Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (476 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant and Hackh's Chemical Dictionary, 5th ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Amine.
Where it fits in the MeSH classification
- Broader topics
- Organic Chemicals
- Narrower topics
- 1-Naphthylamine; 2-Naphthylamine; Allylamine; Amino Alcohols; Aminopyridines; Aniline Compounds; Benzylamines; Biogenic Amines; Butylamines; Catecholamines; Chloramines; Cyclohexylamines; Ethylamines; Gabapentin
Research landscape
PubMed indexes 1,087,579 records tagged with the MeSH heading “Amines” (counts retrieved 2026-10-31). 113,060 of them (10.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 583,259 records.
Reviews account for 67,380 records (6.2%) and meta-analyses for 4,032. Randomized controlled trials number 52,854 (4.9%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 583,259 |
| 2000-2009 | 194,604 |
| 2010-2019 | 196,656 |
| 2020 onward | 113,060 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 67,380 | 6.2% |
| Meta-analyses | 4,032 | 0.4% |
| Randomized controlled trials | 52,854 | 4.9% |
Method: PubMed query "Amines"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 42660892 · DOI · PMC13522591 |
| ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42680725 · DOI · PMC13534584 |
| Proteasome mutations associated with CANDLE syndrome cause altered neuronal development by dysregulating polyamine synthesis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42550603 · DOI · PMC13626833 |
Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Parkinson's disease (PD) is defined pathologically by loss of dopamine-producing neurons in the substantia nigra pars compacta (SNc).
- Closing excerpt
- Together, these findings highlight a subtype-specific, cell-autonomous mechanism by which pathogenic LRRK2 impairs PD-vulnerable nigrostriatal synapses and provide a framework for therapeutic strategies targeting early synaptic deficits in PD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (156 words)
Parkinson's disease (PD) is defined pathologically by loss of dopamine-producing neurons in the substantia nigra pars compacta (SNc). Yet synaptic dysfunction emerges much earlier, making it essential to define the mechanisms that drive early nigrostriatal deregulation. In the SNc, molecularly distinct dopamine neuron subtypes show differential susceptibility to PD. Here, we used intersectional genetic mouse models to determine how the PD-linked kinase LRRK2 affects vulnerable dopamine subtypes. Immunofluorescence and proximity-labeling proteomics revealed enriched LRRK2 expression in vulnerable dopamine neuron subclusters. High-resolution imaging showed that pathogenic LRRK2 disrupts presynaptic release-site organization in vulnerable dopamine axons, leading to reduced spontaneous and evoked striatal dopamine release in vivo. Proteomic analyses further showed that mutant LRRK2 increases phosphorylation of RAB3 proteins, impairing their interaction with the active-zone effectors RIM1 and RIM2. Together, these findings highlight a subtype-specific, cell-autonomous mechanism by which pathogenic LRRK2 impairs PD-vulnerable nigrostriatal synapses and provide a framework for therapeutic strategies targeting early synaptic deficits in PD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42660892 · DOI · PMC13522591
ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Polyamines, such as spermidine, are essential regulators of brain development, yet how cells control their uptake and extracellular levels remains unclear.
- Closing excerpt
- Thus, astrocytic polyamine clearance via ATP13A4 tunes extracellular spermidine to shape synapse formation during development.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (153 words)
Polyamines, such as spermidine, are essential regulators of brain development, yet how cells control their uptake and extracellular levels remains unclear. Here we show that ATP13A4, a transport protein enriched in glia and prominently expressed in astrocytes, governs brain polyamine balance. Using biochemical, cellular, and animal models, we find that ATP13A4 imports polyamines into cells and thereby limits their availability outside cells. Loss of ATP13A4 simplifies astrocyte morphology and increases the excitatory connections, or synapses, that astrocytes promote between neurons; adding spermidine reproduces these effects, identifying extracellular spermidine as a synapse-promoting signal. In mice lacking Atp13a4, brain polyamines are redistributed, with reduced levels in the cortex and accumulation in cerebrospinal fluid. This is accompanied by excess excitatory synapses, delayed early development, and mild, female-biased behavioral changes in adulthood. Rare ATP13A4 variants linked to neurodevelopmental disorders disrupt its function. Thus, astrocytic polyamine clearance via ATP13A4 tunes extracellular spermidine to shape synapse formation during development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42680725 · DOI · PMC13534584
Proteasome mutations associated with CANDLE syndrome cause altered neuronal development by dysregulating polyamine synthesis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Loss-of-function mutations in PSMB8/β5i and other components of the 20S proteasome result in multiorgan diseases, such as Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome.
- Closing excerpt
- These findings demonstrate that dysfunction of the proteasome affects neuronal development through overproduction of polyamines via dysregulation of ODC and offer insight into potential therapeutic strategies for CNS-related proteasomal dysfunction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (167 words)
Loss-of-function mutations in PSMB8/β5i and other components of the 20S proteasome result in multiorgan diseases, such as Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) syndrome. Neurocognitive dysfunction associated with CANDLE suggests that proteasomal mutations may impact neuronal function and development early in life. We generated cerebral organoids (COs) from induced pluripotent stem cells (iPSCs) made from patients with CANDLE. The COs from CANDLE iPSCs exhibited impaired neuronal development when compared with COs from healthy control iPSCs. Impaired neuronal maturation in CANDLE COs was correlated with increased polyamines, which were also elevated in CSF from patients with CANDLE. The proteasome-regulated ornithine decarboxylase (ODC), the rate limiting enzyme in polyamine biosynthesis, was elevated in CANDLE neurons. Inhibition of ODC reversed polyamine overproduction and repaired neuronal maturation in CANDLE COs, suggesting a potential therapeutic avenue for intervention. These findings demonstrate that dysfunction of the proteasome affects neuronal development through overproduction of polyamines via dysregulation of ODC and offer insight into potential therapeutic strategies for CNS-related proteasomal dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42550603 · DOI · PMC13626833
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The serotonin theory of depression: a systematic umbrella review of the evidence [4]
- Research article Effectiveness and safety of non-steroidal anti-inflammatory drugs and opioid treatment for knee and hip osteoarthritis: network meta-analysis [5]
- Research article Inhaled Reliever Therapies for Asthma: A Systematic Review and Meta-Analysis [6]
- Research article Association between Maternal Choline, Fetal Brain Development, and Child Neurocognition: Systematic Review and Meta-Analysis of Human Studies [7]
- Research article Drug treatment for panic disorder with or without agoraphobia: systematic review and network meta-analysis of randomised controlled trials [8]
- Research article Dopamine in major depressive disorder: A systematic review and meta-analysis of in vivo imaging studies [9]
References
- Chen C, He Q, Tombesi G, Napier E, Jaconelli M, Moreno-Ramos OA, et al.. Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons. . 2026. PMID 42660892 · DOI · PMC13522591
- van Veen S, Meeus E, Irala D, Sakers K, Liu Z, Savage J, et al.. ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis. . 2026. PMID 42680725 · DOI · PMC13534584
- Winkler CW, Schwarz B, Williams K, Alehashemi S, Foliaki ST, Snow J, et al.. Proteasome mutations associated with CANDLE syndrome cause altered neuronal development by dysregulating polyamine synthesis. . 2026. PMID 42550603 · DOI · PMC13626833
- Moncrieff J, Cooper RE, Stockmann T, Amendola S, Hengartner MP, Horowitz MA. The serotonin theory of depression: a systematic umbrella review of the evidence. Mol Psychiatry. 2023. PMID 35854107 · DOI · PMC10618090
- da Costa BR, Pereira TV, Saadat P, Rudnicki M, Iskander SM, Bodmer NS, et al.. Effectiveness and safety of non-steroidal anti-inflammatory drugs and opioid treatment for knee and hip osteoarthritis: network meta-analysis. BMJ. 2021. PMID 34642179 · DOI · PMC8506236
- Rayner DG, Ferri DM, Guyatt GH, O'Byrne PM, Brignardello-Petersen R, Foroutan F, et al.. Inhaled Reliever Therapies for Asthma: A Systematic Review and Meta-Analysis. JAMA. 2025. PMID 39465893 · DOI · PMC11519786
- Obeid R, Derbyshire E, Schön C. Association between Maternal Choline, Fetal Brain Development, and Child Neurocognition: Systematic Review and Meta-Analysis of Human Studies. Adv Nutr. 2022. PMID 36041182 · DOI · PMC9776654
- Chawla N, Anothaisintawee T, Charoenrungrueangchai K, Thaipisuttikul P, McKay GJ, Attia J, et al.. Drug treatment for panic disorder with or without agoraphobia: systematic review and network meta-analysis of randomised controlled trials. BMJ. 2022. PMID 35045991 · DOI · PMC8767458
- Mizuno Y, Ashok AH, Bhat BB, Jauhar S, Howes OD. Dopamine in major depressive disorder: A systematic review and meta-analysis of in vivo imaging studies. J Psychopharmacol. 2023. PMID 37811803 · DOI · PMC10647912
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.