ReviewInternational journal of molecular sciences2024
Pathogenesis of Cerebral Small Vessel Disease: Role of the Glymphatic System Dysfunction.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- DTI-ALPS index and cognitive impairment in cerebral small vessel disease: a systematic review and meta-analysis.Frontiers in aging neuroscience · 2026Pooled it
- Left-lateralized glymphatic dysfunction is associated with MoCA-measured cognitive impairment in cerebral small vessel disease: A DTI-ALPS study.IBRO neuroscience reports · 2026Article
- Peripheral inflammation impairs glymphatic function, contributing to neurodegeneration in Alzheimer's disease.iScience · 2026Article
- Experimental models of cerebral small vessel disease: Physiological constraints, translational challenges and future directions.The Journal of physiology · 2026Review
- Glymphatic dysfunction is associated with cognitive impairment in white matter hyperintensities: A DTI-based study.IBRO neuroscience reports · 2026Article
- Glymphatic System Dysfunction in Central Nervous System Diseases.CNS neuroscience & therapeutics · 2026Review
- Alterations in the DTI-ALPS index and choroid plexus volume as brain-immune interfacing indicators in neuropsychiatric lupus erythematosus with inflammatory phenotype.Lupus science & medicine · 2026Article
- Astrocyte-blood-brain barrier crosstalk in cerebral small vessel disease: linking barrier dysfunction to neurovascular failure.Frontiers in neurology · 2026Review
- Associations of clinical obesity with arterial stiffness and cerebral small vessel disease: a population-based study.Frontiers in endocrinology · 2026Article
- Insulin resistance in cerebral small vessel disease: a mini review.Frontiers in neuroscience · 2026Review
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- Impaired Flow: Glymphatic Dysfunction in Ischemic Stroke and the Influence of Sex.Journal of molecular neuroscience : MN · 2025Review
- Chronic Glymphatic Dysfunction Modulates Domain-Specific Cognitive Recovery After Stroke: A DTI-ALPS Lesion Stratification Study.CNS neuroscience & therapeutics · 2025Article
- Enlarged perivascular spaces in the basal ganglia region are associated with white matter interstitial fluid content via deep medullary vein dysfunction.Frontiers in human neuroscience · 2025Article
- The Glymphatic System and Its Role in Neurovascular Diseases.Journal of neuroendovascular therapy · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels. CSVD accounts for 25% of strokes and contributes to 45% of dementia. However, the pathogenesis of CSVD remains unclear, involving a variety of complex mechanisms. CSVD may result from dysfunction in the glymphatic system (GS). The GS contains aquaporin-4 (AQP-4), which is in the perivascular space, at the endfeet of the astrocyte. The GS contributes to the removal of waste products from the central nervous system, occupying perivascular spaces and regulating the exchange and movement of cerebrospinal fluid and interstitial fluid. The GS involves astrocytes and aquaporin channels, which are components of the blood-brain barrier, and problems with them may constitute the pathogenesis of CSVD. Vascular risk factors, including diabetes, dilate the perivascular space, disrupting the glymphatic system and the active regulation of AQP-4. CSVD exacerbation due to disorders of the GS is associated with multiple vasculopathies. Dysfunction of the glymphatic system and AQP-4 interferes with the functioning of the blood-brain barrier, which exacerbates CSVD. In a long-term follow-up of CSVD patients with microbleeds, lacunar infarcts, and white matter hyperintensity, several vascular risk factors, including hypertension, increased the risk of ischemic stroke. Dysfunction of the GS may be the cause of CSVD; however, the underlying treatment needs to be studied further.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.