Evidence map›Paper›PMID 25896831›Full record

ArticleBMC neurology2015

DRD and GRIN2B polymorphisms and their association with the development of impulse control behaviour among Malaysian Parkinson's disease patients.

Shahidee Zainal Abidin, Eng Liang Tan, Soon-Choy Chan, Ameerah Jaafar, Alex Xuen Lee, Mohd Hamdi Noor Abd Hamid, Nor Azian Abdul Murad, Nur Fadlina Pakarul Razy, Shahrul Azmin, Azlina Ahmad Annuar and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 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

14 authors at 4 institutions in 1 country.

Shahidee Zainal AbidinNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. shah.68000@gmail.com.
Eng Liang TanDepartment of Medicine, Universiti Kebangsaan Malaysia Medical Center, Bandar Tun Razak Cheras, 56000, Kuala Lumpur, Malaysia. drtanengliang@gmail.com.
Soon-Choy ChanPerdana University Graduate School of Medicine, Perdana University, 43400, Serdang, Selangor, Malaysia. soonchoyc@yahoo.com.
Ameerah JaafarNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. ameerah.jaafar@gmail.com.
Alex Xuen LeeNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. libk201@hotmail.com.
Mohd Hamdi Noor Abd HamidNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. medinoor89@gmail.com.
Nor Azian Abdul MuradUKM Medical Molecular Biology Institute, UKM Medical Center, Jalan Ya'acob Latiff, Bandar Tun Razak, Cheras, 56000, Kuala Lumpur, Malaysia. nor_azian@ppukm.ukm.edu.my.
Nur Fadlina Pakarul RazyUKM Medical Molecular Biology Institute, UKM Medical Center, Jalan Ya'acob Latiff, Bandar Tun Razak, Cheras, 56000, Kuala Lumpur, Malaysia. nurmp89@yahoo.com.
Shahrul AzminDepartment of Medicine, Universiti Kebangsaan Malaysia Medical Center, Bandar Tun Razak Cheras, 56000, Kuala Lumpur, Malaysia. shahrulazmin@hotmail.com.
Azlina Ahmad AnnuarDepartment of Biomedical Science, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia. azlina_aa@um.edu.my.
Shen Yang LimDepartment of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, Malaysia. limshenyang@ymail.com.
Pike-See CheahNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. cheahpikesee@upm.edu.my.
King-Hwa LingNeurobiology and Genetics Group, Genetic and Regenerative Medicine Research Centre, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400, Serdang, Selangor, Malaysia. lkh@upm.edu.my.
Norlinah Mohamed IbrahimDepartment of Medicine, Universiti Kebangsaan Malaysia Medical Center, Bandar Tun Razak Cheras, 56000, Kuala Lumpur, Malaysia. norlinah@ppukm.ukm.edu.my.
Universiti Putra Malaysia · MYUniversity Kebangsaan Malaysia Medical Centre · MYUniversity of Malaya · MYPerdana University · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImpulse control disorder (ICD) and behaviours (ICB) represent a group of behavioural disorders that have become increasingly recognised in Parkinson's disease (PD) patients who previously used dopaminergic medications, particularly dopamine agonists and levodopa. It has been suggested that these medications can lead to the development of ICB through the abnormal modulation of dopaminergic transmission and signalling in the mesocorticolimbic dopaminergic system. Several studies have reported an association between polymorphisms in the dopamine receptor (DRD) and N-methyl-D-aspartate 2B (GRIN2B) genes with the development of ICB in PD (PD-ICB) patients. Thus, this study aimed to investigate the association of selected polymorphisms within the DRD and GRIN2B genes with the development of ICB among PD patients using high resolution melt (HRM) analysis.

methodWe used high resolution melt (HRM) analysis to genotype 11 polymorphisms in 5 DRD genes [DRD1 (rs4532, rs4867798 and rs265981), DRD2 (ANKK1 rs1800497, rs104894220 and rs144999500), DRD3 (rs3732783 and rs6280), DRD4 (rs1800443), and DRD5 (rs144132215)] and 1 polymorphism in GRIN2B (rs7301328) in PD patients with (cases, n = 52) and without (controls, n = 39) ICB. Cases were obtained from two tertiary movement disorder centres [UKMMC (n = 9) and UMMC (n = 43)]. At both centres, the diagnosis of ICB was made using the QUIP questionnaire. Controls were recruited from PD patients who attended UKMMC and were found to be negative for ICB using the QUIP questionnaire.

resultsThe HRM analysis showed that 7 of 11 polymorphisms [DRD1 (rs4532, rs4867798, and rs265981), DRD2 (ANKK1 rs1800497), DRD3 (rs3732783 and rs6280), and GRIN2B (rs7301328)] exhibited a clear distinction between wild-type and variant alleles. Variants of DRD2/ANKK1 rs1800497 (OR = 3.77; 95% CI, 1.38-10.30; p = 0.0044), DRD1 rs4867798 (OR = 24.53; 95% CI, 1.68-357.28; p = 0.0054), DRD1 rs4532 (OR = 21.33; 95% CI, 1.97-230.64; p = 0.0024), and GRIN2B rs7301328 (OR = 25.07; 95% CI, 1.30-483.41; p = 0.0097) were found to be associated with an increased risk of developing ICB among PD patients.

conclusionOur findings suggest that polymorphisms in dopamine [DRD1 (rs4532 and rs4867798) and DRD2/ANKK1 rs1800497] and glutamate (GRIN2B rs7301328) receptor genes confer increased risk of ICB development among PD patients.

Indexed as

AdultAgedDisruptive, Impulse Control, and Conduct DisordersFemaleHumansMalaysiaMaleMiddle AgedParkinson DiseasePolymorphism, GeneticProtein Serine-Threonine KinasesReceptors, Dopamine D1Receptors, Dopamine D2Receptors, N-Methyl-D-AspartateANKK1 protein, humanDRD1 protein, humanDRD2 protein, humanNR2B NMDA receptorProtein Serine-Threonine KinasesReceptors, Dopamine D1Receptors, Dopamine D2Receptors, N-Methyl-D-Aspartate

Identifiers

PMID25896831
PMCPMC4417293
OpenAlexW1965033221

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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.