ReviewMolecular psychiatry2009
Clearance mechanisms of Alzheimer's amyloid-beta peptide: implications for therapeutic design and diagnostic tests.
Review in Molecular psychiatry, 2009. 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 104 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
104 citing papers in PubMed, 238 citations in OpenAlex.
- Tanycytic degeneration impairs tau clearance and contributes to Alzheimer's disease pathology.Cell press blue · 2026Article
- DKK3-LRP1 complex and a chemical inhibitor regulate Aβ clearance in models of Alzheimer's disease.Science advances · 2025Article
- Characterization of endothelin-converting enzyme 1 as a key enzyme in the multienzyme Aβ degradation pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unmasking a Paradox: Roles of the PD-1/PD-L1 Axis in Alzheimer's Disease-Associated Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- On electrostatic interactions of adenosine triphosphate-insulin-degrading enzyme revealed by quantum mechanics/molecular mechanics and molecular dynamics.Quantitative biology (Beijing, China) · 2024Article
- Novel Therapeutic Strategies in Alzheimer's Disease: Pitfalls and Challenges of Anti-Amyloid Therapies and Beyond.Journal of clinical medicine · 2024Review
- Transcriptomic Analysis of Alzheimer's Disease Pathways in a Pakistani Population.Journal of Alzheimer's disease reports · 2024Article
- Role of Oxidative Stress, Methionine Oxidation and Methionine Sulfoxide Reductases (MSR) in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Alleviating the unwanted effects of oxidative stress on Aβ clearance: a review of related concepts and strategies for the development of computational modelling.Translational neurodegeneration · 2023Review
- Deletion of UCP1 in Tg2576 Mice Increases Body Temperature and Exacerbates Alzheimer's Disease-Related Pathologies.International journal of molecular sciences · 2023Article
- Comparison of Oleocanthal-Low EVOO and Oleocanthal against Amyloid-β and Related Pathology in a Mouse Model of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Article
- Linking Cognitive Impairment with Amyloid-β Accumulation in Alzheimer's Disease: Insights from Behavioral Tests and FTIR Spectroscopy.Journal of Alzheimer's disease reports · 2023Article
- Subclinical cognitive deficits are associated with reduced cerebrovascular response to visual stimulation in mid-sixties men.GeroScience · 2022Article
- Sustained high body temperature exacerbates cognitive function and Alzheimer's disease-related pathologies.Scientific reports · 2022Article
- Age, sex and APOE-ε4 modify the balance between soluble and fibrillar β-amyloid in non-demented individuals: topographical patterns across two independent cohorts.Molecular psychiatry · 2022Article
- Immunotherapy for Alzheimer's disease: targeting β-amyloid and beyond.Translational neurodegeneration · 2022Review
- Exploring the Therapeutic Potential of Phytochemicals in Alzheimer's Disease: Focus on Polyphenols and Monoterpenes.Frontiers in pharmacology · 2022Review
- Extracellular vesicles derived from astrocyte-treated with haFGFTheranostics · 2022Article
- The Beneficial Role of Exercise on Treating Alzheimer's Disease by Inhibiting β-Amyloid Peptide.Molecular neurobiology · 2021Review
- Chronic oral administration of adipoRon reverses cognitive impairments and ameliorates neuropathology in an Alzheimer's disease mouse model.Molecular psychiatry · 2021Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Currently, the 'amyloid hypothesis' is the most widely accepted explanation for the pathogenesis of Alzheimer's disease (AD). According to this hypothesis, altered metabolism of the amyloid-beta (Abeta) peptide is central to the pathological cascade involved in the pathogenesis of AD. Although Abeta is produced by almost every cell in the body, a physiological function for the peptide has not been determined, and the pathways by which Abeta leads to cognitive dysfunction and cell death are unclear. Numerous therapeutic approaches that target the production, toxicity and removal of Abeta are being developed worldwide. Although therapeutic treatment for AD may be imminent, the value and effectiveness of such treatment are largely dependent on early diagnosis of the disease. This review summarizes current knowledge of Abeta clearance, transport and degradation, and evaluates the use of such information in the development of diagnostic tools. The conflicting results of plasma Abeta ELISAs are discussed, as are the more promising results of Abeta imaging by positron emission tomography. Current knowledge of Abeta-binding proteins and Abeta-degrading enzymes is analysed in the context of a potential therapy for AD. Transport across the blood-brain barrier by the receptor for advanced glycation end products and efflux via the multi-ligand lipoprotein receptor LRP-1 is also reviewed. Enhancing clearance and degradation of Abeta remains an attractive therapeutic strategy, and improved understanding of Abeta clearance may lead to advances in diagnostics and interventions designed to prevent or delay the onset of 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.