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RESEARCH PAPER ANALYSIS

Higher glymphatic system activity is linked to longer prodromal stage in isolated REM sleep behavior disorder: a possible protective factor.

In patients with isolated REM sleep behavior disorder, higher DTI-ALPS indices—indicative of better glymphatic function—were associated with longer prodromal symptom duration and substantially delayed phenoconversion to alpha-synucleinopathy.

PMID41997950
JournalNPJ Parkinson's disease
Publication Date2026-04-17
Ingested2026-04-28 08:58 PM
EXECUTIVE SUMMARY

What the AI sees

In patients with isolated REM sleep behavior disorder, higher DTI-ALPS indices—indicative of better glymphatic function—were associated with longer prodromal symptom duration and substantially delayed phenoconversion to alpha-synucleinopathy.

WHY IT MATTERS

Research significance

Points to glymphatic function as a noninvasive biomarker to stratify prodromal PD risk and a plausible, potentially modifiable target (e.g., sleep optimization, AQP4/vascular approaches) for interventions to delay conversion, while noting that causality and therapeutic efficacy remain to be proven.

ABSTRACT

Source abstract

Isolated rapid eye movement sleep behavior disorder (iRBD) is recognized as a prodromal stage of alpha-synucleinopathies. While glymphatic dysfunction has been investigated in Parkinson's disease, its role in iRBD remains incompletely understood. This study evaluated the association between glymphatic function and the speed-modulating effect to alpha-synucleionpathy conversion. Fifty-six patients (67.2 ± 7.1 [mean age ± SD]) with an iRBD and 48 control subjects (61.5 ± 10.0) underwent brain magnetic resonance imaging. Glymphatic function was evaluated using the diffusion tensor imaging along the perivascular space (DTI-ALPS) method with manual acquisition of the ALPS-index. The mean time from symptom onset to MRI acquisition (T1) was 7.05 ± 5.08 years, while among converters the mean time from symptom onset to phenoconversion (T2) was 11.07 ± 5.68 years. Higher ALPS-index was positively correlated with longer iRBD symptom duration (rho = 0.409, p = 0.002). Although the ALPS-index did not predict phenoconversion in the entire cohort, post-hoc analysis of converters revealed that patients with higher ALPS-index exhibited more than nine years longer time to conversion than patients with lower ALPS-index (χ² = 13.075, p < 0.001). These findings suggest that preserved glymphatic function may be associated with prolonged prodromal stability in iRBD.

SUPPORTING PAPER SET

32 more papers to review

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B, Biointerfaces 86.0 13 Neuroprotective roles of klotho: Molecular pathways and therapeutic implications for cognitive health in neurological and psychiatric diseases. Experimental physiology 84.0 14 Flavonoid Rutin Reduces Intestinal Inflammation in an Experimental Model of Parkinson's Disease. Neurotoxicity research 70.0 15 Nanostructured Lipid Carriers Enhance Brain Delivery and Antioxidant Efficacy of a Small-Molecule MAO B Inhibitor for Neurodegenerative Disease Therapy. Molecular pharmaceutics 78.0 16 Pathophysiological Role of the Gut Brain Axis in Parkinson's Disease: From Microbial Metabolites and Intestinal Permeability to Central Neuroinflammation. Current neurovascular research 86.0 17 Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review. Current issues in molecular biology 86.0 18 Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders. Neuroprotection (Chichester, England) 76.0 19 Integrative network pharmacology delineates dual GPCR and non-GPCR mechanisms of blended and individual Taikong Blue lavender and Pingyin rose essential oils in neurodegenerative and psychiatric disorders. Computers in biology and medicine 65.0 20 Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets. Experimental neurology 78.0 21 Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy. Frontiers in pharmacology 75.2 22 Molecular mechanisms underlying Parkinson's disease and role of phytochemicals, α-synuclein, sirtuins, and incretin mimetics in potential therapy. Frontiers in pharmacology 75.0 23 Lipid droplets in neurodegenerative diseases: pathological drivers and therapeutic vulnerabilities. Cell death discovery 82.0 24 Brain-gut-microbiota axis: a review on the bidirectional regulatory mechanisms between gut microbiota and brain and their disease interactions. Frontiers in microbiology 74.0 25 Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review. Biomolecules & biomedicine 84.0 26 Neurosyphilis and Parkinsonism: Overlapping Pathophysiology and Emerging Therapeutic Insights. Current neurovascular research 76.0 27 Molecular biochemistry of soluble epoxide hydrolase in lipid mediator pathways and neuroinflammatory responses. The Journal of steroid biochemistry and molecular biology 82.0 28 Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential. Cell stress 83.3 29 Neuroprotective Role of Exercise-based Physiotherapy Combined with Pharmacological Agents in Parkinson's Disease. Central nervous system agents in medicinal chemistry 64.0 30 Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder. Signal transduction and targeted therapy 84.0 31 HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches. Inflammopharmacology 78.0 32 Beyond acid-base dyshomeostasis: Dynamic instability of neuronal lysosomal pH as a pathogenic mechanism and therapeutic target in neurological diseases. Biochemical pharmacology 88.0
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