ReviewFrontiers in synaptic neuroscience2016
SNAP-25, a Known Presynaptic Protein with Emerging Postsynaptic Functions.
Review in Frontiers in synaptic neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 2 of them syntheses that pooled it.
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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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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
116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.
- Value of blood neural cell-derived small extracellular vesicles in the diagnosis and prediction of Alzheimer's disease: A systematic review.The journal of prevention of Alzheimer's disease · 2025Pooled it
- High Rate of Recurrent De Novo Mutations in Developmental and Epileptic Encephalopathies.American journal of human genetics · 2017Pooled it
- The Use of Botulinum Toxin in the Management of Headache Disorders.Handbook of experimental pharmacology · 2021Trial
- Article
- Preoperative Plasma and Cerebrospinal Fluid SNAP-25 Levels Predict Delayed Neurocognitive Recovery in Elderly Patients: A Prospective Observational Study.CNS neuroscience & therapeutics · 2026Observational
- Proteomic maps of synapses and synaptic vesicles across the central and enteric nervous systems.Communications biology · 2026Article
- Identification of moderate effect size genes in autism spectrum disorder through a novel gene pairing approach.Communications biology · 2026Article
- Emergent latent neurotoxic effects of manganese following nominal chronic exposures in human stem cell and Caenorhabditis elegans models.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Role of eCIRP in Mediating Post-ischemia Microglial Phagocytosis via TREM-2 Receptor: Insights from Porcine and Mouse Cellular Models.Molecular neurobiology · 2026Article
- Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.Biogerontology · 2026Review
- Article
- Altered synaptic and astrocytic proteins in Lewy body disorders associated withBrain communications · 2026Article
- Transcriptomic profile of the hippocampus of rat strains with contrasting nervous system excitability.PloS one · 2026Article
- Chronic gut inflammation differentially modulates mitochondrial and antioxidant transcriptional programs in limbic brain structures.Scientific reports · 2025Article
- Proteomic profiling of Alzheimer's disease and Vascular dementia reveals unique underlying signatures.medRxiv : the preprint server for health sciences · 2025Article
- Loss of Fanconi anemia proteins causes a reliance on lysosomal exocytosis.Cell death & disease · 2025Article
- Computational Modelling Suggests Bacteriostatic Saline Does Not Reverse Botulinum Toxin-Induced Brow Ptosis.Toxins · 2025Article
- Elevated NEGR1 in brain induces anxiety or depression-like phenotypes and synaptic dysfunction.Molecular psychiatry · 2025Article
- Unraveling Predominantly Inattentive ADHD (ADHD-PI): Insights from Proteomic Analysis of the Striatum of Thyroid Hormone-Responsive Protein (THRSP)-Overexpressing Mice.Molecular neurobiology · 2025Article
- Microglial replacement in a Sandhoff disease mouse model reveals myeloid-derived β-hexosaminidase is necessary for neuronal health.Nature communications · 2025Article
56 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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of synaptic specializations is their dependence on highly organized complexes of proteins that interact with each other. The loss or modification of key synaptic proteins directly affects the properties of such networks, ultimately impacting synaptic function. SNAP-25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channels subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulating intracellular calcium dynamics. The SNAP-25 gene has been associated with distinct brain diseases, including Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia and bipolar disorder, indicating that the protein may act as a shared biological substrate among different "synaptopathies". The mechanisms by which alterations in SNAP-25 may concur to these psychiatric diseases are still undefined, although alterations in neurotransmitter release have been indicated as potential causative processes. This review summarizes recent work showing that SNAP-25 not only controls exo/endocytic processes at the presynaptic terminal, but also regulates postsynaptic receptor trafficking, spine morphogenesis, and plasticity, thus opening the possibility that SNAP-25 defects may contribute to psychiatric diseases by impacting not only presynaptic but also postsynaptic functions.
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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.