ReviewFrontiers in physiology2020
The Role of Basement Membranes in Cerebral Amyloid Angiopathy.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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
28 citing papers in PubMed, 59 citations in OpenAlex.
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- Review
- Associations of Cognitive Impairment with Putative Glymphatic-Related Imaging Indices and Cortical Atrophy in Cerebral Amyloid Angiopathy.Biomedicines · 2026Article
- Basement membrane remodeling with fibroblast activation and cystatin C aggregation in cerebral vessels of hereditary cystatin C amyloid angiopathy.Acta neuropathologica communications · 2026Article
- Functions of the basal lamina and ApoE in cerebral amyloid angiopathy.Fluids and barriers of the CNS · 2025Review
- Targeting Transferrin Receptor 1 for Enhancing Drug Delivery Through the Blood-Brain Barrier for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- The life cycle of type IV collagen.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- A collagen IV fluorophore knock-in toolkit reveals trimer diversity in C. elegans basement membranes.The Journal of cell biology · 2025Article
- Gastrointestinal exposure to silica nanoparticles induced Alzheimer's disease-like neurotoxicity in mice relying on gut microbiota and modulation through TLR4/NF-κB and HDAC.Journal of nanobiotechnology · 2025Article
- Improvements in Exercise for Alzheimer's Disease: Highlighting FGF21-Induced Cerebrovascular Protection.Neurochemical research · 2025Review
- Capillary basal lamina in human brain and spinal cord has fibrillar collagen type I and type III: Ignorance may not be bliss.Free neuropathology · 2025Article
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- Tension at the gate: sensing mechanical forces at the blood-brain barrier in health and disease.Journal of neuroinflammation · 2024Review
- iPSC-derived blood-brain barrier modeling reveals APOE isoform-dependent interactions with amyloid beta.Fluids and barriers of the CNS · 2024Article
- Utility of cerebrovascular imaging biomarkers to detect cerebral amyloidosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Differences in the cerebral amyloid angiopathy proteome in Alzheimer's disease and mild cognitive impairment.Acta neuropathologica · 2024Article
- Amyloid-β (Aβ) immunotherapy induced microhemorrhages are associated with activated perivascular macrophages and peripheral monocyte recruitment in Alzheimer's disease mice.Molecular neurodegeneration · 2023Article
- Effects of Voluntary Physical Exercise on the Neurovascular Unit in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- In vivo methods for imaging blood-brain barrier function and dysfunction.European journal of nuclear medicine and molecular imaging · 2023Review
- The emerging role of the HTRA1 protease in brain microvascular disease.Frontiers in dementia · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Dementia is a neuropsychiatric syndrome characterized by cognitive decline in multiple domains, often leading to functional impairment in activities of daily living, disability, and death. The most common causes of age-related progressive dementia include Alzheimer's disease (AD) and vascular cognitive impairment (VCI), however, mixed disease pathologies commonly occur, as epitomized by a type of small vessel pathology called cerebral amyloid angiopathy (CAA). In CAA patients, the small vessels of the brain become hardened and vulnerable to rupture, leading to impaired neurovascular coupling, multiple microhemorrhage, microinfarction, neurological emergencies, and cognitive decline across multiple functional domains. While the pathogenesis of CAA is not well understood, it has long been thought to be initiated in thickened basement membrane (BM) segments, which contain abnormal protein deposits and amyloid-β (Aβ). Recent advances in our understanding of CAA pathogenesis link BM remodeling to functional impairment of perivascular transport pathways that are key to removing Aβ from the brain. Dysregulation of this process may drive CAA pathogenesis and provides an important link between vascular risk factors and disease phenotype. The present review summarizes how the structure and composition of the BM allows for perivascular transport pathways to operate in the healthy brain, and then outlines multiple mechanisms by which specific dementia risk factors may promote dysfunction of perivascular transport pathways and increase Aβ deposition during CAA pathogenesis. A better understanding of how BM remodeling alters perivascular transport could lead to novel diagnostic and therapeutic strategies for CAA patients.
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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.