ReviewFrontiers in neuroscience2017
Alzheimer's Disease: The Role of Microglia in Brain Homeostasis and Proteopathy.
Review in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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.
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Who cites it
79 citing papers in PubMed.
- Interplay of oxidative stress and neuroinflammation in alzheimer's: insights into age-driven pathogenesis.Inflammopharmacology · 2026Review
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Trends in Nanoparticle-based Strategies for the Management of Neuroinflammation.CNS & neurological disorders drug targets · 2026Review
- Ginsenoside Re mitigates AβJournal of ginseng research · 2026Article
- The Potential of Coenzyme Q10 in Alzheimer's Disease: Reducing IL-17 Induced Inflammation and Oxidative Stress for Neuroprotection.Current drug research reviews · 2026Review
- Imaging brain inflammation and blood brain barrier permeability in neurological and psychiatric diseases: a review.Journal of neuroinflammation · 2025Review
- Engineered 3D immuno-glial-neurovascular human miBrain model.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Boosting angiotensin-converting enzyme (ACE) in microglia protects against Alzheimer's disease in 5xFAD mice.Nature aging · 2025Article
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.Journal of cell communication and signaling · 2025Article
- Selenoprotein P is a target for regulating extracellular vesicle biogenesis and secretion from activated microglia in vivo.Cell reports · 2024Article
- Article
- A Human Brain-Chip for Modeling Brain Pathologies and Screening Blood-Brain Barrier Crossing Therapeutic Strategies.Pharmaceutics · 2024Article
- Evaluation of altered cell-cell communication between glia and neurons in the hippocampus of 3xTg-AD mice at two time points.bioRxiv : the preprint server for biology · 2024Article
- Altered glia-neuron communication in Alzheimer's Disease affects WNT, p53, and NFkB Signaling determined by snRNA-seq.Cell communication and signaling : CCS · 2024Article
- Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq.bioRxiv : the preprint server for biology · 2024Article
- Associations between solar and geomagnetic activity and cognitive function in the Normative Aging study.Environment international · 2024Article
- The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets.Frontiers in aging neuroscience · 2024Review
- Arsenic and Tau Phosphorylation: a Mechanistic Review.Biological trace element research · 2023Review
- Coordinated Transcriptional Waves Define the Inflammatory Response of Primary Microglial Culture.International journal of molecular sciences · 2023Article
- Comparison of Monoamine Oxidase-A, Aβ Plaques, Tau, and Translocator Protein Levels in Postmortem Human Alzheimer's Disease Brain.International journal of molecular sciences · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Brain aging is central to late-onset Alzheimer's disease (LOAD), although the mechanisms by which it occurs at protein or cellular levels are not fully understood. Alzheimer's disease is the most common proteopathy and is characterized by two unique pathologies: senile plaques and neurofibrillary tangles, the former accumulating earlier than the latter. Aging alters the proteostasis of amyloid-β peptides and microtubule-associated protein tau, which are regulated in both autonomous and non-autonomous manners. Microglia, the resident phagocytes of the central nervous system, play a major role in the non-autonomous clearance of protein aggregates. Their function is significantly altered by aging and neurodegeneration. This is genetically supported by the association of microglia-specific genes,
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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.