related Pattern Expression in 20 Patients with Isolated Rapid Eye Movement Sleep Behavior Disorder Shows Prodromal Progression

Kogan, Rosalie V.; Janzen, Annette; Meles, Sanne K.; Sittig, Elisabeth; Renken, Remco; Gurvits, Vita; Mayer, Geert; Leenders, Klaus L.; Oertel, Wolfgang H.

doi:10.1002/mds.28260

Cited by 37 publications

(40 citation statements)

References 26 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There was a trend toward elevated PDRP expression in the converters than in the nonconverters, which is grossly similar to a prior study by Holtbernd et al 17 More importantly, most PD converters showed the increased PDRP expression along with the decreased RBDRP expression, and this tendency was not observed in patients who developed DLB or MSA. The PDRP expression in our PD converters are in line with a recent longitudinal study by Kogan et al 27 who reported that all 4 iRBD patients who developed PD had suprathreshold PDRP expression at baseline and its greater increase over approximately 4 years of follow‐up. Given the current results, one could speculate that the RBDRP tends to fade away, being replaced by the disease‐specific pattern of the phenoconversion diagnosis.…”

Section: Discussionsupporting

confidence: 90%

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

et al. 2021

View full text Add to dashboard Cite

A BS TRACT: Background: It remains unclear whether and how the isolated rapid eye movement (REM) sleep behavior disorder (iRBD)-related metabolic pattern (RBDRP) changes with disease progression in iRBD. Objective: To examine longitudinal changes in RBDRP expression in iRBD patients and to explore trajectories of relative metabolic activities of individual brain regions constituting RBDRP. Methods: In this cohort study, 25 iRBD patients (mean age [AEstandard deviation], 69.2 AE 5.3 years; 12 [48%] patients were men) and 24 age-matched healthy controls were included. The patients underwent at least two 18 F-fluorodeoxyglucose positron emission tomography scans at baseline and at the 2-year and/or 4-year followups. We measured the RBDRP expression of the patients and controls which was validated by reproduction in a separate iRBD cohort (n = 13). Results: At baseline, the RBDRP expression discriminated iRBD patients from healthy controls. However, the RBDRP expression z scores tended to decrease over time in the patients, especially with longer follow-ups, and this tendency was observed even in patients with high-risk of phenoconversion. Furthermore, the degree of RBDRP expression at baseline did not predict the disease conversion. The RBDRP breakdown was mainly provoked by the attenuation of relative hypermetabolism in the frontal cortex including premotor areas and relative hypometabolism in the occipital cortex. The putaminal metabolic activity increased steadily with the disease progression. Conclusions: The RBDRP expression in iRBD patients was altered significantly over time. Some of the brain metabolic changes seem to represent attempted functional compensation against ongoing neurodegeneration. The RBDRP expression measurement at one time point may not be a reliable biomarker for predicting disease conversion.

show abstract

Section: Discussionsupporting

confidence: 90%

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

et al. 2021

View full text Add to dashboard Cite

show abstract

“…However, in contrast to the clinical score of the signature, which requires 16 variables in order to yield one patient‐specific clinical score (including the first 3 parts of the UPDRS, 3 different quantitative motor tasks, an extensive neuropsychological with enough cognitive tasks to generate composite scores for the attention and executive functions, episodic memory and learning, and visuospatial domains), the MRI signature has the advantage of only requiring a single anatomic T1‐weighted MRI scan. Several imaging markers have been proposed to identify patients with PD at higher risk of cognitive decline; 63–67 however, they often involved modalities and analytical procedures that are costly, highly technical, or hard to access. There is therefore a need for a more cost‐efficient brain marker that could be implemented in large clinical trials, especially in order to select patients that would be more likely to evolve toward a phenotype in which cognition becomes significantly affected.…”

Section: Discussionmentioning

confidence: 99%

A Prodromal Brain‐Clinical Pattern of Cognition in Synucleinopathies

Rahayel

Postuma

Montplaisir

et al. 2020

Annals of Neurology

View full text Add to dashboard Cite

Objective Isolated (or idiopathic) rapid eye movement sleep behavior disorder (iRBD) is associated with dementia with Lewy bodies (DLB) and Parkinson's disease (PD). Biomarkers are lacking to predict conversion to a dementia or a motor‐first phenotype. Here, we aimed at identifying a brain‐clinical signature that predicts dementia in iRBD. Methods A brain‐clinical signature was identified in 48 patients with polysomnography‐confirmed iRBD using partial least squares between brain deformation and 27 clinical variables. The resulting variable was applied to 78 patients with iRBD followed longitudinally to predict conversion to a synucleinopathy, specifically DLB. The deformation scores from patients with iRBD were compared with 207 patients with PD, DLB, or prodromal DLB to assess if scores were higher in DLB compared to PD. Results One latent variable explained 31% of the brain‐clinical covariance in iRBD, combining cortical and subcortical deformation and subarachnoid/ventricular expansion to cognitive and motor variables. The deformation score of this signature predicted conversion to a synucleinopathy in iRBD (p = 0.036, odds ratio [OR] = 2.249; 95% confidence interval [CI] = 1.053–4.803), specifically to DLB (OR = 4.754; 95% CI = 1.283–17.618, p = 0.020) and not PD (p = 0.286). Patients with iRBD who developed dementia had scores similar to clinical and prodromal patients with DLB but higher scores compared with patients with PD. The deformation score also predicted cognitive performance over 1, 2, and 4 years in patients with PD. Interpretation We identified a brain‐clinical signature that predicts conversion in iRBD to more severe/dementing forms of synucleinopathy. This pattern may serve as a new biomarker to optimize patient care, target risk reduction strategies, and administer neuroprotective trials. ANN NEUROL 2021;89:341–357

show abstract

“…All but one [33] of the included articles investigated global cognition (13,171 Five studies employed data suitable for meta-analysis on screening tests (MoCA or versions of the MMSE) for incident PD, varying between 0.61 and 1.92, with a pooled estimate of 1.08 (95% CI 0.66-1.77, Figure 3A).…”

Section: Global Cognition: Screening Testsmentioning

confidence: 99%

Prodromal Cognitive Deficits and the Risk of Subsequent Parkinson’s Disease

et al. 2022

View full text Add to dashboard Cite

Background: There is growing interest in identifying individuals who are in the prodromal phase of Parkinson’s disease (PD), as these individuals are potentially suitable for inclusion in intervention trials to prevent clinically manifest PD. However, it is less clear whether—and to what extent—cognitive deficits are present in prodromal PD. Methods: A systematic query was conducted through PubMed and Embase for prospective observational cohort studies that (a) assessed cognitive performance in individuals free of manifest PD at baseline and (b) subsequently followed up participants for incident PD. We grouped the results by cognitive domain, and for domains that had been reported in at least three separate studies, we performed random-effects, inverse variance meta-analyses based on summary statistics. Results: We identified nine articles suitable for inclusion, with a total of 215 patients with phenoconversion and 13,524 individuals remaining disease-free at follow-up. The studies were highly heterogeneous in study design, study population, and cognitive test batteries. Studies that included only cognitive screening measures such as MMSE or MoCA reported no association between worse cognitive performance and onset of manifest PD (combined odds ratio 1.08; 95% confidence interval 0.66–1.77). By contrast, studies that used extensive cognitive testing batteries found that global cognitive deficits were associated with an increased risk of manifest PD. In domain-specific analyses, there was evidence for an association between worse executive functioning (OR 1.45; 95% CI 1.10–1.92), but not memory (OR 1.20; 95% CI 0.85–1.70) or attention (OR 0.98; 95% CI 0.23–4.26), and clinically manifest PD. Conclusion: Although some caution due to high heterogeneity among published studies is warranted, the available evidence suggests that global and executive cognitive deficits are prodromal features of PD. Collaborative prospective studies with extensive cognitive test batteries are required to shed light on domain-specific deficits, temporal relations, and subgroup differences in prodromal cognitive deficits in PD.

show abstract

Four‐Year Follow‐up of [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography–Based Parkinson's Disease–Related Pattern Expression in 20 Patients with Isolated Rapid Eye Movement Sleep Behavior Disorder Shows Prodromal Progression

Cited by 37 publications

References 26 publications

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

A Prodromal Brain‐Clinical Pattern of Cognition in Synucleinopathies

Prodromal Cognitive Deficits and the Risk of Subsequent Parkinson’s Disease

Contact Info

Product

Resources

About

Four‐Year Follow‐up of [18F]Fluorodeoxyglucose Positron Emission Tomography–Based Parkinson's Disease–Related Pattern Expression in 20 Patients with Isolated Rapid Eye Movement Sleep Behavior Disorder Shows Prodromal Progression

Cited by 37 publications

References 26 publications

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

Longitudinal Changes in Isolated Rapid Eye Movement Sleep Behavior Disorder‐Related Metabolic Pattern Expression

A Prodromal Brain‐Clinical Pattern of Cognition in Synucleinopathies

Prodromal Cognitive Deficits and the Risk of Subsequent Parkinson’s Disease

Contact Info

Product

Resources

About

Four‐Year Follow‐up of [¹⁸F]Fluorodeoxyglucose Positron Emission Tomography–Based Parkinson's Disease–Related Pattern Expression in 20 Patients with Isolated Rapid Eye Movement Sleep Behavior Disorder Shows Prodromal Progression