ArticleJournal of neuroinflammation2017
Proteomic anaysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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.
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Who cites it
64 citing papers in PubMed, 104 citations in OpenAlex.
- Nicotinamide riboside supplementation restores microglial health and improves cognition in aged male mice.GeroScience · 2026Article
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- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Age-impaired remyelination is associated with dysregulated microglial transitions.Nature communications · 2025Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025Review
- Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research.Molecular neurodegeneration · 2025Review
- Review
- Age-associated microglial transcriptome leads to diminished immunogenicity and dysregulation of MCT4 and P2RY12/P2RY13 related functions.Cell death discovery · 2025Article
- Elevated expression of the retrotransposon LINE-1 drives Alzheimer's disease-associated microglial dysfunction.Acta neuropathologica · 2024Article
- Advancements in Targeting Macrophage Senescence for Age-Associated Conditions.Aging and disease · 2024Review
- Microglia either promote or restrain TRAIL-mediated excitotoxicity caused by AβJournal of neuroinflammation · 2024Article
- TREM1 disrupts myeloid bioenergetics and cognitive function in aging and Alzheimer disease mouse models.Nature neuroscience · 2024Article
- Non-invasiveFrontiers in cellular neuroscience · 2024Review
- Metabolic Control of Microglia.Advances in neurobiology · 2024Review
- The proteomic landscape of microglia in health and disease.Frontiers in cellular neuroscience · 2024Review
- Brain macrophage development, diversity and dysregulation in health and disease.Cellular & molecular immunology · 2023Review
- The Role of Acyl-CoA β-Oxidation in Brain Metabolism and Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAge is the primary risk factor for many diseases. As such, age is a critical co-factor for examination in order to understand the progression and potential intervention in disease progression. Studies examining both the phenotype and transcriptome of aged microglia demonstrated a propensity for the development of a pro-inflammatory phenotype. Less well studied is the concomitant blunting of anti-inflammatory aspects of microglial function with age which also impact plasticity and repair in the CNS.
methodsThis study utilizes mass spectrometry-based proteomics to compare primary microglia from young and aged animals.
resultsThis study revealed alterations in three clusters of inter-related proteins. The three pathways were inflammatory signaling, mitochondrial function, and cellular metabolism. Analysis of these clusters identified the protein rapamycin-insensitive companion of mTOR (RICTOR), a component of the mTORC2 complex, as a novel upstream regulator of several biological functions that are altered with age and potentially linked to phenotype development. A decrease in mTORC2-dependent AKT S473 phosphorylation, as assessed by insulin growth factor (IGF) treatment, was observed in aged microglia. This novel finding was confirmed by genetic manipulation of the microglial cell line. BV2 cells with diminished RICTOR displayed a phenotype that was strikingly similar to that of aged microglia. This finding is particularly relevant as the mTOR pathway already has a number of pharmacological modulators used clinically.
conclusionsThe results suggest that microglia from aged mice show changes in cellular metabolism and energy regulation that might underlie the alterations in inflammatory signaling. Modulation of one pathway identified in our bioinformatic analysis, RICTOR, may provide an avenue by which deleterious aspects of the aging microglia can be attenuated. If successful, this could mean potentially delaying or diminishing the progress of diseases for which progressive inflammation is involved.
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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.