Chromosome 18p11

Indian J Psychiatry. 2013 Oct-Dec; 55(4): 371–375.

doi: 10.4103/0019-5545.120567

PMCID: PMC3890926

Chromosome 18p11.2 harbors susceptibility marker: D18S452, for bipolar

affective disorder

Mutahar Andrabi, Arshad Hussain, Fouzia Rashid, Sheikh Ozair Nissar, Idrees Ayoub Shah, Yasir Hasan Rather,

Waseem Hassan Ahangar, and Nazir Ahmad Dar

Department of Biochemistry, University of Kashmir, Jammu and Kashmir, India

Department of Psychiatry, Government Medical College, Srinagar, Jammu and Kashmir, India

Ram Manohar Lohia Hospital, New Delhi, India

Address for correspondence: Dr. Nazir Ahmad Dar, Department of Biochemistry, University of Kashmir, Hazratbal, Srinagar - 190 006,

Jammu and Kashmir, India. E-mail: [email protected]

Copyright : © Indian Journal of Psychiatry

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported,

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aim:

The aim of our study was to investigate whether the tandem repeat polymorphism in D18S452

microsatellite marker at locus 18p11.2 is a risk factor of bipolar affective disorder (BPAD) in Kashmiri

population.

Materials and Methods:

The repeat polymorphism in D18S452 was evaluated by polymerase chain reaction (PCR) analysis of

in 74 diagnosed BPAD patients and 74 controls subjects.

Results:

Tandem repeat (300 bp*) allele frequency was found to be 1.35% in controls and 8.108% in cases. The

tandem repeat (250 bp*) allele frequency was found to be in 91.89% in cases and 98.65% in controls.

The 252 bp/252 bp genotype was found to be present in 89.18% of cases and 98.64% of controls, the

300 bp/300 bp genotype in 5.40% of cases and 1.35% of controls and the 252 bp/300 bp variant in

5.40% of cases and none among the controls. Although the proportion of patients homozygous for

tandem repeat (300 bp/300 bp) was higher in cases than in controls, the difference was not

statistically significant when 252 bp/252 bp genotype was taken as reference (odds ratio

[OR]=4.4242; 95% confidence interval [CI] 0.4822-40.5924); P=0.1529). However, when the

frequency of heterozygous genotype (252 bp/300 bp) was compared with 252 bp/252 bp statistical

significance was observed (OR=8.0603; 95% CI 1.1112-58.4646; P=0.0383).

Conclusion:

This is the first study reporting a significant association between D18S452 maker with tandem repeat

polymorphism in heterozygous condition (252 bp/300 bp) and the development of BPAD in Kashmiri

population.

1 2

1

1

2

Chromosome 18p11.2 harbors susceptibility marker: D18S452, for bipolar... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890926/?report=printable

1 of 13 1/27/2014 5:56 PM

Keywords: Allele frequency, bipolar disorder, genetic locus, linkage study, tandem repeats

INTRODUCTION

Bipolar affective disorder (BPAD) is a major psychiatric problem with multifactorial etiology affecting

approximately 1% of population[1] and with all other bipolar spectrum disorders the prevalence will

be as high as 5%.[2] Bipolar disorder is the sixth leading cause of medical disability world-wide

among people 15-44 years of age and the estimated disability-adjusted life years of bipolar disorder

outrank all cancers and primary neurologic disorders.[3] It is equally prevalent in males and

females.[1] Family[4], twin[5] and adoption studies[6] have established that there is a multiple

genetic contribution to bipolar disorder and regarding the mechanism of transmission it is thought to

be consistent with the epistatic action of several genes with modest individual effect sizes.[7,8,9]

Although the limits of phenotypic expression are not known, the family studies suggest that bipolar I,

bipolar II recurrent major (unipolar) depression and schizoaffective disorder are part of a bipolar

spectrum.[4]

Since most psychiatric disorders show a complex mode of inheritance and transmission, the BPAD is

no more an exception. Without identifying the genes involved, the mechanism that underlies the

pathophysiology of bipolar disorder cannot be elucidated and therefore it is not possible to think of

any relief and treatment to victims of the disorder. In the direction of identifying causative genetic

markers, various linkage studies on large pedigree cohorts have led to reproducible identification of

several susceptibility loci. These include regions on chromosomes 4q, 12q, 13q, 18, 21q and

22q.[10,11,12,13,14,15,16,17,18] Various types of studies have identified chromosome 18p as a highly

potential and susceptible locus, which carry a few candidate genes for affective mood disorder.

[9,19,20,21,22,23,24,25,26] To investigate this region, further studies like case-control for a marker

D18S452 (locus 18p11.2) association with BPAD is warranted. Microsatellite marker D18S452

contains 26 dinucleotide repeats (cytosine-adenine (CA)) (http://genome.ucsc.edu/cgi-bin

/hgTracks?org=human). Though, the incidence of BPAD in Kashmir is significant yet there has been

no genetic study from Kashmir until date and the existence of any genetic predisposition in this

population remains totally untouched and unexplored. The molecular and epidemiological studies

remain open for research and seem to be promising in addressing the various queries of BPAD

etiology in this area. Therefore, the current work was undertaken to determine the structure of the

marker and evaluation of any association between the chromosomal susceptibility locus and BPAD.

MATERIALS AND METHODS

Study subjects

The BPAD seems very frequent and a serious health problem in Kashmir Valley. All people who suffer

from such ailments report to the Psychiatric Disease Hospital at Srinagar, Kashmir for diagnosis and

treatments. Patients were diagnosed with the disorder by psychiatrists who used diagnostics and

statistical manual IV based instrument called Mini-International Neuropsychiatric interview at the

hospital Srinagar. Those confirmed to have BPAD without having any comorbid condition such as

thyroid disorder, migraine, panic disorder and/or eating disorder were enrolled as cases. All the

diagnosed patients were included irrespective of any grade (whether or not on medication), age or

gender. Controls were recruited from the general medicine wards of Shri Maharaja Hari Singh

Hospital, Srinagar following the referral pattern of sex and age matched patients. None of the controls

had a personal or family history of any psychiatric disorder which was confirmed by a consultant

psychiatrist. The study was approved by the Departmental Research Committee of the Department of

Biochemistry University of Kashmir Srinagar and Board of Research Studies, University of Kashmir. A

total of 148 subjects were taken in this study out of which 74 were cases and rests 74 were controls.


2 of 13 1/27/2014 5:56 PM

After the detailed explanation of the study, all the subjects provided written informed consent.

Sample collection and deoxyribonucleic acid extraction

Around (3 ml) peripheral blood was collected from each subject in sterilized plastic vials containing

ethylenediaminetetraacetic acid (0.5M; pH-8.0) and stored at −20°C for further analysis. DNA was

isolated by a standard phenol-chloroform extraction method.[27] The quality of the genomic DNA

was examined by gel electrophoresis using 0.8% agarose gel. The quantity of the DNA was estimated

by making appropriate dilutions to determine the optical density at 260 nm and 280 nm by double

beam spectrophotometer (spectron 2206) and the concentration was determined using equation:

DNA (μg/ml) = A × 50 × dilution factor

The ratio of A /A was calculated and the DNA samples for which the ratio was 1.7-1.9 were

considered for the future use.

Genotyping

Polymerase chain reaction (PCR) was performed in total volume of 25 μl. The PCR reactions mixture

composed of 50-150 ng genomic DNA; 0.2 mM dNTPs; 0.4 pmoles/μl of each primer; 1.5 U of Taq

polymerase in 1 × PCR buffer and 200 nM each of the forward primer: 5′-TGG GGC ATA CAT AGT

GCA AA-3′ and reverse primer: 5′-AGG CCT TTT GCT AGT TGG GT-3′. PCR cycling parameters were

a 4 min denaturation cycle at 94°C and 34 cycles of the following: 94°C for 45 s 59.2°C for 30 s and

72°C for 45 s and a final extension at 72°C for 5 min. The amplified products were visualized on a 3%

agarose gel using ethidium bromide.

Statistical analysis

The χ test was used for the comparison of the allele and genotype frequency between the cases and

controls. The distribution of the genotype frequencies in both groups did not deviate from the Hardy-

Weinberg equilibrium. The odds ratio (OR) were calculated as estimates of relative risk for disease

and 95% confidence intervals (CIs) were calculated for all observed allele frequencies. P < 0.05 was

considered as statistically significant. The SPSS statistical software package (version 11.5 SPSS

Chicago IL) was used for the statistical analysis.

RESULTS

Genotypic and allelic frequencies

In the present study, 74 BPAD cases and 74 matched controls belonging to the Kashmir division were

analyzed for D18S452 polymorphism. We found six types of alleles corresponding to base pair size:

200 bp; between 200 and 252 bp; 252 bp; between 252 and 300 bp; 300 bp; between 300 and 350

bp. On analyzing the allelic frequency two main groups turned out – rare and frequent genotype with

respect to the locus. Only two subjects (one from each case [1.35%] and control group [1.35%]) had

allelotype corresponding to 200 bp. There was just one case representation from each 200 bp to 250

bp; between 252 bp and 300 bp and 300-350 bp alleotypes. A single subject had from controls had

300 bp allelotype. 63 patients (87.16%) and 72 controls (97.297%) had allelotype corresponding to

252 bp. Seven patients (7.43%) had allelotype corresponding to 300 bp [Figure 1 and Table 1].

Since the alleles corresponding to bp size 200, between 200 and 252 bp, between 252 and 300 bp,

between 300 and 350 bp were very rare we considered them as minor alleles and grouped them under

two main classes of major alleles; 252 bp* (containing alleles of size up to 252 bp) and 300 bp*

(containing alleles corresponding to more than 252 bp).

260

260 280

2


3 of 13 1/27/2014 5:56 PM

The tandem repeat (300 bp*) allele frequency was found to be 1.35% in the controls and 8.108% in

cases. The tandem repeat (252 bp*) allele frequency was found to be 91.89% in cases and 98.65% in

controls. The 252 bp/252 bp genotype was found to be present in 89.18% of the cases and 98.64% of

the controls the 252 bp/300 bp variant in 5.40% of the cases and none among the controls and the

300 bp/300 bp genotype in 5.40% of cases and 1.35% of controls [Tables 2 and 3].

It was observed that although the proportion of individuals who were homozygous for the tandem

repeat (300 bp/300 bp) was higher in cases than in controls the difference was not statistically

significant when using 252 bp/252 bp genotype as a reference (OR=4.4242; 95% CI 0.4822-40.5924);

P=0.1529). However, it was observed that the frequency of the heterozygous genotype (252 bp/300

bp) when compared with 252 bp/252 bp showed statistical significance (OR=8.0603; 95% CI

1.1112-58.4646; P=0.0383).

General characteristics of the study population

Various general characteristics of the study population like mean age gender dwelling and socio-

economic status were analyzed between cases and controls, but no statistical significance was

observed [Table 4].

D18S452 genotypes and clinic pathological variables

Table 5 shows the genotype frequencies of D18S452 polymorphism relating to age gender dwelling

socio-economic status BPAD subtype family history and age at onset. No statistical significance was

attained.

DISCUSSION

Overall results suggests that there is a significant association between D18S452 maker with tandem

repeat polymorphism in heterozygous condition (252 bp/300 bp) and the development of BPAD in

Kashmiri population. The susceptible marker was not explored earlier and its analysis reveals

important information regarding the types and frequency of alleles. On the basis of the frequency in

the subject, the identified six alleles can be sorted into two categories – frequent and rare one. The

allele size determined by the number of dinucleotide (CA) ranged from 200 to 350 bp. The allele 252

bp was predominant in both cases and controls but the 252/300 bp allele was found only in cases

(5.40%) and importantly in none of the controls. Most of the alleles are more or less similar in the

cases and a significant association between tandem repeat polymorphism in heterozygous condition

(252 bp/300 bp) and the development of BPAD in Kashmiri population turns out. There can be many

possible ways by which the genotype can contribute to the development of BPAD. It can influence at

organizational level of chromosome, its accessibility to various factors and regulatory proteins.

Chromosomal locus 18p11.2 harbors many candidate genes like NAPG[28] GNAL[29] NDUFV2[24]

and VAPA.[30] It may be possible that this marker is directly or indirectly involved in the regulation

of neighboring genes. It is also possible that this locus may be in linkage disequilibrium with other

genes.

The result of our study further adds to the data from several other studies which have also shown an

association between chromosomal locus 18p and the risk of BPAD. In one study, chromosome 18p has

been shown to be a highly susceptible locus for the affective mood disorder[19] Further, support for

this region comes from evidence suggesting potential overlap with schizophrenia; Schwab et al.,

reported a possible schizophrenia locus on 18p11.2 and demonstrated that evidence for linkage in

these schizophrenia families increased when individuals with affective diagnoses were also included

in the analysis.[31] A susceptibility gene on chromosome 18 and a parent-of-origin effect have been

suggested for BPAD.[13] In studies of persons with chromosome 18p - deletions, there have been


4 of 13 1/27/2014 5:56 PM

reports of paranoid psychosis, depression and subclinical obsessive compulsive disorder.[32] In

studies of 18qsyndromes, there have also been individual reports of violent/aggressive behaviors.[33]

There is one report of a behavioral/psychiatric problem in a case of chromosome 18p tetrasomy; an

individual who had a history of aggressive, self-injurious and destructive behavior.[34] There is also a

report of a family with a pericentric inversion of chromosome 18, in which three individuals (two with

dup (18p)/del (18q) and one with dup (18q)/del (18p), all displayed depression and anxiety.[35]

We also tried to correlate many clinico-phenotypic conditions like BPAD subtype, age at on set and

other general characteristics with D18S452 polymorphism, but we could not find any significant

association [Table 5].

It may pave a way to understand the development of the BPAD. It can serve us a lead from where we

can further explore the biological significance of the identified genotypes and their association with

BPAD. The management and therapeutic targets may be identified by designing additional studies on

such findings. Bigger sample size, biological characterization of the genotypes in the susceptible and

sequencing of such repetitive DNA sequences by modern sequencing technology seems inevitable for

further substantiation of our findings.

CONCLUSION

Overall our study suggests that there is a significant association between tandem repeat

polymorphism in heterozygous condition (252 bp/300 bp) and the development of BPAD in Kashmiri

population. We identified the alleles of the marker D18S452 most of which are a frequent. There are

various possible ways by which the 252/300 bp genotype can influence the development of the BPAD.

Further studies are required for better understanding of the roles of the genotypes in BAPD

pathophysiology.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

REFERENCES

1. Goodwin FK, Jamison KR. New York: Oxford University Press; 1990. Manic Depressive Illness.

2. Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE. Lifetime prevalence and

age-of-onset distributions of DSM-IV disorders in the national comorbidity survey replication. Arch

Gen Psychiatry. 2005;62:593–602. [PubMed: 15939837]

3. Rodgers A, Ezzati M, Vander Hoorn S, Lopez AD, Lin RB, Murray CJ, et al. Distribution of major

health risks: Findings from the global burden of disease study. PLoS Med. 2004;1:E27.

[PMCID: PMC523844] [PubMed: 15526049]

4. Gershon ES, Hamovit J, Guroff JJ, Dibble E, Leckman JF, Sceery W, et al. A family study of

schizoaffective, bipolar I, bipolar II, unipolar, and normal control probands. Arch Gen Psychiatry.

1982;39:1157–67. [PubMed: 7125846]

5. Bertelsen A, Harvald B, Hauge M. A Danish twin study of manic-depressive disorders. Br J

Psychiatry. 1977;130:330–51. [PubMed: 558030]

6. Mendlewicz J, Rainer JD. Adoption study supporting genetic transmission in manic – Depressive

illness. Nature. 1977;268:327–9. [PubMed: 887159]

7. Risch N, Botstein D. A manic depressive history. Nat Genet. 1996;12:351–3. [PubMed: 8630482]


5 of 13 1/27/2014 5:56 PM

8. Berrettini WH. Genetics of psychiatric disease. Annu Rev Med. 2000;51:465–79.

[PubMed: 10774477]

9. Bennett P, Segurado R, Jones I, Bort S, McCandless F, Lambert D, et al. The wellcome trust

UK-Irish bipolar affective disorder sibling-pair genome screen: First stage report. Mol Psychiatry.

2002;7:189–200. [PubMed: 11840312]

10. Craddock N, Owen M, Burge S, Kurian B, Thomas P, McGuffin P. Familial cosegregation of major

affective disorder and Darier's disease (keratosis follicularis) Br J Psychiatry. 1994;164:355–8.

[PubMed: 8199789]

11. Berrettini WH, Ferraro TN, Goldin LR, Weeks DE, Detera-Wadleigh S, Nurnberger JI, Jr, et al.

Chromosome 18 DNA markers and manic-depressive illness: Evidence for a susceptibility gene. Proc

Natl Acad Sci U S A. 1994;91:5918–21. [PMCID: PMC44108] [PubMed: 8016089]

12. Straub RE, Lehner T, Luo Y, Loth JE, Shao W, Sharpe L, et al. A possible vulnerability locus for

bipolar affective disorder on chromosome 21q22.3. Nat Genet. 1994;8:291–6. [PubMed: 7874172]

13. Stine OC, Xu J, Koskela R, McMahon FJ, Gschwend M, Friddle C, et al. Evidence for linkage of

bipolar disorder to chromosome 18 with a parent-of-origin effect. Am J Hum Genet. 1995;57:1384–94.

[PMCID: PMC1801428] [PubMed: 8533768]

14. Blackwood DH, He L, Morris SW, McLean A, Whitton C, Thomson M, et al. A locus for bipolar

affective disorder on chromosome 4p. Nat Genet. 1996;12:427–30. [PubMed: 8630499]

15. Adams LJ, Mitchell PB, Fielder SL, Rosso A, Donald JA, Schofield PR. A susceptibility locus for

bipolar affective disorder on chromosome 4q35. Am J Hum Genet. 1998;62:1084–91.

[PMCID: PMC1377083] [PubMed: 9545396]

16. Craddock N, Jones I. Genetics of bipolar disorder. J Med Genet. 1999;36:585–94.

[PMCID: PMC1762980] [PubMed: 10465107]

17. Friddle C, Koskela R, Ranade K, Hebert J, Cargill M, Clark CD, et al. Full-genome scan for linkage

in 50 families segregating the bipolar affective disease phenotype. Am J Hum Genet.

2000;66:205–15. [PMCID: PMC1288327] [PubMed: 10631152]

18. Badenhop RF, Moses MJ, Scimone A, Mitchell PB, Ewen-White KR, Rosso A, et al. A genome

screen of 13 bipolar affective disorder pedigrees provides evidence for susceptibility loci on

chromosome 3 as well as chromosomes 9, 13 and 19. Mol Psychiatry. 2002;7:851–9.

[PubMed: 12232778]

19. Ginns EI, St Jean P, Philibert RA, Galdzicka M, Damschroder-Williams P, Thiel B, et al. A

genome-wide search for chromosomal loci linked to mental health wellness in relatives at high risk

for bipolar affective disorder among the old order Amish. Proc Natl Acad Sci U S A. 1998;95:15531–6.

[PMCID: PMC28077] [PubMed: 9861003]

20. Bassett AS. Chromosomal aberrations and schizophrenia. Autosomes. Br J Psychiatry.

1992;161:323–34. [PMCID: PMC3188307] [PubMed: 1393302]

21. McInnes LA, Escamilla MA, Service SK, Reus VI, Leon P, Silva S, et al. A complete genome screen

for genes predisposing to severe bipolar disorder in two Costa Rican pedigrees. Proc Natl Acad Sci U S

A. 1996;93:13060–5. [PMCID: PMC24046] [PubMed: 8917544]

22. Mukherjee O, Meera P, Ghosh S, Kubendran S, Kiran K, Manjunath KR, et al. Evidence of linkage

and association on 18p11.2 for psychosis. Am J Med Genet B Neuropsychiatr Genet.

2006;141B:868–73. [PubMed: 16941653]


6 of 13 1/27/2014 5:56 PM

23. Chavarría-Siles I, Walss-Bass C, Quezada P, Dassori A, Contreras S, Medina R, et al.

TGFB-induced factor (TGIF): A candidate gene for psychosis on chromosome 18p. Mol Psychiatry.

2007;12:1033–41. [PubMed: 17440433]

24. Washizuka S, Iwamoto K, Kakiuchi C, Bundo M, Kato T. Expression of mitochondrial complex I

subunit gene NDUFV2 in the lymphoblastoid cells derived from patients with bipolar disorder and

schizophrenia. Neurosci Res. 2009;63:199–204. [PubMed: 19135101]

25. Li X, Zhang J, Wang Y, Ji J, Yang F, Wan C, et al. Association study on the NAPG gene and

bipolar disorder in the Chinese Han population. Neurosci Lett. 2009;457:159–62.

[PubMed: 19429185]

26. Washizuka S, Iwamoto K, Kazuno AA, Kakiuchi C, Mori K, Kametani M, et al. Association of

mitochondrial complex I subunit gene NDUFV2 at 18p11 with bipolar disorder in Japanese and the

National Institute of Mental Health Pedigrees. Biol Psychiatry. 2004;56:483–9. [PubMed: 15450783]

27. Blin N, Stafford DW. A general method for isolation of high molecular weight DNA from

eukaryotes. Nucleic Acids Res. 1976;3:2303–8. [PMCID: PMC343085] [PubMed: 987581]

28. Weller AE, Dahl JP, Lohoff FW, Ferraro TN, Berrettini WH. Analysis of variations in the NAPG

gene on chromosome 18p11 in bipolar disorder. Psychiatr Genet. 2006;16:3–8. [PubMed: 16395123]

29. Tsiouris SJ, Breschel TS, Xu J, McInnis MG, McMahon FJ. Linkage disequilibrium analysis of

G-olf alpha (GNAL) in bipolar affective disorder. Am J Med Genet. 1996;67:491–4.

[PubMed: 8886169]

30. Lohoff FW, Weller AE, Bloch PJ, Nall AH, Ferraro TN, Berrettini WH. Association between

polymorphisms in the vesicle-associated membrane protein-associated protein A (VAPA) gene on

chromosome 18p and bipolar disorder. J Neural Transm. 2008;115:1339–45. [PubMed: 18665321]

31. Schwab SG, Hallmayer J, Lerer B, Albus M, Borrmann M, Hönig S, et al. Support for a

chromosome 18p locus conferring susceptibility to functional psychoses in families with

schizophrenia, by association and linkage analysis. Am J Hum Genet. 1998;63:1139–52.

[PMCID: PMC1377479] [PubMed: 9758604]

32. Babovic-Vuksanovic D, Jenkins SC, Ensenauer R, Newman DC, Jalal SM. Subtelomeric deletion of

18p in an adult with paranoid schizophrenia and mental retardation. Am J Med Genet A.

2004;124A:318–22. [PubMed: 14708108]

33. Mahr RN, Moberg PJ, Overhauser J, Strathdee G, Kamholz J, Loevner LA, et al. Neuropsychiatry

of 18q- syndrome. Am J Med Genet. 1996;67:172–8. [PubMed: 8723044]

34. Swingle HM, Ringdahl J, Mraz R, Patil S, Keppler-Noreuil K. Behavioral management of a

long-term survivor with tetrasomy 18p. Am J Med Genet A. 2006;140:276–80. [PubMed: 16411237]

35. Vermeulen SJ, Speleman F, Vanransbeeck L, Verspeet J, Menten B, Verschraegen-Spae MR, et al.

Familial pericentric inversion of chromosome 18: Behavioral abnormalities in patients heterozygous

for either the dup (18p)/del (18q) or dup (18q)/del (18p) recombinant chromosome. Eur J Hum

Genet. 2005;13:52–8. [PubMed: 15470365]

Figures and Tables


7 of 13 1/27/2014 5:56 PM

Figure 1

Representative gel picture showing 3% agarose gel electrophoresis after polymerase chain reaction lane 1 represents

negative control; lane 2 and 4 represents homozygous condition (300 bp); lane 3 represents homozygous condition

(252-300 bp) lane 5 represents homozygous condition (200 bp); lane 6 represents heterozygous condition (252

bp/300-350 bp); lane 7-10, 12 and 14 represents homozygous condition (252 bp); lane 13 represents homozygous

condition (200-252 bp). Lane 11 represents 50 bp ladders


8 of 13 1/27/2014 5:56 PM

Table 1

Frequency of D18S452 alleles (major and minor alleles) in the study population


9 of 13 1/27/2014 5:56 PM

Table 2

Frequency of D18S452 alleles (after grouping) in the study population


10 of 13 1/27/2014 5:56 PM

Table 3

Genotypic frequencies of D18S452 polymorphism in the study population


11 of 13 1/27/2014 5:56 PM

Table 4

General characteristics of the study population


12 of 13 1/27/2014 5:56 PM

Table 5

Correlation between D18S452 polymorphism and clinico-pathological characteristics

Articles from Indian Journal of Psychiatry are provided here courtesy of Medknow Publications


13 of 13 1/27/2014 5:56 PM

Documents

Chromosome 18p11