ReviewMolecular neurobiology2004
Atypical antiinflammatory activation of microglia induced by apoptotic neurons: possible role of phosphatidylserine-phosphatidylserine receptor interaction.
Review in Molecular neurobiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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
36 citing papers in PubMed, 88 citations in OpenAlex.
- Investigate the effects of donor breast milk and formula milk on metabolites in preterm infants through non-targeted metabolomics.BMC nutrition · 2026Article
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Exogenous phosphatidylserine protects against mesenteric ischemia-reperfusion with associated Akt/mTOR pathway upregulation.Scientific reports · 2025Article
- Article
- Phosphatidylserine, inflammation, and central nervous system diseases.Frontiers in aging neuroscience · 2022Review
- Protein arginine methyltransferase 8 modulates mitochondrial bioenergetics and neuroinflammation after hypoxic stress.Journal of neurochemistry · 2021Article
- Neuroprotective phosphatidylserine liposomes alleviate depressive-like behavior related to stroke through neuroinflammation attenuation in the mouse hippocampus.Psychopharmacology · 2021Article
- Review
- Exploring the molecular approach of COX and LOX in Alzheimer's and Parkinson's disorder.Molecular biology reports · 2020Review
- Loss of the Extracellular Matrix Molecule Tenascin-C Leads to Absence of Reactive Gliosis and Promotes Anti-inflammatory Cytokine Expression in an Autoimmune Glaucoma Mouse Model.Frontiers in immunology · 2020Article
- ATP8A2-related disorders as recessive cerebellar ataxia.Journal of neurology · 2020Article
- An In VivoMolecular neurobiology · 2018Article
- GABA-containing liposomes: neuroscience applications and translational perspectives for targeting neurological diseases.Nanomedicine : nanotechnology, biology, and medicine · 2018Review
- An in vivoAnnals of clinical and translational neurology · 2018Article
- Comparing Effects of Transforming Growth Factor β1 on Microglia From Rat and Mouse: Transcriptional Profiles and Potassium Channels.Frontiers in cellular neuroscience · 2018Article
- Molecular Anti-inflammatory Mechanisms of Retinoids and Carotenoids in Alzheimer's Disease: a Review of Current Evidence.Journal of molecular neuroscience : MN · 2017Review
- Pharmacological Tools to Activate Microglia and their Possible use to Study Neural Network Patho-physiology.Current neuropharmacology · 2017Review
- Phagocytosis of microglia in the central nervous system diseases.Molecular neurobiology · 2014Review
- Modulating neurotoxicity through CX3CL1/CX3CR1 signaling.Frontiers in cellular neuroscience · 2014Review
- Celecoxib attenuates systemic lipopolysaccharide-induced brain inflammation and white matter injury in the neonatal rats.Neuroscience · 2013Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the central nervous system (CNS), apoptosis plays an important role during development and is a primary pathogenic mechanism in several adult neurodegenerative diseases. A main feature of apoptotic cell death is the efficient and fast removal of dying cells by macrophages and nonprofessional phagocytes, without eliciting inflammation in the surrounding tissue. Apoptotic cells undergo several membrane changes, including the externalization of so-called "eat me" signals whose cognate receptors are present on professional phagocytes. Among these signals, the aminophospholipid phosphatidylserine (PS) appears to have a crucial and unique role in preventing the classical pro-inflammatory activation of macrophages, thus ensuring the silent and safe removal of apoptotic cells. Although extensively studied in the peripheral organs, the process of recognition and removal of apoptotic cells in the brain has only recently begun to be unraveled. Here, we summarize the evidence suggesting that upon interaction with PS-expressing apoptotic neurons, microglia may no longer promote the inflammatory cascade, but rather facilitate the elimination of damaged neurons through antiinflammatory and neuroprotective functions. We propose that the anti-inflammatory microglial phenotype induced through the activation of the specific PS receptor (PtdSerR), expressed by resting and activated microglial cells, could be relevant to the final outcome of neurodegenerative diseases, in which apoptosis seems to play a crucial role.
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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.