ReviewThe Journal of clinical investigation2018
Blood will out: vascular contributions to Alzheimer's disease.
Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
58 citing papers in PubMed.
- Transcriptional analyses identify pericyte-centered signaling programs altered by sex and brain region in Alzheimer's Disease.Communications biology · 2026Article
- Urban greenspace and dementia: Measures, mechanisms, and methodological guidance.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Aβ₁₋₄₀ Enhances Platelet Sensitivity to Thrombin via NADPH Oxidase-ROS Signaling and Integrin αBiomolecules & therapeutics · 2026Article
- Intracranial stenosis and longitudinal progression of Alzheimer's disease pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Targeting hypercoagulability in ischemic stroke modulates fibrin-driven microglial polarization via JAK-STAT pathway.Journal of neuroinflammation · 2025Article
- An antibody targeting high-molecular-weight kininogen blocks contact system activation in a model of polymicrobial sepsis.Journal of thrombosis and haemostasis : JTH · 2025Article
- Synergistic effects of the Aβ/fibrinogen complex on synaptotoxicity, neuroinflammation, and blood-brain barrier damage in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The association of high-density lipoprotein cargo proteins with brain volume in older adults in the Atherosclerosis Risk in Communities (ARIC).Journal of Alzheimer's disease : JAD · 2025Article
- G-Protein Signaling in Alzheimer's Disease: Spatial Expression Validation of Semi-supervised Deep Learning-Based Computational Framework.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Lecanemab blocks the effects of the Aβ/fibrinogen complex on blood clots and synapse toxicity in organotypic culture.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Lecanemab Blocks the Effects of the Aβ/Fibrinogen Complex on Blood Clots and Synapse Toxicity in Organotypic Culture.bioRxiv : the preprint server for biology · 2024Article
- Deficiency of NLRP3 protects cerebral pericytes and attenuates Alzheimer's pathology in tau-transgenic mice.Frontiers in cellular neuroscience · 2024Article
- Neprilysin inhibitors and risk of Alzheimer's disease: A future perspective.Journal of cellular and molecular medicine · 2024Review
- A possible mechanism for the enhanced toxicity of beta-amyloid protofibrils in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Acute and Chronic Macrophage Differentiation Modulates TREM2 in a Personalized Alzheimer's Patient-Derived Assay.Cellular and molecular neurobiology · 2023Article
- Defining blood-induced microglia functions in neurodegeneration through multiomic profiling.Nature immunology · 2023Article
- Review
- Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.International journal of molecular sciences · 2023Review
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Cellular mechanisms of fibrin (ogen): insight from neurodegenerative diseases.Frontiers in neuroscience · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
The fundamental pathology in Alzheimer's disease (AD) is neuronal dysfunction leading to cognitive impairment. The amyloid-β peptide (Aβ), derived from amyloid precursor protein, is one driver of AD, but how it leads to neuronal dysfunction is not established. In this Review, I discuss the complexity of AD and possible cause-and-effect relationships between Aβ and the vascular and hemostatic systems. AD can be considered a multifactorial syndrome with various contributing pathological mechanisms. Therefore, as is routinely done with cancer, it will be important to classify patients with respect to their disease signature so that specific pathologies, including vascular pathways, can be therapeutically targeted.
Indexed as
Identifiers
What OpenQuestion holds
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.