ReviewJournal of Alzheimer's disease : JAD2017
Dynamics of the Complement, Cytokine, and Chemokine Systems in the Regulation of Synaptic Function and Dysfunction Relevant to Alzheimer's Disease.
Review in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Alzheimer's Disease and Inflammation Research: A Systematic Bibliometric Review and Network Visualization of the Published Literature Between 2000 and 2023.Recent advances in inflammation & allergy drug discovery · 2026Pooled it
- Novel cell markers with altered expression in brain aging and Alzheimer's disease: A review.IBRO neuroscience reports · 2026Article
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- Effects of Cerebrospinal Fluids from Alzheimer and Non-Alzheimer Patients on Neurons-Astrocytes-Microglia Co-Culture.International journal of molecular sciences · 2024Article
- Role of Blood-Brain Barrier Dysfunction in Delirium following Non-cardiac Surgery in Older Adults.Annals of neurology · 2023Article
- The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer's disease: a narrative review.Neural regeneration research · 2023Review
- Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- A Role for Blood-brain Barrier Dysfunction in Delirium following Non-Cardiac Surgery in Older adults.medRxiv : the preprint server for health sciences · 2023Article
- CX3CL1 Pathway as a Molecular Target for Treatment Strategies in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The Cytokine CX3CL1 and ADAMs/MMPs in Concerted Cross-Talk Influencing Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Microglia-Mediated Neurovascular Unit Dysfunction in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- Crosstalk between Microglia and Neurons in Neurotrauma: An Overview of the Underlying Mechanisms.Current neuropharmacology · 2022Review
- Dysregulated protein phosphorylation: A determining condition in the continuum of brain aging and Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2021Article
- Maresin 1 attenuates pro-inflammatory activation induced by β-amyloid and stimulates its uptake.Journal of cellular and molecular medicine · 2021Article
- Microglial autophagy is impaired by prolonged exposure to β-amyloid peptides: evidence from experimental models and Alzheimer's disease patients.GeroScience · 2020Article
- Alzheimer's Disease, Oligomers, and Inflammation.Journal of Alzheimer's disease : JAD · 2018Review
- Bidirectional Microglia-Neuron Communication in Health and Disease.Frontiers in cellular neuroscience · 2018Review
- A Critical Assessment of Research on Neurotransmitters in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common form of dementia affecting nearly 45 million people worldwide. However, the etiology of AD is still unclear. Accumulations of amyloid-β plaques and tau tangles, neuroinflammation, and synaptic and neuronal loss are the major neuropathological hallmarks of AD, with synaptic loss being the strongest correlating factor with memory and cognitive impairment in AD. Many of these pathological hallmarks influence each other during the onset and progression of the disease. Recent genetic evidence suggests the possibility of a causal link between altered immune pathways and synaptic dysfunction in AD. Emerging studies also suggest that immune system-mediated synaptic pruning could initiate early-stage pathogenesis of AD. This comprehensive review is toward understanding the crosstalk of neuron-microglia-astrocyte and dynamics of complement, cytokine, and chemokine systems in the regulation of synaptic function and dysfunction relevant to AD. We start with summarizing several immune pathways, involving complements, MHC-I and CX3CL1, which mediate synaptic elimination during development and in AD. We then will discuss the potential of targeting these molecules as therapeutic interventions or as biomarkers for AD.
Indexed as
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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.