ReviewJournal of molecular biology2019
Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk.
Review in Journal of molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 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
141 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.
- Pooled it
- Distinct Transposable Element Transcript Patterns in Microglia Across Aging and Alzheimer's Disease.Aging cell · 2026Article
- Gut Microbiome Changes in Preclinical Alzheimer's Disease.Nutrients · 2026Review
- Alzheimer's Disease Risk AllelebioRxiv : the preprint server for biology · 2026Article
- Timing of microglial ablation determines protection from tau-mediated neurodegeneration and cognitive decline.Acta neuropathologica communications · 2026Article
- Alzheimer's disease risk protein SorLA regulates ER homeostasis and lipid metabolism in human microglia, with conserved effects in neurons.Acta neuropathologica · 2026Article
- Functional border-associated macrophages limit Alzheimer's Disease progression.bioRxiv : the preprint server for biology · 2026Article
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Interplay between CD33 and TREM2 in Alzheimer's Disease: Potential Mechanistic Insights into Microglial Function in Amyloid Pathology.ACS chemical neuroscience · 2026Review
- Targeting Microglial Phagocytosis for Alzheimer's Disease Management: Natural, Pharmacological, Nanoparticle, and Gene Therapy Approaches.CNS & neurological disorders drug targets · 2026Review
- TREM2 and microglial immunity in Alzheimer's disease: mechanisms, genetics, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Trends in Nanoparticle-based Strategies for the Management of Neuroinflammation.CNS & neurological disorders drug targets · 2026Review
- Exploring the role of infectious pathogens in Alzheimer's disease neuroinflammation.Frontiers in cellular and infection microbiology · 2026Review
- Evaluating Microglial Contributions to the Neurovascular Unit in Health and Neurodegeneration Using HumanbioRxiv : the preprint server for biology · 2025Article
- DDT exposure induces microglial activation and disease-associated microglial signatures: Relevance to mechanisms of Alzheimer's disease.Neurotoxicology · 2025Article
- A Multimodal Atlas Reveals the Anatomical Distribution of Medium Spiny Neuron Subtypes and a Novel RGS6+ Population in the Primate Striatum.bioRxiv : the preprint server for biology · 2025Article
- Integrating Genomic, eQTL, and Mendelian Randomization Analyses to Identify Microglial Drug Targets in Multiple Sclerosis.Journal of cellular and molecular medicine · 2025Article
- Amyloid precursor protein and C99 are subunits in human microglial Hv1 channels that enhance current and inflammatory mediator release.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Astrocytes as Metabolic Sensors Orchestrating Energy-Driven Brain Vulnerability in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- Anti-Amyloid Monoclonal Antibodies for Alzheimer's Disease: Evidence, ARIA Risk, and Precision Patient Selection.Journal of personalized medicine · 2025Review
81 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Research into the function of microglia has dramatically accelerated during the last few years, largely due to recent genetic findings implicating microglia in virtually every neurodegenerative disorder. In Alzheimer's disease (AD), a majority of risk loci discovered through genome-wide association studies were found in or near genes expressed most highly in microglia leading to the hypothesis that microglia play a much larger role in disease progression than previously thought. From this body of work produced in the last several years, we find that almost every function of microglia has been proposed to influence the progression of AD from altered phagocytosis and synaptic pruning to cytokine secretion and changes in trophic support. By studying key Alzheimer's risk genes such as TREM2, CD33, ABCA7, and MS4A6A, we will be able to distinguish true disease-modulatory pathways from the full range of microglial-related functions. To successfully carry out these experiments, more advanced microglial models are needed. Microglia are quite sensitive to their local environment, suggesting the need to more fully recapitulate an in vivo environment to study this highly plastic cell type. Likely only by combining the above approaches will the field fully elucidate the molecular pathways that regulate microglia and influence neurodegeneration, in turn uncovering potential new targets for future therapeutic development.
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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.