ReviewProteomics2023
Advances in proteomic phenotyping of microglia in neurodegeneration.
Review in Proteomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Single-Cell Nanodroplet Processing Proteomics Pipeline for Analysis of Human-Derived Microglia.Proteomics · 2026Article
- Glial-Dopamine crosstalk: Astrocytic and microglial gatekeepers of neuroinflammation, plasticity, and motivation.AIMS neuroscience · 2026Review
- Single-cell nanodroplet processing proteomics pipeline for analysis of human-derived microglia.bioRxiv : the preprint server for biology · 2025Article
- TGF-β Signaling in Microglia: A Key Regulator of Development, Homeostasis and Reactivity.Biomedicines · 2024Review
- Brain resident microglia in Alzheimer's disease: foe or friends.Inflammopharmacology · 2024Review
- Microglia as integrators of brain-associated molecular patterns.Trends in immunology · 2024Review
- Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer's pathology.Nature communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Microglia are dynamic resident immune cells of the central nervous system (CNS) that sense, survey, and respond to changes in their environment. In disease states, microglia transform from homeostatic to diverse molecular phenotypic states that play complex and causal roles in neurologic disease pathogenesis, as evidenced by the identification of microglial genes as genetic risk factors for neurodegenerative disease. While advances in transcriptomic profiling of microglia from the CNS of humans and animal models have provided transformative insights, the transcriptome is only modestly reflective of the proteome. Proteomic profiling of microglia is therefore more likely to provide functionally and therapeutically relevant targets. In this review, we discuss molecular insights gained from transcriptomic studies of microglia in the context of Alzheimer's disease as a prototypic neurodegenerative disease, and highlight existing and emerging approaches for proteomic profiling of microglia derived from in vivo model systems and human brain.
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.