ArticleGlia2015
APOE genotype-dependent modulation of astrocyte chemokine CCL3 production.
Article in Glia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- A haptoglobin (HP) structural variant alters the effect of APOE alleles on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Pooled it
- Mutation-specific neuropathologic signatures in MAPT-associated frontotemporal lobar degeneration.Acta neuropathologica · 2026Article
- Is there a role for apolipoprotein E in perinatal brain injury?Molecular and cellular pediatrics · 2026Review
- Transcriptomic analysis identifies candidate molecular mechanisms underlying SCF+G-CSF-reduced neuropathology in aged APP/PS1 mice.Frontiers in aging neuroscience · 2026Article
- Impaired macroautophagy in oligodendrocyte precursor cells suppresses neuronal plasticity via a senescence-associated signaling.Science advances · 2025Article
- Anti-Inflammatory Effects of GPR55 Agonists and Antagonists in LPS-Treated BV2 Microglial Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Neuronal glutathione loss leads to neurodegeneration involving gasdermin activation.Scientific reports · 2023Article
- A multi-hit hypothesis for an APOE4-dependent pathophysiological state.The European journal of neuroscience · 2022Review
- Role of Chemokines in the Development and Progression of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- The roles of chemokines following intracerebral hemorrhage in animal models and humans.Frontiers in molecular neuroscience · 2022Review
- Spatiotemporal patterns of gliosis and neuroinflammation in presenilin 1/2 conditional double knockout mice.Frontiers in aging neuroscience · 2022Article
- Effects of prolactin on movement disorders and APOE, GFAP, and PRL receptor gene expression following intracerebral hemorrhage in rats.Iranian journal of basic medical sciences · 2021Article
- COVID-19 enters the expanding network of apolipoprotein E4-related pathologies.Redox biology · 2021Review
- Innate Immune System Activation and Neuroinflammation in Down Syndrome and Neurodegeneration: Therapeutic Targets or Partners?Frontiers in aging neuroscience · 2021Review
- APOE ε4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer's disease.Alzheimer's research & therapy · 2020Article
- Commentary: APOE e4 Genotype Predicts Severe COVID-19 in the UK Biobank Community Cohort.Frontiers in immunology · 2020Article
- Invited Review: APOE at the interface of inflammation, neurodegeneration and pathological protein spread in Alzheimer's disease.Neuropathology and applied neurobiology · 2019Review
- Leonurine suppresses neuroinflammation through promoting oligodendrocyte maturation.Journal of cellular and molecular medicine · 2019Article
- Mimicry of Central-Peripheral Immunity in Alzheimer's Disease and Discovery of Neurodegenerative Roles in Neutrophil.Frontiers in immunology · 2019Article
- Tau and neuroinflammation: What impact for Alzheimer's Disease and Tauopathies?Biomedical journal · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Apolipoprotein E (apoE) is well known as a regulator of cholesterol homeostasis, and is increasingly recognized to play a prominent role in the modulation of innate immune response, including cell-to-cell communication and migration. Alzheimer's disease (AD) is a slowly progressive neurodegenerative disorder characterized by neuroinflammation that appears to be an important component of the pathophysiology of the disease. Astrocytes are the majority cell type in brain, exerting significant influence over a range of central nervous system activities, including microglial-mediated neuroinflammatory responses. As the resident innate immune effector cells of the brain, microglia respond to soluble chemical signals released from tissue during injury and disease by mobilizing to lesion sites, clearing toxic molecules, and releasing chemical signals of their own. While microglial-mediated neuroinflammation in the AD brain remains an area of intense investigation, the mechanisms underlying reinforcement and regulation of these aberrant microglial responses by astrocytes are largely unstudied. Moreover, although inheritance of APOE ɛ4 represents the greatest genetic risk factor for sporadic AD, the mechanism by which apoE isoforms differentially influence AD pathophysiology is unknown. Here we show that APOE ɛ4 genotype specifically modulates astrocyte secretion of potent microglial chemotactic agents, including CCL3, thus providing evidence that APOE modulation of central nervous system (CNS) innate immune response is mediated through astrocytes.
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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.