ArticleInternational journal of molecular sciences2021
Impact of Amyloid-β on Platelet Mitochondrial Function and Platelet-Mediated Amyloid Aggregation in Alzheimer's Disease.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Aβ₁₋₄₀ Enhances Platelet Sensitivity to Thrombin via NADPH Oxidase-ROS Signaling and Integrin αBiomolecules & therapeutics · 2026Article
- Alzheimer's Disease-Thrombosis Comorbidity: A Growing Body of Evidence from Patients and Animal Models.Cells · 2025Review
- What Information do Systemic Pathological Changes Bring to the Diagnosis and Treatment of Alzheimer's Disease?Neuroscience bulletin · 2025Review
- Associations between platelet indices and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: the CABLE study.Alzheimer's research & therapy · 2025Article
- Platelets and diseases: signal transduction and advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- One immune cell to bind them all: platelet contribution to neurodegenerative disease.Molecular neurodegeneration · 2024Review
- Platelets and Neurodegenerative Diseases: Current Knowledge and Future Perspectives.International journal of molecular sciences · 2024Review
- Article
- Modulatory effects of dietary saturated fatty acids on platelet mitochondrial function following short-term exposure to ambient Particulate Matter (PMJournal of toxicology and environmental health. Part A · 2024Article
- Platelet mitochondria, a potent immune mediator in neurological diseases.Frontiers in physiology · 2023Review
- Platelet-derived microparticles provoke chronic lymphocytic leukemia malignancy through metabolic reprogramming.Frontiers in immunology · 2023Article
- Neutrophil Extracellular Traps in Cerebral Ischemia/Reperfusion Injury: Friend and Foe.Current neuropharmacology · 2023Review
- Platelets from early-stage Alzheimer patients show enhanced amyloid binding, an elevated open canalicular system and sex-specific differences in their activation profile.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlzheimer's disease (AD) is characterized by an accumulation of amyloid β (Aβ) peptides in the brain and mitochondrial dysfunction. Platelet activation is enhanced in AD and platelets contribute to AD pathology by their ability to facilitate soluble Aβ to form Aβ aggregates. Thus, anti-platelet therapy reduces the formation of cerebral amyloid angiopathy in AD transgenic mice. Platelet mitochondrial dysfunction plays a regulatory role in thrombotic response, but its significance in AD is unknown and explored herein.
methodsThe effects of Aβ-mediated mitochondrial dysfunction in platelets were investigated in vitro.
resultsAβ40 stimulation of human platelets led to elevated reactive oxygen species (ROS) and superoxide production, while reduced mitochondrial membrane potential and oxygen consumption rate. Enhanced mitochondrial dysfunction triggered platelet-mediated Aβ40 aggregate formation through GPVI-mediated ROS production, leading to enhanced integrin αII
conclusionsMitochondrial dysfunction contributes to platelet-mediated Aβ aggregate formation and might be a promising target to limit platelet activation exaggerated pathological manifestations in AD.
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.