ReviewImmunologic research2005
Role of formyl peptide receptor-like 1 (FPRL1/FPR2) in mononuclear phagocyte responses in Alzheimer disease.
Review in Immunologic research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Genome-wide Association Study of Dimensional Psychopathology Using Electronic Health Records.Biological psychiatry · 2018Pooled it
- Therapeutic Options for Alzheimer's Disease and Aging-Associated Cognitive Decline: State of the Art in the ACH2.0 Paradigm.International journal of molecular sciences · 2026Review
- Alzheimer's Is a Multiform Disease of Sustained Neuronal Integrated Stress Response Driven by the C99 Fragment Generated Independently of AβPP; Proteolytic Production of Aβ Is Suppressed in AD-Affected Neurons: Evolution of a Theory.International journal of molecular sciences · 2025Review
- Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer's disease.Cellular & molecular immunology · 2025Article
- Article
- Quintessential Synergy: Concurrent Transient Administration of Integrated Stress Response Inhibitors and BACE1 and/or BACE2 Activators as the Optimal Therapeutic Strategy for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- ACH2.0/E, the Consolidated Theory of Conventional and Unconventional Alzheimer's Disease: Origins, Progression, and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- On the Inadequacy of the Current Transgenic Animal Models of Alzheimer's Disease: The Path Forward.International journal of molecular sciences · 2024Article
- Next Generation Therapeutic Strategy for Treatment and Prevention of Alzheimer's Disease and Aging-Associated Cognitive Decline: Transient, Once-in-a-Lifetime-Only Depletion of Intraneuronal Aβ (International journal of molecular sciences · 2023Article
- The Amyloid Cascade Hypothesis 2.0 for Alzheimer's Disease and Aging-Associated Cognitive Decline: From Molecular Basis to Effective Therapy.International journal of molecular sciences · 2023Article
- The Amyloid Cascade Hypothesis 2.0: Generalization of the Concept.Journal of Alzheimer's disease reports · 2023Article
- Principles of Design of Clinical Trials for Prevention and Treatment of Alzheimer's Disease and Aging-Associated Cognitive Decline in the ACH2.0 Perspective: Potential Outcomes, Challenges, and Solutions.Journal of Alzheimer's disease reports · 2023Article
- Antibody-Mediated Clearance of Brain Amyloid-β: Mechanisms of Action, Effects of Natural and Monoclonal Anti-Aβ Antibodies, and Downstream Effects.Journal of Alzheimer's disease reports · 2023Review
- Acute-serum amyloid A and A-SAA-derived peptides as formyl peptide receptor (FPR) 2 ligands.Frontiers in endocrinology · 2023Review
- Aβ and Tau Interact with Metal Ions, Lipid Membranes and Peptide-Based Amyloid Inhibitors: Are These Common Features Relevant in Alzheimer's Disease?Molecules (Basel, Switzerland) · 2022Review
- suPAR: An Inflammatory Mediator for Kidneys.Kidney diseases (Basel, Switzerland) · 2022Review
- Structural basis of FPR2 in recognition of AβNature communications · 2022Article
- The Amyloid Cascade Hypothesis 2.0: On the Possibility of Once-in-a-Lifetime-Only Treatment for Prevention of Alzheimer's Disease and for Its Potential Cure at Symptomatic Stages.Journal of Alzheimer's disease reports · 2022Article
- Regulatory Roles of Antimicrobial Peptides in the Nervous System: Implications for Neuronal Aging.Frontiers in cellular neuroscience · 2022Review
- The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1-42)-Induced Neuroinflammation in Mouse Models of Alzheimer's Disease.Molecular neurobiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer disease (AD) is the most common neurodegenerative disease, affecting approx 4 million people in the United States in the year 2000 alone. Amyloid beta (Abeta) deposition, activated glial cells, and neuritic degeneration are the characteristic features of AD. Although the precise cause of AD has yet to be determined, a bulk of evidence suggests that inflammatory responses elicited by elevated Abeta peptides play an important role in the pathogenic process of the disease. In AD brain, mononuclear phagocytes (microglia) accumulate at the sites of Abeta peptide deposition. In vitro, Abeta peptides activate mononuclear phagocytes to release neurotoxic mediators. A number of cell-surface molecules have been reported to act as putative receptors for Abeta peptides, among which the G protein-coupled formyl peptide receptor-like 1 (FPRL1) and its mouse homolog FPR2 have been shown to be expressed by activated microglial cells and mediate the chemotactic activity of the 42 amino acid form of Abeta (Abeta42). FPRL1 also participates in Abeta42 internalization in macrophages and its cytotoxicity for neuronal cells. Therefore, FPRL1 may be involved in the inflammatory aspects of AD. This review discusses recent findings relevant to the function and regulation of FPRL1/FPR2 in mononuclear phagocytes by pro- and antiinflammatory signals and its potential as a therapeutic target 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.