US 2013 0072391A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0072391 A1 KANG et al. (43) Pub. Date: Mar. 21, 2013

(54) COMPOSITION, KIT, AND METHOD FOR Publication Classification DAGNOSINGADHD RISK (51) Int. Cl. C40B 30/04 (2006.01) C40B 40/06 (2006.01) (75) Inventors: Changwon KANG, Daejeon (KR): C7H 2L/04 (2006.01) Eunjoon KIM, Daejeon (KR); Jae-Won GOIN 2L/64 (2006.01) Kim, Seoul (KR); Eunjin KIM, Daejeon (52) U.S. Cl. (KR); Hyejung WON, Daejeon (KR): USPC ...... 506/9: 436/501; 435/6.11:506/16; Won MAH, Daejeon (KR); Soo-Churl 536/23.5 CHO, Seoul (KR) (57) ABSTRACT The following disclosure relates to a technology of genotyp (73) Assignees: SNU R&DB FOUNDATION, Seoul ing a particular single nucleotide polymorphism (SNP) hav ing significant association with attention deficit hyperactivity (KR); KOREA ADVANCED disorder (ADHD) and using the SNP genotypes for predicting INSTITUTE OF SCIENCE AND the risk of ADHD. The present invention relates to providing TECHNOLOGY, Daejeon (KR) a method of predicting ADHD risk by identifying the nucle otide of rS5508181 SNP in GIT1, which is C or T at the 24926.101st residue on human 17, and a linkage (21) Appl. No.: 13/446,711 disequilibrium block harboring rs5508181. Further, the present invention relates to a composition for diagnosing ADHD risk, including a probe for detecting the SNP or a primer for amplifying the chromosomal region, and a diag (22) Filed: Apr. 13, 2012 nosing kit having the probe immobilized on a Surface thereof. Therefore, the method, the composition and the kit for diag (30) Foreign Application Priority Data nosing ADHD risk according to the following disclosure are useful technologies that can conveniently classify riskgroups Sep. 20, 2011 (KR) ...... 10-2011-0094918 for ADHD at high sensitivity. US 2013/0072391 A1 Mar. 21, 2013

COMPOSITION, KIT, AND METHOD FOR tors (Premont R. T. et al., Proc. Natl. Acad. Sci. USA 95: DAGNOSINGADHD RISK 14082-14087, 1998; Claig A. et al., Proc. Natl. Acad. Sci. USA97: 1119-1124, 2000). It has been known that, in rodent CROSS-REFERENCE TO RELATED brains, GIT1 affects various nerve functions, including Syn APPLICATIONS apse formation, and in particular, Git1-null mice (Gitl) showed impaired dendritic outgrowth, reduced spine density, 0001. This application claims priority under 35 U.S.C. impaired fear responses and reduced adaptation to new and S119 to Korean Patent Application No. 10-2011-0094918, changing environments (Menon P. et al., Brain Res 1317:218 filed on Sep. 20, 2011 in the Korean Intellectual Property 226, 2010; Schmalzigauget al., Neurosci. Lett. 458:79-93, Office, the disclosure of which is incorporated herein by 2009). Therefore, the present inventors noticed these func reference in its entirety. tions of GIT1, and analyzed the association of the GIT1 with ADHD susceptibility through a patient-control study, TECHNICAL FIELD and as a result, first found that a single nucleotide polymor 0002 The following disclosure relates to a technology of phism (SNP) located in an intron of the GIT1 gene is signifi typing a particular single nucleotide polymorphism (SNP) cantly associated with ADHD susceptibility. having significant association with attention deficit hyperac 0006. The SNP is a polymorphism with high frequency, tivity disorder (ADHD) and using the SNP genotypes as a which is present on the at a ratio of 0.1% marker to predict the risk of ADHD, and more particularly to (about 1 nucleotide per 1000 nucleotides). SNP refers to a a composition for diagnosing ADHD risk, including a poly position in a genome where one nucleotide (or base pair) is nucleotide having CorT nucleotide at the 24926.101st residue substituted with another nucleotide (or base pair), for on human and a method of predicting the risk example, one genome has a C nucleotide while another of ADHD by identifying the nucleotide of rs5508181 SNP in genome has T nucleotide. In addition, an individual may have the GIT1 gene. Further, the present invention relates to a only one allele in both copies of autosomal composition for diagnosing the risk of ADHD, including a (homozygous genotype, for example, T/T), while another probe for typing the SNP or a primer for amplifying the individual may have two differentalleles in the two autosome chromosomal region, and a diagnosing kit having the probe copies (heterozygous genotype, for example, C(T). This immobilized on a surface thereof. variation of one nucleotide may cause synthesis of variant 0003. Therefore, the method of predicting, and the com amino acids due to variation of codon (missense mutation) or position and the kit for diagnosing according to the following synthesis of a truncated protein due to generation of a stop disclosure are useful technologies that can conveniently clas codon (nonsense mutation). Therefore, it is obvious that pres sify risk groups for ADHD at high sensitivity, so as to prevent ence or absence of the polymorphism is associated with sev in advance or early detect the risk groups. eral disorders (Patent Document 1; Korean Patent Registra tion No. 10-1012601, Patent Document 2: Korean Patent BACKGROUND Registration No. 10-1057262), and it has been strongly rec ognized that it is important to accurately determine presence 0004 Attention deficit hyperactivity disorder (ADHD) is and absence of polymorphism (SNP typing), for the purpose more common in childhood than adulthood, and is referred to of diagnosis, genetic screening or treatment, or the like. In as a state characterized by persistentinattention, hyperactiv addition, SNP is a polymorphism maker that is used when ity, and impulsivity. When these symptoms are ignored with related to genetic predisposition to disorders or medi out being treated, they lead to continuous difficulties in lives cine reactivity are searched for, and receives attention as throughout childhood, and in many cases, these symptoms important genetic information for tailor-made medical treat may linger even during the adolescence and adulthood (Bar ment. key R. A., Attention deficit hyperactivity disorder. A Hand 0007. Therefore, the present inventors identified that the book for Diagnosis and Treatment, Guilford, N.Y., 2006). SNP located in an intron of the GIT1 gene can be used to 0005. It has been reported that neurochemical factors, predict genetic disposition for ADHD, and completed the genetic factors, and environmental factors are the causes of ADHD. Particularly, an association between dopamine, present invention. which is a neurotransmitter, and ADHD has been known CITED DOCUMENTS (Swanson J M et al., Neuropsychol. Rev. 17:39-59, 2007). Many ADHD susceptibility loci identified by genome linkage Patent Documents or association studies do not contain dopamine-related genes Such as dopamine carriers (Franke B. et al., Hum. Genet. 0008 (Patent Document 1) Korean Patent No. 126:13-50, 2009). Therefore, various genetic predispositions 10-10 12601: Composition for Predicting the Risk of are determined to affect this disorder. Recent genome-wide Developing Breast Cancer, Registration Date: 2011 Jan. linkage and association study results in relation to ADHD 27, Applicant: MACROGEN INC have reported that several ADHD-susceptibility associated 0009 (Patent Document 2) Korean Patent No. genetic variations may be located in a chromosomal locus 10-1057262: Biomarker for diagnosis of aspirin hypersen comprising of 17q11, 17 ul, and 17p12 on human chromo sitivity, method for manufacturing the same, and method some 17 (Ogdie M. N. et al., Am. J. Hum. Genet. 75:661-668, for diagnosis of aspirin hypersensitivity using the same, 2004; Ogdie M N et al., Am. J. Hum. Genet. 72:1268-1279, Registration Date: 2011 Aug. 9, Applicant: Soonchunhy 2003: Acros-Burgos Met al., Am. J. Hum. Genet. 75:998 ang University Industry Academy Cooperation Foundation 1014, 2004). GIT1, which is one of proteins encoded by genes present in this locus, is one of adaptor proteins with a GTPase Non-Patent Documents activating protein domain, and it is known to regulate various 0010 (Non-patent Document 1) Swanson J. M. et al., G protein-coupled receptors including B2-adrenergic recep Neuropsychol. Rev. 17:39-59, 2007 US 2013/0072391 A1 Mar. 21, 2013

0011 (Non-patent Document 2) Franke B. et al., Hum. 0025. Meanwhile, a linkage disequilibrium (hereinafter, Genet, 126:13-50, 2009 LD) region is a region where a particular section on the 0012 (Non-patent Document 3) Ogdie M. N. et al., Am. J. genome is so short that a cross-over hardly occurs for gen Hum. Genet. 75:661-668, 2004 erations. Therefore, genetic information located in the section 0013 (Non-patent Document 4) Ogdie M N et al., Am. J. is the same and almost conserved for generations. The SNP Hum. Genet. 72:1268-1279, 2003 having a significant association with the risk of ADHD, of the 0014 (Non-patent Document 5) Acros-Burgos M. et al., present invention, is a variation presentata particularlocus on Am. J. Hum. Genet. 75:998-1014, 2004 genome. In addition, polymorphisms are explored where cor 0015 (Non-patent Document 6) Premont R.T. et al., Proc. relation coefficiency (r-square) with the ADHD-associated Natl. Acad. Sci. USA95: 14082-14087, 1998 rs550818 SNP is exhibited 0.95 or more, and polymorphisms 0016 (Non-patent Document 7) Claig A. et al., Proc. Natl. are explored where an LD (D") with the ADHD-associated Acad. Sci. USA 97: 1119-1124, 2000 rS550818 SNP is exhibited 0.95 or more. Therefore, all other variations located in the LD block harboring the rs550818 0017 (Non-patent Document 8) Menon P. et al., Brain SNP in the GIT1 gene also have the same genetic information Res. 1317:218-226, 2010 as the SNP, and thus, the LD block harboring the rs550818 0018 (Non-patent Document 9) Schmalzigauget al., Neu SNP in the GIT1 gene can be also provided as a composition rosci. Lett. 458:79-93, 2009 for diagnosing ADHD risk. 0026. Based on these, genes of each subject can be ana SUMMARY lyzed using the composition for diagnosing ADHD risk of the 0019. An embodiment of the present invention is directed present invention. The composition for diagnosing ADHD to providing a composition for diagnosing attention deficit risk may include a probe having a chromosomal region that hyperactivity disorder (ADHD) risk, including a polynucle includes a predetermined SNP having a significant associa otide having C or T at the 24926.101st nucleotide residue on tion with ADHD and a complementary sequence, and a the human chromosome 17, which is rs550818 SNP in the primer for amplifying the chromosomal region. GIT1 gene, or a region in the vicinity of the SNP. Another 0027. A specific method for this gene analysis is not par embodiment of the present invention is directed to providing ticularly limited, and all the gene detection methods known to a composition for diagnosing ADHD risk, including a probe the technical fields to which the present invention pertains having a chromosomal region that includes a particular SNP may be employed. The genetic species may include all the having a significant association with ADHD and a comple biological species isolated from the subjects. The genetic mentary sequence, and/or a primer for amplifying the chro species is preferably any one selected from the group consist mosomal region. Still another embodiment of the present ing of for example, hair, blood, tissues, cells, serum, plasma, invention is directed to providing a method of predicting the saliva, Sputum, and urine, and the blood is more preferable, risk of ADHD, by identifying a nucleotide of a particular SNP but the genetic species is not limited thereto. having a significant association with ADHD with respect to a 0028. In the above method, the subject means all animals genetic species taken from a human Subject. Such as a human, a monkey, a dog, a goat, a pig, a mouse, and 0020 Still another embodiment of the present invention is the like. directed to providing a kit for diagnosing the risk of ADHD, 0029. The present invention provides a method of predict including a microarray. ing the risk of ADHD, the method including: 0021. An embodiment of the present invention is directed 0030) 1) isolating a nucleic acid species from a biological to providing a method of predicting the risk of attention species derived from a Subject; deficit hyperactivity disorder (ADHD), by identifying or typ 0031) 2) identifying the nucleotide of rs550818 single ing the nucleotide of a single nucleotide polymorphism nucleotide polymorphism (SNP) in the GIT1 gene from the (SNP) in the GIT1 gene having significant association with nucleic acid isolated from stage 1) at the 24926.101st nucle ADHD, and then afterward measuring the risk of ADHD otide residue on human chromosome 17; and based on information of the SNP genotypes. 0032 3) determining the risk of ADHD to be high when 0022. In the present invention, one SNPrs550818, located the alleles or genotype of rS550818 that is identified in stage at the 24926.101st nucleotide residue on the human chromo 2) has one or more T nucleotide. some 17 (Genome Build 36.3) was identified to have signifi 0033. In the above method, any method known in the art cant association with ADHD risk. In the wildtype, nucleotide may be used to isolate the nucleic acid from the biological C is located at the above SNP position, however, when it is species of the Subject. For example, in the case in which changed into nucleotide T due to variation, the variant T nucleic acid of interest is present in a cell, in order to produce dominantly acts in development of ADHD. Hence, when at pure nucleic acid, first, an extract of the cell is prepared, and least one of two alleles is nucleotide T, the risk of ADHD then, differential precipitation, column chromatography, would be significantly increased. extraction with organic solvent, and the like may be further 0023. As such, based on the information of the SNP in the performed. The extract may be prepared using a standard present invention, the nucleotide of the SNP is identified from technology in the corresponding art, for example, chemical or the whole genome of a subject with undeveloped ADHD in mechanical dissolution of a cell. Then, in order to remove any order to determine whether or not the risk of ADHD is high in contamination and interference protein, for example, the the subject, and thus, the risk of ADHD in the subject can be extract may be subjected to filtration and/or centrifugal sepa predicted. ration, and/or may also be treated with chaotropic salts such 0024. For this reason, one SNP, rs550818, located at the as guanidium isothiocynate or urea, or organic solvents such 24926.101st nucleotide residue on the human chromosome 17 as phenyl and/or chloroform. When the chaotropic salt is in the present invention is provided as a composition for used, the salt may be preferably removed from the nucleic diagnosing the risk of ADHD. acid containing species. This procedure may be performed US 2013/0072391 A1 Mar. 21, 2013 using standard techniques in the art, Such as, precipitation, a preferable method, a matrix-assisted laser desorption/ion filtration, size exclusion chromatography, and the like. The ization-time of flight (MALDI-TOF) may be used. The nucleic acid isolated from the cells or tissues by the above MALDI-TOF may include a method where a matrix molecule method may be directly purified, or a predetermined region is mixed with a biopolymer to be analyzed and then a pulse may be specifically amplified using an amplification method laser is applied thereto, thereby to ionize a biopolymer. such as PCR or real time PCR (RT-PCR) and separated. The 0037. When laser is applied to the matrix molecule, for nucleic acid includes cDNA synthesized from mRNA as well example, 3-hydorXypicolinic acid and an analysis material, as DNA. Meanwhile, PCR or RT-PCR may be performed on the matrix molecule absorbs the laser and transmits energy the whole nucleic acid sequences of the Subject, but it may be and proton to the analysis material, so that the matrix mol performed on only a region in the vicinity of an SNP. In the ecule is ionized. The analysis material is operated by a prin above method, nucleotide sequencing of the isolated nucleic ciple where the mass is analyzed by calculating the amount of acid may be performed by various methods known in the art. time it takes for the analysis material to fly together with the For example, direct nucleotide sequencing of nucleic acid ionized matrix and reach a detector on the opposite side under may be performed by a dideoxy method, or nucleotide the vacuum condition. The analysis material having a small sequencing of the SNP region may be performed by hybrid amount of mass quickly reaches the detector. Based on the izing a probe including a sequence of the SNP region or a thus obtained mass difference and the sequence of the SNP probe complementary thereto with the DNA and measuring region that is previously known, the SNP in DNA may be the hybridization degree obtained therefrom. The hybridiza typed. tion degree may be confirmed by labeling a target DNA with 0038 Meanwhile, the present invention provides a a detectable label to specifically detect only the hybridized microarray for predicting the risk of ADHD. target DNA, or by using an electric signal detection method or 0039. The microarray means that the polynucleotide is the like. Specifically, at least one method selected from the immobilized in divided regions on a Surface of a Substrate at group consisting of hybridization by a microarray, allele a high density, and the regions may be arranged on the Sub specific probe hybridization, allele-specific amplification, strate at densities of, for example, 400/cm or higher, 10/ sequencing, 5' nuclease digestion, molecular beacon assay, cm, or 10/cm. oligonucleotide ligation assay, size analysis, and single 0040. The microarray in the present invention preferably Stranded conformation polymorphism may be performed, but includes a polynucleotide hybridizing with C or T nucleotide the present invention is not limited thereto. of the rs550818 SNP in the GIT1 gene, or a complementary 0034. In the above method, the sequencing of a polynucle polynucleotide thereof, but is not limited thereto. As for the otide including a sequence of the SNP region may include microarray in the present invention, a micropipetting method hybridizing the nucleic acid species with the polynucleotide using a piezoelectric type, a method usingapin type spotter or immobilized in the microarray; and detecting the hybridiza the like is preferably employed in order to immobilize the tion result. probe, used as a probing DNA molecule, on the substrate of 0035. In addition, peptide nucleic acids (PNAS), which are the microarray, but the present invention is not limited one of the various DNA analogues, may be included as the thereto. The substrate of the microarray is preferably coated probe including a sequence of the SNP region. In PNA, a with at least one activator selected from the group consisting phosphodiester bond of DNA is substituted with a peptide of amino-silane, poly-L-lysine, and aldehyde, but is not lim bond and PNA has adenine, thymine, guanine, and cytosine, ited thereto. In addition, the substrate may be at least one like DNA, and thus, PNA may bring about a nucleotide selected from the group consisting of silicon wafer, glass, specific hybridizing reaction with DNA and RNA. In particu quartz, metals, nylon films, nitrocellulose membranes, and lar, unlike natural nucleic acids that electrically repulse each plastics, but is not limited thereto. Therefore, the microarray other due to a frame of phosphate bond exhibiting a negative in the present invention may provide a kit for predicting the charge, PNA binds to the natural nucleic acid in the hybrid risk of ADHD. izing reaction more strongly than DNA since a frame thereof 0041. The kit may include the polynucleotide as a primer consists of the peptide bond that does not exhibit an electric and, at the same time, a reagent necessary for amplification. charge, and this bond is not affected by salt concentration. In The kit may further include any one selected from the reactive addition, PNA is not degraded by a biodegradable enzyme reagent group consisting of a buffer, reverse transcriptase for Such as nuclease or protease, and thus, may have higher synthesizing cDNA from RNA, dNTPs and rNTP (premixing stability than DNA or RNA. As such, when PNA that enables type or separate feeding type), labeling reagents, and washing complementary recognition of the natural nucleic acids and buffer, which are used in hybridization. Preferably, there may has excellent hybridization bonding strength and stability is be provided those including a primer for amplifying the labeled with a fluorescent substance, and reacts with the region in the vicinity of thers5508118 SNP in the GIT1 gene. target nucleic acid to occur a hybridizing reaction, a mis 0042. The primer in the present invention may amplify the matched portion thereof is degraded and removed by the SNP region, which is a target portion, and the size thereof and nuclease, and thereby to be used, as a fluorescence resonance the locus thereof binding to a template are not limited. Any energy transfer (FRET), to analyze the SNP. one skilled in the art can easily design the primer by using 0036) Another stage for the sequencing of a polynucle conventional primer selection software. The primer has, for otide including a sequence of the SNP region may include an example, a nucleotide sequence corresponding to the SNP analysis method capable of improving discrimination power region, and the 3' terminal nucleotides of the primer may and specificity in detection of nucleotide Substitution, inser consist of a complementary sequence (in a specific primer) or tion, and deletion, by designing the probe where the nucle a non-complementary sequence (in a non-specific primer) to otide of the SNP complementary to the target gene is posi the nucleotides of the SNP region. The non-specific primer tioned at the central portion of the probe and five to six may include non-complementary sequence in other regions nucleotides are positioned at the left and right thereof, but as as well as the 3' terminal nucleotides thereof. US 2013/0072391 A1 Mar. 21, 2013

0043. The kit in the present invention may be a kit, of 0048 Meanwhile, unless technical and scientific terms which the polynucleotide or a probe derived therefrom is used herein are defined otherwise, they have meanings under hybridized with nucleic acids in a species and the risk of stood by those skilled in the art to which the present invention ADHD for a subject is diagnosed from the hybridized result. pertains. In this case, the kit may include the probe and reagents nec 0049. In addition, the repetitive descriptions of the same essary for hybridization. The reagent necessary for hybrid technical constitutions and functions as the prior art will be ization may include for example a hybridizing buffer. The omitted. nucleic acids may be amplified or may not be amplified. Therefore, the kit may further include a reagent necessary for Example 1 amplifying the nucleic acid. The nucleic acid may be labeled with a detectable label. Examples of the detectable label as Study Subjects Such may further include any one selected from the group 0050. The present invention included genomic DNAs of a consisting of streptavidin-like phosphatase conjugate, chemi total of 388 Koreans in order to study an association between fluorescent, and chemiluminescent, and are not limited an ADHD patient group and a control group. Blood samples thereto. of the objects were collected under the approval by the Seoul 0044) Therefore, the kit in the present invention may National University Hospital Institutional Review Board include a mismatch probe complementary to the entire region (IRB). Association analysis was performed based on the except the SNP region and a perfect match probe complemen genotypes of 192 patients with ADHD and 196 age-matched tary to the entire region including the SNP region. The probe controls without ADHD. Specifically, genome DNAs were may be in a type of microarray Such that it is immobilized in extracted from the blood samples obtained from the study a plurality of divided regions on a substrate. When the target subjects using PuregeneTM DNA purification kit (Gentra, sequence is detected in a hybridizing reaction using the per Minneapolis, Minn.). After the concentration of the extracted fect match probe and the target sequence is not detected in a DNA was measured using PicoGreen (Molecular Probes, hybridizing reaction using the mismatch probe, a sequence Eugene, Oreg.) fluorescent dye that specifically quantifies associated with ADHD is determined to be present in the only double-stranded DNAs, the blood was stored at a con species, and the risk of ADHD of the subject is determined centration of 2.5 ng/ul Suitable for genotyping. from the results. 0045. In the kit, the fluorescent may be used at least one Example 2 selected from the group consisting of Cy3, Cy5, poly L-lysine-fluorescein isothiocyanate (FITC), rhodamine-B- <2-1> Selection of Gene Polymorphism isothiocyanate (RITC), and rhodamine, but is not limited 0051. The present inventors selected 27 SPNs within a thereto. 19-kilobase (kb) region in human chromosome 17 encom 0046. From the above result, the method for predicting the passing the GIT1 gene as analysis objects based on the Inter risk of ADHD in the present invention is characterized by national HapMap Project database, and then analyzed their analyzing a nucleotide sequence of the genetic species association with ADHD risk comparing the ADHD patient obtained from the human subject, and then, if the nucleotide and control groups. at the 24926.101st nucleotide residue on chromosome 17 cor responds to T, classifying the human Subject as a high risk <2-2> Genotyping group of ADHD. 0052. The GIT1 SNPs were genotyped using the Mass AR DETAILED DESCRIPTION OF EMBODIMENTS RAY system (Sequenom, San Diego, Calif.) including the matrix assisted laser desorption and ionization-time of flight 0047. Hereinafter, the present invention will be described (MALDI-TOF) mass spectrometry. Sequences of two prim in more detail by specific embodiments. However, the present ers for polymerase chain reaction (PCR) and a primer for invention is not limited to the following embodiments, and it nucleotide extension reaction used in the genotyping are is apparent to those skilled in the art that various modifica shown in Table 1 below, and these primers were designed tions and changes can be made within the idea and technical using the SpectroDESIGN 3.1 program (Sequenom, San Scope of the present invention. Diego, Calif.). TABLE 1. Sequences of the three primers used for each SNP typing Amplification Amplification Extension SNP forward backward reaction

rs31.10496 ACGTTGGATGCACAAATCA ACGTTGGATGCTCCTGCTT TCACTGCCGCTCTGGCACC CTGCCGCTCTG GTTAAGATGGG G

S1 O17529 ACGTTGGATGCCAGGGCAG ACGTTGGATGTATAGTCAG GATCTGAGGTCTGTGGTCC GATCATAAATG CCTTCCATGCC TAC

rs374. 4626 ACGTTGGATGTTTCTCCCC ACGTTGGATGTCTCAAGGG GGACCTTTCCGCAGCCTGA CGTGACCTTTC TGGAGGAGATG GTCGTA

S3.115.095 ACGTTGGATGTTAACCTCT ACGTTGGATGTGTGATGCT CACTGTTTCTTCATCACAG CTGAGCCACTG GCTTGCAACTG AGG

US 2013/0072391 A1 Mar. 21, 2013

0053. The PCR was performed using 5 ul of an aqueous Example 3 solution where 200 nM of each PCR primer of Table 1 was added to 2.5 ng of genome DNA, 1x buffer, 1 mM of MgCl, Statistical Analysis 200 uM of dNTP mixture, and 0.1 unit of HotStart Taq poly merase mixture. The PCR was run under the reaction condi 0054. In the statistical analysis of the present invention, tions of an initial denaturation stage of 94°C. for 15 minutes, Hardy-Weinberg equilibrium (HWE) was analyzed using a followed by 45 cycles of 94° C. for 20 seconds, 56°C. for 30 chi-square test for independence, and association between the seconds, and 72°C. for 1 minute, and a final elongation stage risk of ADHD and each polymorphism was tested using logis of 72° C. for 3 minutes. After the PCR, 0.3 units of shrimp tic regression analysis with adjustment for gender and IQ alkaline phosphatase (SAP) was added, followed by incuba score in comparisons between the ADHD patient group and tion at 37° C. for 20 minutes and 85°C. for 5 minutes, thereby the control group. All statistical analyses were done using the removing residual dNTPs. The nucleotide extension reaction SPSS 15 program. was performed by adding 50 uM of dNTP terminator mix, 625 nM of extension primer mix, and 0.5 units of Thermose Example 4 quenase enzyme to the resultant reaction. After initial dena turation was performed at 94°C. for 30 seconds, 40 cycles of Association with ADHD Susceptibility 94° C. for 5 seconds, 52° C. for 5 seconds, and 80° C. for 5 seconds were repeated. After 16 ul of distilled water and 3 mg 0055 Association analysis with ADHD susceptibility for of clean resin were added thereto, the final reaction product 27 SNPs in the GIT1 gene of the present invention was done. was transferred onto SpectroChip (Sequenom, San Diego, As the result, as shown in Table 3, the risk of ADHD was Calif.), and then genotyping was done using mass spectrom higher by about 2.66 times in the subjects carrying the het etry. As a genotyping result of 27 SNPs in Example 1, Table erozygote C/T genotype at the rs550818 SNP than those 2 shows that only 8 SNPs exhibited polymorphism (heterozy carrying the homozygote C/C genotype (OR=2.66, 95% gosity 0) in the patient and control groups. CI=1.33-5.31, P=0.0056). Therefore, as a result of associa tion analysis with ADHD susceptibility using the SNP geno TABLE 2 types, it was confirmed that the heterozygote C/T genotype or carriage ofT nucleotide allele in thers550818 SNP has strong Genotype frequency of SNP in GITl association with an increase in the risk of ADHD in compari Position on Major Minor Hetero son with homozygote CC genotype or non-carriage of T SNP ID chromosome Location allele allele Zygosity nucleotide. rS3110496 24.941897 Promoter 300 92 O.36 rS1017529 24936541 intron 1 362 30 O.14 TABLE 3 rS3744626 24935683 intron 1 247 145 O.47 rs3115095 2493S4O4 intron 1 359 33 O.15 Association of rS550818 SNP in rS1128913 24933936 Exon 4 384 O O GIT1 with the risk of ADHD rS894.606 2493.3478 intron 4 255 137 O.45 rS36053O49 24.931747 intron 7 392 O O Patient Control rs378S960 2493.1466 intron 7 346 46 O.21 Geno- group group OR rs479SS15 2493.09.25 intron 7 392 O O type (n = 192) (n = 196) (95% CI) P rS3548.1649 249.28389 Exon 12 392 O O CC 155 178 1 rS41274278 24927873 Intron 13 390 O O rSSS956,743 2492.7872 Intron 13 392 O O (80.7%) (90.8%) CT 36 18 2.66 O.OOS6 rS34131428 24927598 Intron 14 392 O O rS1154.8561 249274.96 Exon 15 392 O O (18.8%) (9.2%) (1.33-5.31) TT 1 O ENSSNP11225832 249.27446 Exon 15 392 O O rs34O15437 24927033 Exon 17 392 O O (0.5%) (0%) rS361O9144 24926.614 Exon 19 392 O O rSSSO818 24926.101 Intron 20 374 18 O.09 rs55778351 24925677 3' UTR 392 O O 0056. The rs550818 SNP marker in the GIT1 gene has a rS41274276 24925.454 3' UTR 392 O O significant association with ADHD Susceptibility, and thus, rS321.1044 249251.84 3' UTR 392 O O rSS7467547 24925095 3' UTR 392 O O the SNP can be used to constitute the composition and the kit rS11548.559 24925.064 3' UTR 392 O O for diagnosing the risk of ADHD by SNP analysis. rS6OOO6SSS 24924.984 3' UTR 392 O O 0057. Further, according to the method of predicting the rSSS677368 249.24775 3' UTR 392 O O rS1154.8562 249.24722 3' UTR 392 O O risk of ADHD of the present invention, the analysis of genetic rs565977 24922954 Downstream 295 97 0.37 information (SNP) and research on clinical factors such as gender, IQ scores, and the like, are performed in parallel, so that accuracy can be further improved.

SEQUENCE LISTING

<16 Os NUMBER OF SEO ID NOS: 81

<21 Os SEQ ID NO 1 &211s LENGTH: 30 &212s. TYPE: DNA US 2013/0072391 A1 Mar. 21, 2013

- Continued <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3110496 forward primer <4 OOs, SEQUENCE: 1 acgttggatg cacaaatcac to cqctctg 3 O

<210s, SEQ ID NO 2 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs1017529 forward primer <4 OOs, SEQUENCE: 2 acgttggatg C cagggcagg at Cataaatg 3 O

<210s, SEQ ID NO 3 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3744626 forward primer <4 OOs, SEQUENCE: 3 acgttggatgtttct c cc cc gtgacctitt c 3 O

<210s, SEQ ID NO 4 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3115095 forward primer <4 OOs, SEQUENCE: 4 acgttggatgttalacct ct c tdagccactg 3 O

<210s, SEQ ID NO 5 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs1128913 forward primer <4 OOs, SEQUENCE: 5 acgttggatg aagcaa.cccc caaga caaag 3 O

<210s, SEQ ID NO 6 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs394.606 forward primer <4 OOs, SEQUENCE: 6 acgttggatg gccaattaat aaacgctgcc 3 O

<210s, SEQ ID NO 7 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs36053 049 forward primer

<4 OO > SEQUENCE: 7 US 2013/0072391 A1 Mar. 21, 2013

- Continued acgttggatgaac acct cat t caac cagcc 3 O

<210s, SEQ ID NO 8 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3785960 forward primer <4 OOs, SEQUENCE: 8 acgttggatg atacacatgc acgcatgcac 3 O

<210s, SEQ ID NO 9 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 4795515 forward primer <4 OOs, SEQUENCE: 9 acgttggatg agcgaga.ccc caact cittaa 3 O

<210s, SEQ ID NO 10 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs35481649 forward primer <4 OOs, SEQUENCE: 10 acgttggatg actictogggc attaaag.cgg 3 O

<210s, SEQ ID NO 11 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 41274278 forward primer <4 OOs, SEQUENCE: 11 acgttggatg ctic ctago ct caataactgc 3 O

<210s, SEQ ID NO 12 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 55956 743 forward primer <4 OOs, SEQUENCE: 12 acgttggatg ctic ctago ct caataactgc 3 O

<210s, SEQ ID NO 13 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34131428 forward primer <4 OOs, SEQUENCE: 13 acgttggatgtcagcgaga gatgagggit 29

<210s, SEQ ID NO 14 US 2013/0072391 A1 Mar. 21, 2013

- Continued

&211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548561 forward primer <4 OOs, SEQUENCE: 14 acgttggatgaaagggct tc agggcagag 29

<210s, SEQ ID NO 15 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: ENSSNP11225832 forward primer <4 OOs, SEQUENCE: 15 acgttggatgaaagggct tc agggcagag 29

<210s, SEQ ID NO 16 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34015437 forward primer <4 OOs, SEQUENCE: 16 acgttggatg agtgaagggc acagotgag 29

<210s, SEQ ID NO 17 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3610.9144 forward primer <4 OOs, SEQUENCE: 17 acgttggatg ggtggaagttc titcct ctittg 3 O

<210s, SEQ ID NO 18 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs650818 forward primer <4 OOs, SEQUENCE: 18 acgttggatg taggctgga ccttggactt 3 O

<210s, SEQ ID NO 19 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 55778351 forward primer <4 OOs, SEQUENCE: 19 acgttggatg gaggtgcatg gaatgttggg 29

<210s, SEQ ID NO 2 O &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 41274276 forward primer US 2013/0072391 A1 Mar. 21, 2013 10

- Continued

<4 OOs, SEQUENCE: 2O acgttggatg accCC catga gcc agttcag 3 O

<210s, SEQ ID NO 21 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3211044 forward primer <4 OOs, SEQUENCE: 21 acgttggatgtcgtgttga gtgtgtggg 29

<210s, SEQ ID NO 22 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 57467547 forward primer <4 OOs, SEQUENCE: 22 acgttggatgtcgtgttga gtgtgtggg 29

<210s, SEQ ID NO 23 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548559 forward primer <4 OOs, SEQUENCE: 23 acgttggatgtcgtgttga gtgtgtggg 29

<210s, SEQ ID NO 24 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs6OOO6555 forward primer <4 OOs, SEQUENCE: 24 acgttggatg citcgc.ccctt citctatogaac 3 O

<210s, SEQ ID NO 25 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 556 77368 forward primer <4 OOs, SEQUENCE: 25 acgttggatg acccaccacc acacagg tag 3 O

<210s, SEQ ID NO 26 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548562 forward primer <4 OOs, SEQUENCE: 26 acgttggatg acccaccacc acacagg tag 3 O US 2013/0072391 A1 Mar. 21, 2013 11

- Continued

<210s, SEQ ID NO 27 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 565977 forward primer <4 OOs, SEQUENCE: 27 acgttggatg cgagaggagg taactgttag 3 O

<210s, SEQ ID NO 28 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3110496 reverse primer <4 OOs, SEQUENCE: 28 acgttggatg ct cctgcttgttalagatggg 3 O

<210s, SEQ ID NO 29 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs1017529 reverse primer <4 OOs, SEQUENCE: 29 acgttggatg tatagt cago citt coatgcc 3 O

<210s, SEQ ID NO 3 O &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3744626 reverse primer <4 OOs, SEQUENCE: 30 acgttggatgtct Caagggit ggaggagatg 3 O

<210s, SEQ ID NO 31 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3115095 reverse primer <4 OOs, SEQUENCE: 31 acgttggatgttgatgctg. Cttgcaactg 3 O

<210s, SEQ ID NO 32 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs1128913 reverse primer <4 OOs, SEQUENCE: 32 acgttggatgttgcacaaa to cagdatc 3 O

<210s, SEQ ID NO 33 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence US 2013/0072391 A1 Mar. 21, 2013 12

- Continued

22 Os. FEATURE: <223> OTHER INFORMATION: rs394.606 reverse primer <4 OOs, SEQUENCE: 33 acgttggatgagtatictaag Cagggcacac 3 O

<210s, SEQ ID NO 34 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs36053 049 reverse primer <4 OOs, SEQUENCE: 34 acgttggatg gct tcaggga tigtgactaac 3 O

<210s, SEQ ID NO 35 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3785960 reverse primer <4 OOs, SEQUENCE: 35 acgttggatg taalacc caga cct ct tccag 3 O

<210s, SEQ ID NO 36 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 4795515 reverse primer <4 OOs, SEQUENCE: 36 acgttggatg Ctggaaatgg agatgacagc 3 O

<210s, SEQ ID NO 37 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs35481649 reverse primer <4 OO > SEQUENCE: 37 acgttggatg cctgcgt.ca.g. t catalaggg 29

<210s, SEQ ID NO 38 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 41274278 reverse primer <4 OOs, SEQUENCE: 38 acgttggatgtctgcagaga gagacctaag 3 O

<210s, SEQ ID NO 39 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65956 743 reverse primer

<4 OOs, SEQUENCE: 39 US 2013/0072391 A1 Mar. 21, 2013 13

- Continued acgttggatgtctgcagaga gagacctaag 3 O

<210s, SEQ ID NO 4 O &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34131428 reverse primer <4 OOs, SEQUENCE: 4 O acgttggatgttctic.cgc.ct gcagottgttg 3 O

<210s, SEQ ID NO 41 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548561 reverse primer <4 OOs, SEQUENCE: 41 acgttggatg agtgaacggg C9gaacaca 29

<210s, SEQ ID NO 42 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: ENSSNP11225832 reverse primer <4 OOs, SEQUENCE: 42 acgttggatg agtgaacggg C9gaacaca 29

<210s, SEQ ID NO 43 &211s LENGTH: 29 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34015437 reverse primer <4 OOs, SEQUENCE: 43 acgttggatg cacactgact c catccagc 29

<210s, SEQ ID NO 44 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3610.9144 reverse primer <4 OOs, SEQUENCE: 44 acgttggatg gtctctgttt t ctggacctg 3 O

<210s, SEQ ID NO 45 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs650818 reverse primer <4 OOs, SEQUENCE: 45 acgttggatgaatcc catct gatcgctacc 3 O

<210s, SEQ ID NO 46 &211s LENGTH: 30 US 2013/0072391 A1 Mar. 21, 2013 14

- Continued

&212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65778351 reverse primer <4 OOs, SEQUENCE: 46 acgttggatgttagtgctgc cacacticcict 3 O

<210s, SEQ ID NO 47 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 41274276 reverse primer <4 OOs, SEQUENCE: 47 acgttggatg ggagacitatg tacaaaggag 3 O

<210s, SEQ ID NO 48 &211s LENGTH: 28 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3211044 reverse primer <4 OOs, SEQUENCE: 48 acgttggatg at Cagggagg cagctggc 28

<210s, SEQ ID NO 49 &211s LENGTH: 28 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs67467547 reverse primer <4 OOs, SEQUENCE: 49 acgttggatg at Cagggagg cagctggc 28

<210s, SEQ ID NO 50 &211s LENGTH: 28 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548559 reverse primer <4 OOs, SEQUENCE: 50 acgttggatg at Cagggagg cagctggc 28

<210s, SEQ ID NO 51 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs6OOO6555 reverse primer <4 OOs, SEQUENCE: 51 acgttggatg accctagoca gcacacattc 3 O

<210s, SEQ ID NO 52 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65677368 reverse primer US 2013/0072391 A1 Mar. 21, 2013 15

- Continued <4 OOs, SEQUENCE: 52 acgttggatg at Cactacct gcacctgctg 3 O

<210s, SEQ ID NO 53 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs 11548562 reverse primer <4 OOs, SEQUENCE: 53 acgttggatg at Cactacct gcacctgctg 3 O

<210s, SEQ ID NO 54 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs 565977 reverse primer <4 OOs, SEQUENCE: 54 acgttggatggggaatggaa aattcaaggg 3 O

<210s, SEQ ID NO 55 &211s LENGTH: 2O &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs31.10496 extension reaction primer <4 OO > SEQUENCE: 55 t cactgcc.gc. tctggcaccg

<210s, SEQ ID NO 56 &211s LENGTH: 22 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs 1017529 extension reaction primer <4 OOs, SEQUENCE: 56 gatctgagglt Ctgtggtcct ac 22

<210s, SEQ ID NO 57 &211s LENGTH: 25 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs3744626 extension reaction primer <4 OO > SEQUENCE: 57 ggacct titcc gcagcctgag ticgta 25

<210s, SEQ ID NO 58 &211s LENGTH: 22 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: 223 OTHER INFORMATION: rs3115095 extension reaction primer <4 OOs, SEQUENCE: 58 cactgtttct t catcacaga gq 22 US 2013/0072391 A1 Mar. 21, 2013 16

- Continued <210s, SEQ ID NO 59 &211s LENGTH: 23 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs1128913 extension reaction primer <4 OO > SEQUENCE: 59 agacaaagtic caccc.catca agt 23

<210s, SEQ ID NO 60 &211s LENGTH: 26 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs394.606 extension reaction primer <4 OOs, SEQUENCE: 60 caattaataa acgctg.ccgt cagtica 26

<210s, SEQ ID NO 61 &211s LENGTH: 17 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs36053 049 extension reaction primer <4 OOs, SEQUENCE: 61 agcgcacgtg cctaatt 17

<210s, SEQ ID NO 62 &211s LENGTH: 2O &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs378596O extension reaction primer <4 OOs, SEQUENCE: 62 tagaat caga C catagaagt

<210s, SEQ ID NO 63 &211s LENGTH: 2O &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 4795515 extension reaction primer <4 OOs, SEQUENCE: 63 attatctaat CCt CCCtcCC

<210s, SEQ ID NO 64 &211s LENGTH: 19 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs35481649 extension reaction primer <4 OOs, SEQUENCE: 64

19

<210s, SEQ ID NO 65 &211s LENGTH: 17 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: US 2013/0072391 A1 Mar. 21, 2013 17

- Continued <223> OTHER INFORMATION: rs 41274278 extension reaction primer <4 OOs, SEQUENCE: 65 gCagggaggc caa.cacc 17

<210s, SEQ ID NO 66 &211s LENGTH: 25 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65956 743 extension reaction primer <4 OOs, SEQUENCE: 66 t cctagocto aataactgcc ccctg 25

<210s, SEQ ID NO 67 &211s LENGTH: 17 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34131428 extension reaction primer <4 OO > SEQUENCE: 67 gacago actt tdcaccc 17

<210s, SEQ ID NO 68 &211s LENGTH: 18 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548561 extension reaction primer <4 OOs, SEQUENCE: 68 agggcagagc Caggttca 18

<210s, SEQ ID NO 69 &211s LENGTH: 18 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: ENSSNP11225832 extension reaction primer <4 OOs, SEQUENCE: 69 ggcggalacac acacccat 18

<210s, SEQ ID NO 70 &211s LENGTH: 21 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs34015437 extension reaction primer <4 OO > SEQUENCE: 7 O agctgaggca gacacic cctt t 21

<210s, SEQ ID NO 71 &211s LENGTH: 17 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3610.9144 extension reaction primer <4 OOs, SEQUENCE: 71 aacct citt co citt coag 17 US 2013/0072391 A1 Mar. 21, 2013 18

- Continued

<210s, SEQ ID NO 72 &211s LENGTH: 2O &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs650818 extension reaction primer <4 OOs, SEQUENCE: 72 c caaccttgg actittaa.gc.c

<210s, SEQ ID NO 73 &211s LENGTH: 30 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65778351 extension reaction primer <4 OO > SEQUENCE: 73 acgttggatgttagtgctgc cacacticcict 3 O

<210s, SEQ ID NO 74 &211s LENGTH: 23 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs 41274276 extension reaction primer <4 OOs, SEQUENCE: 74 cc catgagcc agttcagocc tac 23

<210s, SEQ ID NO 75 &211s LENGTH: 22 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs3211044 extension reaction primer <4 OO > SEQUENCE: 75 ggactgtc.cg ggtagc.cagt tt 22

<210s, SEQ ID NO 76 &211s LENGTH: 17 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs67467547 extension reaction primer <4 OO > SEQUENCE: 76 agct tcc.ctt coccacc 17

<210s, SEQ ID NO 77 &211s LENGTH: 2O &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548559 extension reaction primer <4 OO > SEQUENCE: 77 gatggaccag gcct Coggaa

<210s, SEQ ID NO 78 &211s LENGTH: 22 &212s. TYPE: DNA US 2013/0072391 A1 Mar. 21, 2013

- Continued <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs6OOO6555 extension reaction primer <4 OO > SEQUENCE: 78 gaatcaaaaa ccact tcc ct c c 22

<210s, SEQ ID NO 79 &211s LENGTH: 19 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs65677368 extension reaction primer <4 OO > SEQUENCE: 79

CCC agggaag aag.cgggat 19

<210s, SEQ ID NO 8O &211s LENGTH: 18 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs11548562 extension reaction primer <4 OOs, SEQUENCE: 80 acagcct tcc Caggctgc 18

<210s, SEQ ID NO 81 &211s LENGTH: 18 &212s. TYPE: DNA <213> ORGANISM: Artificial sequence 22 Os. FEATURE: <223> OTHER INFORMATION: rs665977 extension reaction primer <4 OOs, SEQUENCE: 81 cgaggalaggt ggggacala 18

What is claimed is: 5. The method of claim 4, wherein the biological species is 1. A composition for diagnosing the risk of attention deficit at least one selected from the group consisting of hair, blood, hyperactivity disorder (ADHD), the composition comprising tissues, cells, serum, plasma, Saliva, sputum, and urine. a polynucleotide including rS550818 single nucleotide poly 6. The method of claim 4, wherein the stage 2) is performed morphism (SNP) in the GIT1 gene, which exhibits C or T by at least one method selected from the group consisting of nucleotide at the 24926.101st nucleotide residue on human hybridization by microarrays, allele-specific probe hybrid chromosome 17. ization, allele-specific amplification, sequencing, 5' nuclease 2. The composition of claim 1, further comprising a linkage digestion, molecular beacon assay, oligonucleotide ligation disequilibrium block harboring the rs550818 SNP in the assay, size analysis, and single-stranded conformation poly GIT1 gene. morphism. 3. The composition of claim 1, further comprising a probe 7. A method for predicting the risk of attention deficit having a chromosomal region including an SNP having a hyperactivity disorder (ADHD), the method comprising significant association with ADHD and a complementary determining a single nucleotide polymorphism (SNP) by a sequence, and/or a primer. polymerase chain reaction (PCR) using a probe having a 4. A method for predicting the risk of attention deficit sequence of thers550818 SNP in the GIT1 gene, a primer, or hyperactivity disorder (ADHD), the method comprising: both of the probe and the primer. 1) isolating a nucleic acid species from a biological species 8. The method of claim 7, wherein the PCR is a real time derived from a subject; PCR (RT-PCR) or a PCR using a PNA probe. 2) identifying the nucleotide of rs550818 single nucleotide polymorphism (SNP) in the GIT1 gene, which is the 9. A microarray for diagnosing the risk of ADHD, the 24926.101st nucleotide residue on human chromosome microarray comprising a polynucleotide having C or T of 17, from the nucleic acid isolated from stage 1); and rs550818 single nucleotidepolymorphism (SNP) in the GIT1 3) determining the risk of ADHD to be high when the gene, or a complementary polynucleotide thereof. genotype of rS550818 SNP that is identified in stage 2) 10. The microarray of claim 9, wherein the polynucleotide carries T nucleotide. or the complementary polynucleotide is immobilized on a US 2013/0072391 A1 Mar. 21, 2013 20 substrate of the microarray coated with at least one activator streptavidin-like phosphatase conjugate, chemifluorescent, selected from the group consisting of amino-silane, poly-L- and chemiluminescent for hybridization. lysine, and aldehyde. 14. The kit of claim 13, further comprising any one selected from the reactive reagent group consisting of a buffer, reverse 11. The microarray of claim 10, wherein the substrate is at transcriptase for synthesizing cDNA from RNA, dNTPs and least one selected from the group consisting of silicon wafer, rNTP (premixing type or separate feeding type), labeling glass, quartz, metals, nylon films, nitrocellulose membranes, reagents, and washing buffer, which are used in the hybrid and plastics. ization. 12. A kit for diagnosing the risk of attention deficit hyper 15. The kit of claim 13, wherein the fluorescent is at least activity disorder (ADHD), the kit comprising the microarray one selected from the group consisting of Cy3, Cy5, poly of claim 9. L-lysine-fluorescein isothiocyanate (FITC), rhodamine-B- 13. The kit of claim 12, wherein the microarray further isothiocyanate (RITC), and rhodamine. includes any one selected from the group consisting of k k k k k