ArticleMolecular neurodegeneration2018
Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism.
Article in Molecular neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 175 papers, 2 of them syntheses 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.
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Who cites it
175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 271 citations in OpenAlex.
- Glymphatic dysfunction in Alzheimer's disease: a systematic review and meta-analysis of the DTI-ALPS index as an imaging biomarker.Frontiers in aging neuroscience · 2026Pooled it
- Neurodevelopmental Clues to Neurodegeneration.Pediatric neurology · 2021Pooled it
- Pathogenicity of Rift Valley fever virus: Organ-specific clinical outcomes and hidden drivers of virulence - a narrative review.Virulence · 2026Review
- The bone-cerebrovascular axis: effects of bone aging on neurovascular dysfunction and neurodegeneration.The Journal of clinical investigation · 2026Review
- Recent advances in Alzheimer's disease: From molecular mechanisms to therapeutic strategies.Cell · 2026Review
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Friend or foe? Glial-vascular interactions in health and neurodegenerative disease.Pharmacological reviews · 2026Review
- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- Crossing the blood-brain barrier: nanoparticle-based strategies for neurodegenerative disease therapy.Drug delivery and translational research · 2026Review
- Article
- A human blood-brain barrier model reveals pericytes as critical regulators of viral neuroinvasion.iScience · 2026Article
- Mechanistic role of APOE lipidation in Alzheimer's disease pathogenesis.Theranostics · 2026Review
- Differential pericyte pathology in the human retina and brain in diabetes mellitus and Alzheimer's disease.Frontiers in neuroscience · 2026Article
- ApoE expression across the CNS: Who, What, Where, When, and How (much)?Molecular neurodegeneration advances · 2026Review
- Role of tRNA-Derived Fragments and Their Modifications in the Pathogenesis and Treatment of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Functions of the basal lamina and ApoE in cerebral amyloid angiopathy.Fluids and barriers of the CNS · 2025Review
- Orthobiologics and Peptide Therapy for Central Nervous System Repair in Neurodegenerative Conditions.Cells · 2025Review
- Mechanisms of high-density lipoprotein in regulating blood-brain barrier function: insights and implications.Fluids and barriers of the CNS · 2025Review
- Brain pericytes derived from human pluripotent stem cells retain vascular and phagocytic functions under hypoxia.Stem cells (Dayton, Ohio) · 2025Article
- APOE4 Exacerbates Alzheimer-Like Pathologies and Cognitive Deficits Induced by Blood-Derived Aβ in a Mouse Model.Aging cell · 2025Article
115 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundClearance at the blood-brain barrier (BBB) plays an important role in removal of Alzheimer's amyloid-β (Aβ) toxin from brain both in humans and animal models. Apolipoprotein E (apoE), the major genetic risk factor for AD, disrupts Aβ clearance at the BBB. The cellular and molecular mechanisms, however, still remain unclear, particularly whether the BBB-associated brain capillary pericytes can contribute to removal of aggregated Aβ from brain capillaries, and whether removal of Aβ aggregates by pericytes requires apoE, and if so, is Aβ clearance on pericytes apoE isoform-specific.
methodsWe performed immunostaining for Aβ and pericyte biomarkers on brain capillaries (< 6 μm in diameter) on tissue sections derived from AD patients and age-matched controls, and APP
resultsFirst, we found that 35% and 60% of brain capillary pericytes accumulate Aβ in AD patients and 8.5-month-old APP
conclusionsOur data suggest that BBB-associated pericytes clear Aβ aggregates via an LRP1/apoE isoform-specific mechanism. These data support the role of LRP1/apoE interactions on pericytes as a potential therapeutic target for controlling Aβ clearance in AD.
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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.