Evidence map›Paper›PMID 24532984›Full record

ArticleCurrent genomics2013

Polymorphism of the COMT, MAO, DAT, NET and 5-HTT Genes, and Biogenic Amines in Parkinson's Disease.

Jolanta Dorszewska, Michal Prendecki, Anna Oczkowska, Agata Rozycka, Margarita Lianeri, Wojciech Kozubski

Open access · bronzeAbstract read
In one paragraph

Article in Current genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Transcranial photobiomodulation ameliorates midbrain and striatum neurochemical impairments and behavioral deficits in reserpine-induced parkinsonism in rats.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023
    Article
  7. ComparativeFrontiers in neuroscience · 2023
    Article
  8. 5-HTInternational journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Parkinson's disease · 2022
    Article
  12. Review
  13. Interaction of silver nanoparticles with catecholBiochemistry and biophysics reports · 2021
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. The New *G29A and G1222A ofFrontiers in molecular neuroscience · 2018
    Article
  19. Article
  20. Catechol-O-methyltransferase association with hemoglobin A1c.Metabolism: clinical and experimental · 2016
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jolanta DorszewskaLaboratory of Neurobiology, Department of Neurology.
Michal PrendeckiLaboratory of Neurobiology, Department of Neurology.
Anna OczkowskaLaboratory of Neurobiology, Department of Neurology.
Agata RozyckaDepartment of Biochemistry and Molecular Biology.
Margarita LianeriDepartment of Biochemistry and Molecular Biology.
Wojciech KozubskiChair and Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland.
Poznan University of Medical Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epinephrine (E) and sympathetic nerve stimulation were described by Thomas Renton Elliott in 1905 for the first time. Dopamine (DA), norepinephrine (NE), E, and serotonin (5-HT) belong to the classic biogenic amines (or monoamines). Parkinson's disease (PD) is among the diseases in which it has been established that catecholamines may account for the neurodegeneration of central and peripheral catecholamine neural systems. PD is a chronic and progressive neurological disorder characterized by resting tremor, rigidity, and bradykinesia, affecting 2% of individuals above the age of 65 years. This disorder is a result of degeneration of DA-producing neurons of the substantia nigra and a significant loss of noradrenergic neurons in the locus coeruleus. In PD and other related neurodegerative diseases, catecholamines play the role of endogenous neurotoxins. Catechol-O-methyltransferase (COMT) and/or monoamine oxidase (MAO) catalyze the metabolism of monoamines. However, the monoamine transporters for DA, NE, and 5-HT namely DAT, NET, and SERT, respectively regulate the monoamine concentration. The metabolism of catecholamines and 5-HT involves common factors. Monoamine transporters represent targets for many pharmacological agents that affect brain function, including psychostimulators and antidepressants. In PD, polymorphisms of the COMT, MAO, DAT, NET, and 5- HTT genes may change the levels of biogenic amines and their metabolic products. The currently available therapies for PD improve the symptoms but do not halt the progression of the disease. The most effective treatment for PD patients is therapy with L-dopa. Combined therapy for PD involves a DA agonist and decarboxylase, MAOs and COMT inhibitors, and is the current optimal form of PD treatment maintaining monoamine balance.

Indexed as

COMTMAOMonoamine transporters polymorphismPD.

Identifiers

PMID24532984
PMCPMC3924247
OpenAlexW2080538807

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Registered trials

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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.