ReviewJournal of neuroinflammation2024
Peripheral blood amyloid-β involved in the pathogenesis of Alzheimer's disease via impacting on peripheral innate immune cells.
Review in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
33 citing papers in PubMed, 41 citations in OpenAlex.
- Association Between Plasma Amyloid-Beta 42 Ratio and Postoperative Delirium in Elderly Patients Undergoing Major Abdominal Surgery: Secondary Analysis of a Randomized Controlled Trial.Brain and behavior · 2025Trial
- Article
- Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease.Nature aging · 2026Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- A Review of the Effect of Peripheral Amyloid β on the Central Nervous System.Current issues in molecular biology · 2026Review
- Review
- Plasma brain-derived tau: analytical and clinical validation of the first commercial immunoassay.Scientific reports · 2026Article
- Tuft Cells in the Gut Limit Cognitive Disorders by Regulating Gut Homeostasis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Mechanistic modeling of amyloid dynamics relating to Alzheimer's disease progression.Frontiers in aging neuroscience · 2026Article
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Amyloid β Peptide Modifies Membrane Architecture and Surface Electrostatic Properties of Human Red Blood Cells.International journal of molecular sciences · 2025Article
- Disease-disease interactions: molecular links of neurodegenerative diseases with cancer, viral infections, and type 2 diabetes.Translational neurodegeneration · 2025Review
- Plasma brain-derived tau: analytical and clinical validation of the first commercial immunoassay.medRxiv : the preprint server for health sciences · 2025Article
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- Stability and chaos analysis of neurological disorder of complex network with fractional order comparative study.Scientific reports · 2025Article
- Ultrasonic disruption of circulating amyloid β aggregates via phase-change peptide nanoemulsions.Biomaterials · 2025Article
- Bridging systemic metabolic dysfunction and Alzheimer's disease: the liver interface.Molecular neurodegeneration · 2025Review
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Hesperetin-Enhanced Metformin to Alleviate Cognitive Impairment via Gut-Brain Axis in Type 2 Diabetes Rats.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
A key pathological factor of Alzheimer's disease (AD), the most prevalent form of age-related dementia in the world, is excessive β-amyloid protein (Aβ) in extracellular aggregation in the brain. And in the peripheral blood, a large amount of Aβ is derived from platelets. So far, the causality between the levels of peripheral blood Aβ and its aggregation in the brain, particularly the role of the peripheral blood Aβ in the pathology of AD, is still unclear. And the relation between the peripheral blood Aβ and tau tangles of brain, another crucial pathologic factor contributing to the pathogenesis of AD, is also ambiguous. More recently, the anti-Aβ monoclonal antibodies are approved for treatment of AD patients through declining the peripheral blood Aβ mechanism of action to enhance plasma and central nervous system (CNS) Aβ clearance, leading to a decrease Aβ burden in brain and improving cognitive function, which clearly indicates that the levels of the peripheral blood Aβ impacted on the Aβ burden in brain and involved in the pathogenesis of AD. In addition, the role of peripheral innate immune cells in AD remains mostly unknown and the results obtained were controversial. In the present review, we summarize recent studies on the roles of peripheral blood Aβ and the peripheral innate immune cells in the pathogenesis of AD. Finally, based on the published data and our own work, we believe that peripheral blood Aβ plays an important role in the development and progression of AD by impacting on the peripheral innate immune cells.
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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.