注意缺陷多动障碍患儿COMT基因rs6267多态性分析

目的：分析儿茶酚胺氧位甲基转移酶（COMT）基因 rs6267 多态性位点与注意缺陷多动障碍（ADHD）的关联,寻找ADHD的易感基因。方法：采用聚合酶链反应-限制性片段长度多态性技术分析 114 例ADHD 儿童与 76 例正常对照组的 COMT 基因 rs6267 多态性位点频率,并用儿童行为量表（CBCL）评定儿童行为问题。结果：rs6267 多态性各基因型及等位基因在 ADHD 组和正常对照组之间的分布差异无统计学意义（P＞0.05）。基因型为G/G的ADHD患儿的思维问题和违纪问题（分别为1.7±1.9,4.5±3.7)明显多于基因型为G/T的患儿（分别为1.0±0.9,2.2±1.4）（P＜0.05）。结论：COMT 基因 rs6267 多态性可能不是 ADHD 的易感因素;rs6267 多态性可能与 ADHD 的某些临床特征有关。     

青少年特发性脊柱侧弯患儿褪黑素受体1B基因多态性研究

目的 研究褪黑素受体1B(melatonin receptor 1B, MTNR1B)基因启动子区域多态性与青少年特发性脊柱侧弯(adolescent idiopathic scoliosis, AIS)发生发展的关系.方法 本研究包括814例AIS患儿及651例正常对照,所有AIS患儿最大cobb角大于20°.采用PCR-RFLP的方法 对所选取多态性位点(rs4753426、rs7941837)进行基因分型.结果 AIS患儿组rs4753426多态性位点基因型分布为TT 6.5%、TC 41.5%、CC 52.0%,正常对照组为TT 9.5%、TC 44.4%、CC 46.1%.AIS患儿组rs4753426多态性位点等位基因分布为T 27.3%、C 73.7%,正常对照组为T 31.7%、C 68.3%.AIS患儿组与正常对照相比,rs4753426多态性位点基因型分布及等位基因分布差异都有统计学意义(P值分别为0.025,0.009).AIS患儿组rs7941837多态性位点基因型分布为AA 21.2%、AT 50.2%、TT 28.6%,正常对照组为AA 17.6%、AT 50.6%、TT 31.7%.AIS患儿组rs7941837多态性位点等位基因分布为A 46.3%、T 53.7%,正常对照组为A 43.0%、T 57.0%.AIS患儿组与正常对照相比,rs7941837多态性位点基因型分布及等位基因分布差异都无统计学意义(P＞0.05).在已经达到骨骼成熟或者已经接受手术治疗的患儿组,MTNR1B基因启动子区2个多态性位点不同基因型所对应的平均最大Cobb角差异都没有统计学意义(P＞0.05).结论 MTNR1B基因启动子区域多态性位点rs4753426与AIS的发病相关,MTNR1B基因是AIS的一个易感基因,但它可能不是AIS的修饰基因.     

TARC/CCL17 基因多态性与川崎病及其临床特征的相关性分析

目的 探讨我国中部汉族人群中TARC/CCL17 基因的SNP 位点(rs223895、rs223899)多态性与川崎病(Kawasaki disease, KD)及其临床特点的关系。方法 采用病例对照研究方法,选取218 例典型KD 患儿和248 例体检正常儿童作为研究对象。利用PCR-RFLP 的方法测定SNP 位点多态性分布;评估TARC/CCL17基因多态性与KD 临床特点的相关性。结果 KD 患儿SNP 位点(rs223895)的基因型(CC、CT、TT)频率及等位基因频率与正常对照组相比差异有统计学意义(P<0.05),且C 等位基因为风险因子(OR=1.379)。SNP位点(rs223899)的基因型频率及等位基因频率与对照组相比差异无统计学意义。SNP 位点(rs223895)CC 基因型患儿的血红蛋白以及白蛋白水平低于其他基因型(CT+TT)的患儿(P<0.05);而血沉高于其他基因型患儿(P<0.05)。结论 TARC/CCL17 基因SNP 位点(rs223895)与KD 的易感性相关,C 等位基因为风险因子;且该SNP 位点多态性可能影响患者血红蛋白、白蛋白及血沉水平。     

STAT3基因多态性与过敏性紫癜易感性的相关性研究

目的研究信号转导和转录激活因子-3(STAT3)两个位点(rs 2293152、rs 9579700)基因多态性与过敏性紫癜(HSP)易感性及紫癜性肾炎(HSPN)的关系。方法选取2013年9月至2015年9月诊治的180例HSP患儿(HSP组),及同期205例健康体检儿童(对照组),采用序列特异性引物聚合酶链反应(SSP-PCR)法检测STAT3基因内含子11rs 2293152 C/G和内含子23 rs 957970 C/T的单核苷酸多态性(SNP),并进行分析。结果 STAT3基因内含子11中rs 2293152的CC基因型在HSP组(26.1%)的分布频率高于对照组(8.8%),rs2293152C等位基因在HSP组(48.6%)的分布频率高于对照组(32.7%),差异均有统计学意义(P均0.05);而基因型和等位基因在STAT3基因内含子23中rs957970C/T位点的分布在两组间差异无统计学意义(P0.05)。STAT3基因这两个位点的基因型及等位基因分布频率在HSPN和非HSPN组间的差异无统计学意义(P0.05)。结论 STAT3基因内含子11 rs 2293152 C/G的C等位基因可能是儿童HSP的易感基因,而内含子23 rs957970C/T位点的多态性与儿童HSP无相关性;同时这两个基因位点多态性与HSPN亦无相关性。     

ZNF365基因多态性与儿童支气管哮喘的相关性

目的 探讨我国中部湖北地区儿童ZNF365基因的两个SNP位点(rs2393903和rs10995251)的多态性与支气管哮喘及其临床特点的关系。方法 采用病例-对照的研究方法,选取湖北地区221例支气管哮喘患儿和243例同时期体检正常的儿童作为研究对象,利用限制性片段长度多态性分析的方法检测两个SNP位点的多态性分布。结果 哮喘患儿中SNP rs2393903位点的3种基因型(GG、GA、AA)分布及等位基因频率与正常对照组相比差异均无统计学意义;而SNP rs10995251位点的基因型(CC、CT、TT)以及等位基因频率与正常对照组相比差异有统计学意义(P< 0.05),C等位基因为风险因子(OR=1.380)。在哮喘患儿中SNP rs10995251位点CC基因型患儿血清免疫球蛋白E(IgE)的水平高于TT基因型患儿(P< 0.05)。结论 ZNF365基因SNP rs10995251位点的多态性与我国中部湖北地区儿童支气管哮喘的易感性相关;且该位点的多态性可能影响患儿血清IgE水平。     

CHI3L1基因单核苷酸多态性与儿童哮喘易感性的相关性研究

目的 探讨CHI3L1基因单核苷酸多态性(SNP)与儿童哮喘易感性之间的相关性.方法 选取2011年1月至2013年10月确诊为哮喘的316例儿童为哮喘组,同期选取297例健康儿童作为对照组.采集所有研究对象外周血,应用化学发光法和流式细胞术分别检测两组总IgE水平和嗜酸性粒细胞比例,ELISA法检测YKL-40水平;提取外周血细胞基因组DNA,应用Mass ARRAY-IPLEX质谱阵列技术检测CHI3L1基因rs4950928、rs10399805和rs883125位点的单核苷酸多态性,统计分析上述位点基因型及等位基因分布频率.结果 哮喘组总IgE和YKL-40浓度均较对照组显著升高(均PP>0.05).哮喘组rs883125位点的GG基因型频率高于对照组(PPP结论 YKL-40可作为初步诊断儿童哮喘的分子标记物;CHI3L1基因的rs4950928和rs883125多态性可能为儿童哮喘的易感因子;rs4950928位点G等位基因可能是提高哮喘风险的易感因子.     

MPO基因多态性与川崎病及其临床表型的相关性分析

目的探讨我国中部汉族人群中MPO基因的单核苷酸多态性(SNP)位点(rs2333227,—643G/A)多态性与川崎病(KD)及其临床特点的相关性。方法采用病例对照研究方法,选取237例典型KD患儿和249例正常儿童作为研究对象。利用PCR-RFLP的方法测定SNP位点多态性分布;并收集KD患儿临床资料。结果 KD患儿SNP位点(rs2333227)的基因型(GG、GA、AA)频率与正常儿童相比差异有统计学意义(P=0.039),且等位基因频率差异亦存在统计学意义(P=0.012),G等位基因为风险因子。该SNP位点GG基因型的患儿手足水肿的比例高于其他基因型的患儿,差异具有统计学意义(P=0.029)并与腹腔积液的特点相关(P=0.028);该SNP位点多态性与结膜充血、皮疹、冠状动脉损伤肝脏肿大、脾脏肿大、小叶性肺炎等影像学特点无关(P0.05)。结论 MPO基因SNP位点(rs2333227)与KD的易感性相关,G等位基因为风险因子;且该SNP位点多态性可能与部分临床特点相关。     

IL1R1基因多态性与儿童哮喘的相关性

目的 探讨我国中部地区儿童IL1R1 基因的两个SNP 位点(rs1558641 和rs949963)的多态性与哮喘易感性的相关性。方法 采用病例-对照的研究方法,选取来自于我国中部地区的208 例哮喘患儿(哮喘组)和223 例同时期体检正常的儿童(健康对照组)作为研究对象。利用限制性片段长度多态性分析(PCRRFLP)的方法检测IL1R1 基因两个SNP 位点(rs1558641 和rs949963)的多态性分布;酶联免疫吸附试验(ELISA)测定血清中IL1R1 的水平。结果 哮喘组患儿SNP 位点(rs1558641)的基因型及等位基因频率与健康对照组相比差异无统计学意义。而哮喘组患儿SNP 位点(rs949963)GG 基因型的比例显著高于健康对照组(P=0.031),且两组等位基因频率差异也有统计学意义(P=0.018)。哮喘组血清IL1R1 的水平明显高于健康对照组(P=0.011),且SNP 位点(rs949963)GG 基因型的患儿血清IL1R1 水平高于其他基因型(AA+AG)的患儿(P=0.028)。结论 IL1R1 基因SNP 位点(rs949963)的多态性与我国中部地区儿童哮喘的易感性相关,且该位点的多态性可能影响患儿血清中IL1R1 的表达水平。     

谷氨酸/多巴胺系统5个候选基因14个多态性与注意力缺陷多动障碍的关联

目的：注意力缺陷多动障碍(ADHD)是儿童常见行为障碍,病因不明。该文旨在探讨ADHD与5个基因14个多态位点的关系,以及与多位点联合效应的关系,寻找可增加患病风险的某些位点的特定组合。方法：对138名ADHD患者和119名正常对照进行以下遗传学分析：①用PCR-RFLP分析8个SNP位点;用PCR结合PAGE分析DRD4的48 bp VNTR;用基因扫描分析5个微卫星多态。②采用logistic回归法研究12个多态位点对ADHD的联合效应。结果：①ADHD组SNAP-25的T1065G多态性1065T/1065T基因型和1065T等位基因频率均明显高于对照组(均P<0.05),DRD1 的A-48G多态性-48G/-48G频率明显低于对照组(P<0.05)。②发现了一个由2个基因3个SNP位点组成的特定基因型组合与ADHD有关联,其预测水平为77.5%。结论：SNAP-25的T1065G与ADHD可能有关联,1065T/1065T和1065T可能是其危险因素;DRD1的A-48G多态性与ADHD可能有关联,-48G/-48G可能是其保护因素;所发现的特定基因型组合支持“一些位点的特定组合效应增加了ADHD发病风险”的观点。［中国当代儿科杂志,2009,11（8）：617-622］     

信号转导子及转录激活因子2基因rs2066807C→G多态性与支气管哮喘的相关性

目的探讨信号转导子及转录激活因子2(STAT2)基因单核苷酸多态位点rs2066807C→G多态性与潍坊地区汉族人群儿童哮喘的关系。方法应用PCR-限制性内切酶多型性法,对92例支气管哮喘患儿(哮喘组)和98例健康儿童(健康对照组)STAT2基因rs2066807C→G多态性进行检测,计算基因型和等位基因频率,组间比较采用χ2检验。相关疾病的基因型风险率以参与风险及比值比(OR)表示,95%可信区间(95%CI)计算采用Miettinen法。结果STAT2基因rs2066807C→G多态位点CC、CG、GG基因型频率,哮喘组患儿分别为0、3.4%、96.6%,健康对照组分别为0、6.1%、93.9%;C和G等位基因频率,哮喘组为1.6%和98.4%,健康对照组为3.1%和96.9%。哮喘组STAT2基因各基因型和等位基因频率和健康照组比较差异均无统计学意义(Pa>0.05)。携带CG基因型和C等位基因的儿童发生支气管哮喘的相对风险OR值分别为0.34(95%CI:0.05～4.96)和0.33(95%CI:0.05～4.93)(Pa>0.05)。结论STAT2基因rs2066807C→G多态性与潍坊地区儿童支...     

注意缺陷多动障碍与突触体联系蛋白25基因的关联研究

目的 探讨中国汉族人群中注意缺陷多动障碍(ADHD)与突触体联系蛋白25(SNAP-25)基因微卫星(STR)和单核苷酸多态性(SNP)的关系.方法 本组100例,均为学龄期的ADHD患儿,通过唾液取样获取他们及其父母的DNA样本.同时选取符合年龄段的正常儿童97名作为对照组,DNA样本从血液中提取.检测100个ADHD核心家系和97个对照的SNAP-25基因STR,同时对rs363006和rs362549两段SNP进行基因分型,并进行病例对照的关联分析和传递不平衡检验(TDT).结果 SIR病例对照分析结果显示ADHD组和对照组(TAAA)n的等位基因频率和基因型频率差异无统计学意义(P均＞0.05);rs363006和rs362549两段SNP的家系TDT研究表明,SNAP-25基因和ADHD之间不存在关联(P均＞0.05).按照亚型分组后,rs362549在注意缺陷型中有优先传递等位基因A的趋势(x2=8.00,P＜0.01),而在混合型中有优先传递等位基因G的趋势(x2=4.122,P＜0.05).结论 SNAP-25基因STR和上述两段SNP和ADHD之间也许不存在关联,但rs362549这段SNP的多态性和ADHD亚型可能存在关联,尚需扩大样本进一步验证才能得出确切结论.     

脑源性神经营养因子基因单核苷酸多态与注意缺陷多动障碍的关系

目的 探讨脑源性神经营养因子(BDNF)基因单核苷酸多态性(SNP)位点rs6265、rs7103411和rs11030104多态与注意缺陷多动障碍(ADHD)及其亚型之间的关系.方法 根据美国<精神障碍诊断与统计手册>第4 版(DSM-Ⅳ)中ADHD诊断标准,共收集1 842例散发ADHD病例及其组成的1 271个ADHD家系和957例健康对照者分别进行家系和病例对照研究.在美国生物系统公司生产的7900 HT型荧光定量PCR仪提供的技术平台上完成等位基因分型试验,采用遗传分析统计软件Haploview 4.2进行传递不平衡检验(TDT)、χ2检验和单体型分析对ADHD及其表型进行关联分析,并对P值进行置换检验的校正.结果 BDNF基因的SNP位点 rs6265/C、rs11030104/A、rs7103411/T以及CAT单体型在女性单纯ADHD家系中过度传递,在女性单纯ADHD患者中频率明显高于健康对照组(Pa<0.05).BDNF基因rs6265/T和TT基因型、rs11030104/G及GG基因型、rs7103411/C及TT基因型和TGC单体型在男性单纯ADHD混合型(ADHD-C)家系中有过度传递趋势,在男性ADHD-C亚型患儿中频率有高于健康对照组的趋势.结论 BDNF基因单核苷酸多态性变异可能与ADHD的病理机制有关,可能是作用于较精细的同质性较高的ADHD亚组,且这种作用机制存在性别差异.     

The COMT val158met polymorphism is associated with early pubertal development, height and cortical bone mass in girls

Estrogens are involved in accretion of bone mass during puberty. Catechol-O-Methyltransferase (COMT) is involved in the degradation of estrogens. In this cross-sectional study we investigated associations between the COMT val158met polymorphism, which results in a 60-75% difference in enzyme activity between the val (high activity = H) and the met (low activity = L) variant, and skeletal phenotypes in 246 healthy pre/early pubertal girls. Girls with COMT(LL) were 5.4 cm taller than COMT(HH) girls. Dual x-ray absorptiometry showed higher values of bone mineral content (BMC), and larger areas of total body, femur and spine in COMT(LL). Cortical BMC, measured by peripheral quantitative computerized tomography in the tibia, was 9.8% higher in COMT(LL) compared with COMT(HH). This was due to a larger cortical cross sectional area while the cortical volumetric bone mineral density was not associated with COMT genotype. COMT(LL) girls had higher serum levels of free estradiol and insulin like growth factor. Regression models indicated that COMT genotype exerted effects on skeletal growth mainly via a regulation of free estradiol, resulting in an affected pubertal development (Tanner staging). We propose that the COMT(LL) genotype results in higher free estradiol levels and earlier pubertal development, leading to an increased skeletal growth in pre/early pubertal girls. Possible consequences for the adult skeleton however can be determined only after cessation of growth.     

睡眠质量对注意缺陷多动障碍儿童症状的影响:工作记忆的中介作用北大核心CSCD

目的探讨注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)儿童工作记忆在睡眠质量与症状之间的中介作用。方法采用随机整群抽样法从新疆维吾尔自治区喀什市2所小学3~5年级学生中筛选出符合条件的ADHD儿童(110例)及正常对照儿童(124例)为研究对象,采用SNAP-Ⅳ评估量表、匹兹堡睡眠质量指数量表(Pittsburgh Sleep Quality Index,PSQI)、工作记忆任务测试进行调查并比较。结果ADHD组儿童主观睡眠质量、入睡时间、睡眠效率、睡眠障碍评分及PSQI总分高于正常对照组(P<0.001),睡眠质量问题的发生率也高于正常对照组(P<0.001);ADHD儿童工作记忆得分低于正常对照组(P<0.001)。ADHD组工作记忆得分与PSQI总分呈负相关(r_(s)=-0.271,P<0.001),与症状得分呈负相关(r_(s)=-0.439,P<0.001);ADHD组PSQI总分与症状得分呈正相关(r_(s)=0.540,P<0.001)。工作记忆在睡眠质量对ADHD儿童症状影响中起部分中介效应,占总效应的18.10%。结论部分ADHD儿童存在睡眠质量问题,且工作记忆在ADHD儿童睡眠质量与症状之间起中介作用。     

注意缺陷多动障碍患儿Period3基因可变数目串联重复序列多态性分析

目的探讨Period3(Per3)基因18号外显子54 bp可变数目串联重复(VNTR)序列多态性与中国汉族儿童注意缺陷多动障碍(ADHD)伴睡眠障碍的相关性。方法选取2005年8月-2010年5月在本科就诊、符合美国《精神障碍诊断与统计手册(第4版)》诊断标准的166例ADHD患儿为ADHD组,另收集150例健康儿童为对照组。用睡眠障碍量表(SDSC)评分评定儿童睡眠障碍情况,采用PCR技术分析ADHD组患儿与健康对照组儿童Per3基因54 bp-VNTR多态性基因型和等位基因的频率分布。将ADHD患儿根据SDSC量表评分分为有睡眠障碍组和无睡眠障碍组,并比较2组间Per3基因54 bp-VNTR多态性。结果 Per3基因54 bp-VNTR多态性各基因型(Per34/4,Per34/5,Per35/5)及等位基因(Per34,Per35)频率在ADHD组和健康对照组间的分布差异均无统计学意义(Pa>0.05),在伴睡眠障碍组和不伴睡眠障碍组间的分布差异均有统计学意义(Pa<0.05),伴睡眠障碍组携带等位基因Per35明显多于不伴睡眠障碍组(χ2=15.028,P<0.001;OR=2.760,95%CI:1.635～4.658)。结论 Per3基因54 bp-VNTR多态性可能与ADHD的易感性无关,但可能与ADHD伴睡眠障碍有关。     

CLOCK基因T3111C多态性与儿童注意缺陷多动障碍及相关睡眠障碍的关联研究

目的：探讨CLOCK基因3’非编码区SNP 位点T3111C与儿童注意缺陷多动障碍（attention deficit hyperactivity disorder, ADHD）及相关睡眠障碍的关联性。方法：取无亲缘关系的ADHD患儿166名以及正常儿童（对照组）150名,根据睡眠障碍量表（Sleep Disturbance Scale for Children, SDSC）评分筛查睡眠障碍,采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术,检测ADHD组和对照组CLOCK基因的T3111C基因型和等位基因的频率分布。结果：CLOCK基因的T3111C基因型及等位基因频率分布在ADHD组和对照组之间差异有统计学意义（P<0.05）,ADHD组中等位基因C频率显著高于对照组（χ2=7.254,P=0.007, OR=1.740,95%CI=1.160~2.612）。伴有睡眠障碍的ADHD患儿等位基因C频率显著高于不伴有睡眠障碍者（χ2=13.052,P<0.001,OR=2.766,95%CI=1.573~4.865）。结论：CLOCK基因T3111C位点与ADHD易感性存在关联,也是影响ADHD患儿相关睡眠障碍的重要因素。携带C等位基因的个体罹患ADHD以及ADHD相关睡眠障碍的相对风险增高。     

LPHN3 and attention-deficit/hyperactivity disorder: interaction with maternal stress during pregnancy

Background: Attention‐deficit/hyperactivity disorder (ADHD) is a heterogeneous behavioral disorder, complex both in etiology and clinical expression. Both genetic and environmental factors have been implicated, and it has been suggested that gene‐environment interactions may play a pivotal role in the disorder. Recently, a significant association was reported between ADHD and LPHN3 (which codes for latrophilin 3), and replicated in independent samples. Methods: We have examined the association between tag single nucleotide polymorphisms (SNPs) in LPHN3 within the region previously implicated in ADHD. Family based association tests (FBAT) were conducted (n = 380 families) with the categorical diagnosis of ADHD, behavioral and cognitive phenotypes related to ADHD, and response to treatment (given a fixed dose of methylphenidate, 0.5 mg/day). Stratified FBAT analyses, based on maternal smoking and stress during pregnancy, was conducted. Results: Whereas limited association was observed in the total sample, highly significant interaction between four LPHN3 tag SNPs (rs6551665, rs1947274, rs6858066, rs2345039) and maternal stress during pregnancy was noted. Analysis conducted in the sub‐group of mothers exposed to minimal stress during pregnancy showed significant associations with ADHD, behavioral and cognitive dimensions related to ADHD, as well as treatment response. Although extensive association was observed with the candidate SNPs, the findings are partially inconsistent with previously published results with the opposite alleles over‐transmitted in these studies. Conclusions: These results provide evidence for the interaction between a genetic and environmental factor independently shown to be associated with ADHD. If confirmed in independent large studies, they may present a step forward in unraveling the complex etiology of ADHD.     

ADHD symptoms and maturity – a study in primary school children

Aim: To study if age and non-behavioural measures of biological maturity have any associations with attention deficit hyperactivity disorder (ADHD).
Methods: Two hundred fifty-one children 7 to 9 years of age in a Swedish school were screened for ADHD-symptom. ADHD-symptoms were estimated by Conners Abbreviated Questionnaire by both parents and teachers. Motor function, body weight and body height were measured. Skeletal age was estimated through hand radiographs.
Results: Height, weight and skeletal bone-age did correlate significantly with age (rs = 0.44–0.69, p < 0.001) but not with ADHD symptom scores. Motor dysfunction had a weak negative correlation with age (rs =−0.21, p < 0.05). Parent and teacher scores of ADHD-symptoms did not correlate with age.
Conclusion: This study showed that the variables measuring general biological maturity had a strong association with age, whereas motor dysfunction and ADHD symptoms had no significant association with age. ADHD symptoms did not correlate with the variables measuring general biological maturity. These results do not support the hypothesis that a general biological immaturity is an important etiologic factor for ADHD symptomatology.     

ADHD symptoms and maturity--a study in primary school children.

AIM: To study if age and non-behavioural measures of biological maturity have any associations with attention deficit hyperactivity disorder (ADHD). METHODS: Two hundred fifty-one children 7 to 9 years of age in a Swedish school were screened for ADHD-symptom. ADHD-symptoms were estimated by Conners Abbreviated Questionnaire by both parents and teachers. Motor function, body weight and body height were measured. Skeletal age was estimated through hand radiographs. RESULTS: Height, weight and skeletal bone-age did correlate significantly with age (rs = 0.44-0.69, p < 0.001) but not with ADHD symptom scores. Motor dysfunction had a weak negative correlation with age (rs =-0.21, p < 0.05). Parent and teacher scores of ADHD-symptoms did not correlate with age. CONCLUSION: This study showed that the variables measuring general biological maturity had a strong association with age, whereas motor dysfunction and ADHD symptoms had no significant association with age. ADHD symptoms did not correlate with the variables measuring general biological maturity. These results do not support the hypothesis that a general biological immaturity is an important etiologic factor for ADHD symptomatology.