Evidence map›Paper›PMID 28982350›Full record

ArticleBMC medical genetics2017

Pilot study indicate role of preferentially transmitted monoamine oxidase gene variants in behavioral problems of male ADHD probands.

Arijit Karmakar, Rishov Goswami, Tanusree Saha, Subhamita Maitra, Anirban Roychowdhury, Chinmay Kumar Panda, Swagata Sinha, Anirban Ray, Kochupurackal P Mohanakumar, Usha Rajamma and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 5 institutions in 1 country.

Arijit KarmakarManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Rishov GoswamiManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Tanusree SahaManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Subhamita MaitraManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Anirban RoychowdhuryDepartment of Oncogene Regulation, Chittaranjan National Cancer Institute, 37 S.P. Mukherjee Road, Kolkata, 700 026, India.
Chinmay Kumar PandaDepartment of Oncogene Regulation, Chittaranjan National Cancer Institute, 37 S.P. Mukherjee Road, Kolkata, 700 026, India.
Swagata SinhaManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Anirban RayDepartment of Psychiatry, Institute of Post Graduate Medical Education & Research, Kolkata, 700 020, India.
Kochupurackal P MohanakumarCSIR-Indian Institute of Chemical Biology, Laboratory of Clinical & Experimental Neurosciences, Cell Biology & Physiology Division, 4, Raja S.C. Mullick Road, Kolkata, 700 032, India.
Usha RajammaManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India.
Kanchan MukhopadhyayManovikas Biomedical Research and Diagnostic Centre, 482, Madudah, Plot: I-24, Sector-J, Manovikas Kendra, E.M. Bypass, Kolkata, 700 107, India. kanchanmvk@yahoo.com.ORCID 0000-0002-4317-7522
Manovikas Kendra Rehabilitation and Research Institute · INChittaranjan National Cancer Institute · INIndian Institute of Chemical Biology · INInstitute of Post Graduate Medical Education and Research · INMahatma Gandhi University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAttention deficit hyperactivity disorder (ADHD) is an etiologically complex childhood onset neurobehavioral disorder characterized by age-inappropriate inattention, hyperactivity, and impulsivity. Symptom severity varies widely and boys are diagnosed more frequently than girls. ADHD probands were reported to have abnormal transmissions of dopamine, serotonin, and/or noradrenaline. Monoamine oxidase A (MAOA) and B (MAOB), mitochondrial outer membrane bound two isoenzymes, mediate degradation of these neurotransmitters and thus regulating their circulating levels. Case-control analyses in different populations, including Indians, suggested involvement of MAOA and MAOB genes in the etiology of ADHD. Due to high heritability rate of ADHD, we tested familial transmission of MAOA and MAOB variants to ADHD probands in 190 nuclear families having ADHD probands from Indo-Caucasoid ethnicity.

methodsSubjects were recruited following the Diagnostic and Statistical Manual of Mental Disorders-4th edition (DSM-IV). Appropriate scales were used for measuring the behavioral traits in probands. Genotyping was performed through PCR-based amplification of target sites followed by DNA-sequencing and/or gel-electrophoresis. Data obtained were analyzed by family based statistical methods.

resultsOut of 58 variants present in the analyzed sites only 15 were found to be polymorphic (30 bp-uVNTR, rs5906883, rs1465107, rs1465108, rs5905809, rs5906957, rs6323, rs1137070 from MAOA and rs4824562, rs56220155, rs2283728, rs2283727, rs3027441, rs6324, rs3027440 from MAOB). Statistically significant maternal transmission of alleles to male probands was observed for MAOA rs5905809 'G' (p = 0.04), rs5906957 'A' (p = 0.04), rs6323 'G' (p = 0.0001) and MAOB rs56220155 'A' (p = 0.002), rs2283728 'C' (p = 0.0008), rs2283727 'C' (p = 0.0008), rs3027441 'T' (p = 0.003), rs6324 'C' (p = 0.003), rs3027440 'T' (p = 0.0002). Significantly preferential maternal transmissions of different haplotype combinations to male probands were also noticed (p < 0.05), while female probands did not reveal such transmission bias. Behavioral traits of male probands exhibited significant association with gene variants. Age of the mother at pregnancy also revealed association with risk variants of male probands.

conclusionsIt may be inferred that the MAOA and MAOB variants may contribute to the etiology of ADHD in the Indo-Caucasoid population and could be responsible for higher occurrence of ADHD in the boys.

Indexed as

Genetic Predisposition to DiseaseAllelesAttention Deficit Disorder with HyperactivityDiagnostic and Statistical Manual of Mental DisordersFemaleGenotyping TechniquesHaplotypesHumansMaleMonoamine OxidasePilot ProjectsProblem BehaviorWhite PeopleMonoamine Oxidasemonoamine oxidase A, humanADHDBehavioral traitGenotypingIndo-Caucasoid populationLinkage disequilibriumMAOAMAOBMaternal ageMaternal transmission

Identifiers

PMID28982350
PMCPMC5629801
OpenAlexW2761327447

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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.