ArticlePerspectives in medicinal chemistry2014
Revisiting the monoamine hypothesis of depression: a new perspective.
Article in Perspectives in medicinal chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
15 citing papers in PubMed, 46 citations in OpenAlex.
- Validation of high-sensitivity assays to quantitate cerebrospinal fluid and serum β-galactosidase activity in patients with GM1-gangliosidosis.Molecular therapy. Methods & clinical development · 2024Article
- Depression clinical trials worldwide: a systematic analysis of the ICTRP and comparison with ClinicalTrials.gov.Translational psychiatry · 2024Review
- Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction.Brain sciences · 2024Review
- Pharmacotherapies Targeting GABA-Glutamate Neurotransmission for Treatment-Resistant Depression.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Folate and Its Significance in Depressive Disorders and Suicidality: A Comprehensive Narrative Review.Nutrients · 2023Review
- Efficacy, Tolerability, and Safety of Toludesvenlafaxine for the Treatment of Major Depressive Disorder-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2023Review
- St. John's wort (Hypericum perforatum) and depression: what happens to the neurotransmitter systems?Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Antidepressants in Alzheimer's Disease: A Focus on the Role of Mirtazapine.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Is NRXN1 Gene Expression an Important Marker of Treatment of Depressive Disorders? A Pilot Study.Journal of personalized medicine · 2021Article
- Is the Antidepressant Activity of Selective Serotonin Reuptake Inhibitors Mediated by Nicotinic Acetylcholine Receptors?Molecules (Basel, Switzerland) · 2021Review
- Skimmetin/osthole mitigates pain-depression dyad via inhibiting inflammatory and oxidative stress-mediated neurotransmitter dysregulation.Metabolic brain disease · 2021Article
- Recent Studies on Anti-Depressant Bioactive Substances in Selected Species from the GeneraPharmaceuticals (Basel, Switzerland) · 2019Review
- Social Defeat Stress (SDS) in Mice: Using Swiss Mice as Resident.Bio-protocol · 2019Article
- The monoaminergic pathways and inhibition of monoamine transporters interfere with the antidepressive-like behavior of ketamine.IBRO reports · 2018Article
- Blocking p38 Signaling Reduces the Activation of Pro-inflammatory Cytokines and the Phosphorylation of p38 in the Habenula and Reverses Depressive-Like Behaviors Induced by Neuroinflammation.Frontiers in pharmacology · 2018Article
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
As the incidence of depression increases, depression continues to inflict additional suffering to individuals and societies and better therapies are needed. Based on magnetic resonance spectroscopy and laboratory findings, gamma aminobutyric acid (GABA) may be intimately involved in the pathophysiology of depression. The isoelectric point of GABA (pI = 7.3) closely approximates the pH of cerebral spinal fluid (CSF). This may not be a trivial observation as it may explain preliminary spectrophotometric, enzymatic, and HPLC data that monoamine oxidase (MAO) deaminates GABA. Although MAO is known to deaminate substrates such as catecholamines, indoleamines, and long chain aliphatic amines all of which contain a lipophilic moiety, there is very good evidence to predict that a low concentration of a very lipophilic microspecies of GABA is present when GABA pI = pH as in the CSF. Inhibiting deamination of this microspecies of GABA could explain the well-established successful treatment of refractory depression with MAO inhibitors (MAOI) when other antidepressants that target exclusively levels of monoamines fail. If further experimental work can confirm these preliminary findings, physicians may consider revisiting the use of MAOI for the treatment of non-intractable depression because the potential benefits of increasing GABA as well as the monoamines may outweigh the risks associated with MAOI therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.