ReviewCurrent neuropharmacology2019
Synaptic Elimination in Neurological Disorders.
Review in Current neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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Who cites it
63 citing papers in PubMed, 115 citations in OpenAlex.
- Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 2026Review
- The C3-C3aR axis drives rotenone-induced cognitive damage via synaptic engulfment, dark microglia and PANoptosis.Redox biology · 2026Article
- Juvenile myoclonic epilepsy heterogeneity uncovered: Z-mapped imaging endophenotypes of cortical and subcortical structures and their clinical, cognitive and psychiatric features.Brain communications · 2026Article
- Roles of Microglia in Synaptogenesis, Synaptic Pruning, and Synaptic Plasticity in Physiological Conditions and Central Nervous System Disorders.Current neuropharmacology · 2026Review
- Neuroplasticity and immune system are related to altered grey matter networks: a cohort study in sporadic Alzheimer's disease.Brain communications · 2026Article
- Sex-Specific Molecular Architecture of Microglia-Mediated Neuronal Pruning Across the Human Lifespan.Molecular neurobiology · 2025Article
- Cognitive outcomes of deep brain stimulation depend on age and hippocampal connectivity in Parkinson's and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Live Cell Imaging to Monitor Axonal Pruning inBio-protocol · 2025Article
- Increased Synapse Elimination by Inflammatory Cells Contributes to Long-lasting Post-Stroke Memory Dysfunction in Old Mice.bioRxiv : the preprint server for biology · 2025Article
- Unraveling Neurodevelopment: Synergistic Effects of Intrinsic Genetic Programs and Extrinsic Environmental Cues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Neuron-secreted chemokine-like Orion interacts with the glial receptor Draper during mushroom body neuronal remodeling inFrontiers in cell and developmental biology · 2025Article
- Non-canonical Roles of Complement in the CNS: From Synaptic Organizer to Presynaptic Modulator of Glutamate Transmission.Current neuropharmacology · 2025Review
- Neurodegeneration in the cortical sulcus is a feature of chronic traumatic encephalopathy and associated with repetitive head impacts.Acta neuropathologica · 2024Article
- STING Driving Synaptic Phagocytosis of Hippocampal Microglia/Macrophages Contributes to Cognitive Impairment in Sepsis-Associated Encephalopathy in Mice.CNS neuroscience & therapeutics · 2024Article
- Tremendous Fidelity of Vitamin D3 in Age-related Neurological Disorders.Molecular neurobiology · 2024Review
- Brain stars take the lead during critical periods of early postnatal brain development: relevance of astrocytes in health and mental disorders.Molecular psychiatry · 2024Review
- Exploring causal mechanisms of psychosis risk.Neuroscience and biobehavioral reviews · 2024Review
- Recent progress in dendritic pruning ofOpen biology · 2024Review
- A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Monitoring synaptic pathology in Alzheimer's disease through fluid and PET imaging biomarkers: a comprehensive review and future perspectives.Molecular psychiatry · 2024Review
3 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
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapses are well known as the main structures responsible for transmitting information through the release and recognition of neurotransmitters by pre- and post-synaptic neurons. These structures are widely formed and eliminated throughout the whole lifespan via processes termed synaptogenesis and synaptic pruning, respectively. Whilst the first process is needed for ensuring proper connectivity between brain regions and also with the periphery, the second phenomenon is important for their refinement by eliminating weaker and unnecessary synapses and, at the same time, maintaining and favoring the stronger ones, thus ensuring proper synaptic transmission. It is well-known that synaptic elimination is modulated by neuronal activity. However, only recently the role of the classical complement cascade in promoting this phenomenon has been demonstrated. Specifically, microglial cells recognize activated complement component 3 (C3) bound to synapses targeted for elimination, triggering their engulfment. As this is a highly relevant process for adequate neuronal functioning, disruptions or exacerbations in synaptic pruning could lead to severe circuitry alterations that could underlie neuropathological alterations typical of neurological and neuropsychiatric disorders. In this review, we focus on discussing the possible involvement of excessive synaptic elimination in Alzheimer's disease, as it has already been reported dendritic spine loss in post-synaptic neurons, increased association of complement proteins with its synapses and, hence, augmented microglia-mediated pruning in animal models of this disorder. In addition, we briefly discuss how this phenomenon could be related to other neurological disorders, including multiple sclerosis and schizophrenia.
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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.