Evidence map›Paper›PMID 21971001›Full record

ReviewInternational review of neurobiology2011

Behavioral outcomes of monoamine oxidase deficiency: preclinical and clinical evidence.

Marco Bortolato, Jean C Shih

Open access · greenAbstract readReview
In one paragraph

Review in International review of neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 131 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Prominent Neuroprotective Potential of Indole-2-Pharmaceuticals (Basel, Switzerland) · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Individual and Combined Effect ofBehavioral sciences (Basel, Switzerland) · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Combined Antagonism of 5-HTPharmaceuticals (Basel, Switzerland) · 2022
    Article
  20. 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

2 authors at 1 institution in 1 country.

Marco BortolatoDepartment of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, California, USA.
Jean C Shih
University of Southern California · US

Funding

TWO TYPES OF MONOAMINE OXIDASER01MH039085 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SHIH, JEAN CHEN · 1985 to 2013
$2.0M
Interactions of MAO A with vulnerability factors for aggressionR21HD070611 · NICHD · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BORTOLATO, MARCO · 2011 to 2012
$434k
NICHD NIH HHS R21 HD070611NICHD NIH HHS R21HD070611NIMH NIH HHS R01 MH039085NIMH NIH HHS R01MH39085
6 · The paper itself

Abstract

Monoamine oxidase (MAO) isoenzymes A and B are mitochondrial-bound proteins, catalyzing the oxidative deamination of monoamine neurotransmitters as well as xenobiotic amines. Although they derive from a common ancestral progenitor gene, are located at X-chromosome and display 70% structural identity, their substrate preference, regional distribution, and physiological role are divergent. In fact, while MAO-A has high affinity for serotonin and norepinephrine, MAO-B primarily serves the catabolism of 2-phenylethylamine (PEA) and contributes to the degradation of other trace amines and dopamine. Convergent lines of preclinical and clinical evidence indicate that variations in MAO enzymatic activity--due to either genetic or environmental factors--can exert a profound influence on behavioral regulation and play a role in the pathophysiology of a large spectrum of mental and neurodegenerative disorders, ranging from antisocial personality disorder to Parkinson's disease. Over the past few years, numerous advances have been made in our understanding of the phenotypical variations associated with genetic polymorphisms and mutations of the genes encoding for both isoenzymes. In particular, novel findings on the phenotypes of MAO-deficient mice are highlighting novel potential implications of both isoenzymes in a broad spectrum of mental disorders, ranging from autism and anxiety to impulse-control disorders and ADHD. These studies will lay the foundation for future research on the neurobiological and neurochemical bases of these pathological conditions, as well as the role of gene × environment interactions in the vulnerability to several mental disorders.

Indexed as

AnimalsDisease Models, AnimalDopamineEvidence-Based MedicineGenetic Predisposition to DiseaseHumansMental DisordersMonoamine OxidaseNorepinephrineSerotoninDopamineMonoamine OxidaseNorepinephrineSerotonin

Identifiers

PMID21971001
PMCPMC3371272
OpenAlexW1526582769

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.