ReviewMolecular psychiatry2016
The significance of selegiline/(-)-deprenyl after 50 years in research and therapy (1965-2015).
Review in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- L-deprenyl extends lifespan across mammalian species: A meta-analysis of 22 longevity experiments.Ageing research reviews · 2025Pooled it
- Stromal-derived MAOB promotes prostate cancer growth and progression.Science advances · 2024Article
- A sustainable avenue for the synthesis of propargylamines and benzofurans using a Cu-functionalized MIL-101(Cr) as a reusable heterogeneous catalyst.Scientific reports · 2023Article
- Multiomic Analyses of Dopaminergic Neurons Isolated from Human Substantia Nigra in Parkinson's Disease: A Descriptive and Exploratory Study.Cellular and molecular neurobiology · 2022Article
- Expression of neurotrophic factor genes by human adipose stem cells post-induction by deprenyl.Anatomy & cell biology · 2021Article
- Chronic Oral Selegiline Treatment Mitigates Age-Related Hearing Loss in BALB/c Mice.International journal of molecular sciences · 2021Article
- Newly Synthesized Fluorinated Cinnamylpiperazines Possessing Low In Vitro MAO-B Binding.Molecules (Basel, Switzerland) · 2020Article
- Multi-parameter Behavioral Phenotyping of the MPP+ Model of Parkinson's Disease in Zebrafish.Frontiers in behavioral neuroscience · 2020Article
- Different Generations of Type-B Monoamine Oxidase Inhibitors in Parkinson's Disease: From Bench to Bedside.Current neuropharmacology · 2019Review
- Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders.Brain : a journal of neurology · 2017Article
- Presentations to an urban emergency department in Bern, Switzerland associated with acute recreational drug toxicity.Scandinavian journal of trauma, resuscitation and emergency medicine · 2017Article
- Effects on Sperms' Quality of Selegiline in Aged Rats.The open medicinal chemistry journal · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deprenyl/Selegiline (DEP), created by Joseph Knoll in the 1960s, registered in more than 60 countries to treat Parkinson's disease, Alzheimer's disease, major depressive disorder; and used as an anti-aging drug, achieved its place in research and therapy as the first selective inhibitor of B-type monoamine oxidase (MAO-B). The demonstration that the DEP analog (-)-1-phenyl-2-propylaminopentane devoid of MAO inhibitory property, enhanced like DEP the activity of the catecholaminergic brain engine revealed that this effect is unrelated to the selective inhibition of MAO-B. β-Phenylethylamine (PEA), the important trace-amine in the mammalian brain, is known to be a releaser of catecholamines. Amphetamine and methamphetamine, the best known synthetic PEA derivatives are also releasers of catecholamines like their parent compound. DEP is a unique synthetic PEA derivative devoid of the catecholamine releasing property. As the releasing effect conceals the catecholaminergic activity enhancer (CAE) effect, it remained undiscovered until DEP uncovered that PEA is a natural CAE substance; and only releases catecholamines in high concentration. Discovering that tryptamine is a natural enhancer of catecholaminergic and serotonergic neurons catalyzed the development of R-(-)-1-(benzofuran-2-yl)-2-propylaminopentane (BPAP); the most potent and selective enhancer substance, and it exerts its enhancer effect in 0.0001 mg kg
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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.