Genetic Association between Atopy and Behavioral Symptoms in Middle Childhood

The relationship of atopic and behavioral symptoms in a community sample of 66 monozygotic and 141 dizygotic twin pairs, ages 4–11 years, was investigated via mother report questionnaires. Within-person correlation between atopic symptoms and Child Behavior Checklist internalizing symptoms (CBCL-INT) was .21 ( p < .001) for the total sample. Cross-correlations between atopy and CBCL-INT were .26 for monozygotic and .04 for dizygotic twins. A common and specific factor model applied to the data revealed that the cross-correlation between atopy and CBCL-INT was mainly due to genetic influences (77% of the covariance). This study supports the hypothesis that there is a shared genetic risk for atopy and internalizing symptoms.     

The Impact of Family Transition on the Development of Delinquency in Adolescent Boys: A 9-year Longitudinal Study

The purpose of this study was to examine prospectively the impact of family transition on deviant development in a sample of 427 French-Canadian boys participating in a longitudinal study from kindergarten onwards. During the course of the study some boys experienced family transition. We grouped the boys by developmental period and number of marital transitions they experienced: divorced between ages 6 and 11; divorced between ages 12 to 15; remarried between ages 6 and 11; and remarried between ages 12 and 15. From ages 11 to 15 we assessed boys' delinquency and their family processes (parental supervision, punishment, and communication) annually. The results suggest that boys who experienced remarriage between ages 12 and 15 are at greater risk for delinquency. In particular, they showed evidence of comparatively more theft and fighting at earlier ages than their peers from families that had remained intact. At similar points in development, they perceived less expressive parent-child relationships. Finally, these boys also perceived less monitoring by their parents, both overall and at different points in adolescence.     

Attention deficit hyperactivity disorder with reading disabilities: preliminary genetic findings on the involvement of the ADRA2A gene

BACKGROUND: Attention deficit/hyperactivity disorder (ADHD) and reading disability (RD) tend to co-occur and quantitative genetic studies have shown this to arise primarily through shared genetic influences. However, molecular genetic studies have shown different genes to be associated with each of these conditions. Neurobiological studies have implicated noradrenergic function in the aetiology of ADHD that is comorbid with RD. This paper examines the neurobiological evidence and presents preliminary testing of the hypothesis that the ADRA2A receptor gene is contributing to ADHD and comorbid RD. METHODS: One hundred and fifty-two children (140 boys, 12 girls) of British Caucasian origin, aged between 6 and 13 years and with a diagnosis of ADHD, were recruited. The children's reading ability was tested. Children were identified as having ADHD or ADHD plus RD (n=82). DNA was available for 110 parent child trios and 42 parent child duos. Genotyping was undertaken for an ADRA2A polymorphism. RESULTS: For those with ADHD plus RD there was evidence of association with the alpha 2A adrenergic receptor (ADRA2A) polymorphism with the G allele being preferentially transmitted. CONCLUSIONS: The preliminary evidence together with other neurobiological research findings suggests that the ADRA2A gene may contribute to comorbid ADHD and RD and needs to be properly examined.     

ע��ȱ�ݶද�ϰ�����θ�����ͷ�����������̬�Ե��о�

??Abstract??Objective??To study the GRPR polymorphisms in ADHD children and analyze the sequence of the second exon of GRPR. Methods??The DNA was taken from the periphery blood. The PCR of the second exon of 120 children with ADHD and 126 normal children was sequenced. We used Chi-square test to know difference of genotype and haplotype between ADHD and normal control group?? and among inattention?? hyperactivity and impulsivity compound group. Result??There were TT?? CC and TC polymorphisms in the second exon of GRPR in 661 and 450 sits. There was no difference between ADHD and normal control group??χ2 = 0.30??0.52??1.34??0.30??all P > 0.05??. There was no difference among inattention?? hyperactivity and impulsivity compound group??χ2 = 0.37??0.49??0.63??all P > 0.05??. Conclusion??The research has not proved the relationship between ADHD and the second exon of GRPR.     

��Ч�߼��������ζ����ƶ�ͯע��ȱ�ݶද�ϰ��ϲ�Ʒ���ϰ��о�

??Abstract??Objective To study the methylphenidate hydrochloride controlled-release tablets??OROS-MPH??dose titration treatment for children with attention deficit hyperactivity disorder??ADHD??combining conduct disorder??CD??to achieve the best clinical efficacy. Methods According to the DSM-IV diagnostic criteria of attention deficit hyperactivity disorder??ADHD??combining conduct disorder??CD????120 cases of children were randomly divided into the original dose group and dose titration group.Two groups of children accepted the 24-week treatment of OROS-MPH??in which the original dose group were chosen to 18 mg/day?? dose titration group increased to 36 mg/day or 54 mg/day??respectively??in the fifth week and thirteenth week??and after the course of treatment??the following assessments were performed??SNAP-IV scale??Child Behavior Checklist??CBCL??and Treatment Emergent Symptom Scale??TESS??.Results ??1??The best response rate in the dose titration group was significantly higher than original dose group ??P??0.05??.??2??The SNAP-IV hyperactivity / impulsivity?? inattention and confrontation behavior items showed a significant difference between dose titration group and original dose group??P??0.05??.??3??In the CBCL behavior scales??dose titration group and the original dose group showed significant difference in the presence of adverse exchanges??forcedness??hyperactivity??aggression and discipline of the five dimensions??P??0.05??.??4??The incidence of side effects in both groups of children had no significant difference??P??0.05??.Conclusion With different doses of OROS-MPH for the treatment of children with ADHD and CD??effects differ more obviously-the higher dose??36 mg/day-54 mg/day??for the improvement of symptoms is better than lower dose??18 mg/day??.     

ע��ȱ�ݶද�ϰ���ͥ��Ԥ�󻼶����丸ĸ��������������������о�?

目的探讨家庭干预是否能改善注意缺陷多动障碍(ADHD)患儿及其父母的焦虑抑郁情绪。方法对2009年1月至2010年10月在广州市妇女儿童医疗中心心理专科首次就诊的ADHD患儿62例,随机分为对照组31例和研究组31例。研究组在服用药物的基础上进行家庭干预。所有患儿均取得知情同意书。采用儿童焦虑性情绪障碍筛查表(SCARED)、儿童抑郁障碍自评量表(DSRSC)、父母焦虑自评量表(SAS)、父母抑郁自评量表(SDS)分别评定两组患儿及其父母焦虑抑郁情绪。结果研究组治疗4周后SCARED评分为(13.28±0.43)分,较治疗前降低,差异有统计学意义(P<0.01);治疗后12周为(9.31±0.32)分,较治疗前、治疗后1周、对照组治疗后12周降低,差异均有统计学意义(P<0.01)。研究组治疗后4周DSRSC评分为(9.42±0.26)分,与治疗前差异有统计学意义(P<0.01);治疗后12周较治疗前、治疗后1周、对照组治疗后12周降低,差异有统计学意义(P<0.01)。研究组患儿父母SAS评分治疗后4周为(48.16±6.31)分,与治疗前比较,差异有统计学意义(P<0.01);治疗后12周为(41.96±...     

Response Inhibition in AD/HD, CD, Comorbid AD/HD+CD, Anxious, and Control Children: A Meta-analysis of Studies with the Stop Task

The aim of this study was to investigate whether impaired response inhibition is uniquely related to AD/HD or whether deficits in response inhibition are also evident in other psychopathological disorders. Furthermore, the suggestion was examined that anxiety disorders are associated with abnormally high levels of response inhibition. This paper presents the results of a meta-analysis of eight studies in which response inhibition was assessed with the so-called stop task in five groups of children: children with attention deficit/hyperactivity disorder (AD/HD), children with conduct disorder (CD), children with AD/HD+CD, children with anxiety disorders, and control children. A total of 456 children participated in the 8 studies. All children were in the age range 6–12 years. Consistent and robust evidence was found for a response inhibition deficit in AD/HD. However, response inhibition deficits did not distinguish children with AD/HD from children with CD, nor from children with comorbid AD/HD+CD. Contrary to predictions, anxious children did not demonstrate enhanced levels of response inhibition.     

Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility

Attention-deficit hyperactivity disorder (ADHD) is a common childhood neurobehavioural disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. As is the norm for most psychiatric phenotypes, traditional aetiological studies have focused primarily on the interplay between genetic and environmental factors. It is likely that epigenetic factors, i.e., heritable, but reversible changes to genomic function that are independent of DNA sequence, are also important. It is known that epigenetic processes can be induced following exposure to a range of external factors, and thus provide a mechanism by which the environment can lead to long-term alterations in phenotype. In this article we hypothesise that epigenetic dysregulation may mediate the association observed between early-development environmental insults and ADHD. We propose that understanding the epigenetic processes involved in linking specific environmental pathogens to an increased risk for ADHD may offer new possibilities for preventative and therapeutic intervention.     

Genetic and environmental influences on socio-emotional behavior in toddlers: an initial twin study of the infant-toddler social and emotional assessment

BACKGROUND: Relatively little is known about the genetic architecture of childhood behavioral disorders in very young children. METHOD: In this study, parents completed the Infant-Toddler Social and Emotional Assessment, a questionnaire that assesses symptoms of childhood disorders, as well as socio-emotional competencies, for 822 twin pairs (49.3% female; age 17-48 months) participating in the Wisconsin Twin Project. Psychometric, rater bias, and sex-limitation models explored the role of genetic and environmental influences on (1) externalizing and internalizing behavior; (2) less commonly assessed behaviors pertaining to physical and emotional dysregulation, general competencies, social relatedness; and (3) infrequent behaviors such as those associated with pervasive developmental delays. RESULTS: Heritable influences accounted for the majority (56% or more) of variation in behavior that was commonly observed by both parents. The remaining variance was associated with non-shared environmental factors, with the exception of competency and atypical behavior, which were also influenced by shared environmental factors. In contrast, for most behaviors, the variation unique to mother and father ratings was split between variation due to shared environment or rater biases and to measurement error. Little evidence emerged for sex differences in the underlying causes of variation.     

The familial aggregation of the lesser variant in biological and nonbiological relatives of PDD probands: a family history study

OBJECTIVE: To determine the risk of the lesser variant (or PDD-like traits) in the biological and nonbiological second- and third-degree relatives of PDD probands using a screening questionnaire and to investigate the extent to which the risk of the lesser variant differs according to various characteristics of the proband. METHOD: The sample consists of a series of 34 nuclear families with 2 affected PDD children (multiplex, MPX), 44 families with a single PDD child (simplex, SPX), and 14 families who adopted a PDD child. Data on characteristics of the lesser variant in 1362 biological and 337 nonbiological second- and third-degree relatives were collected from parents by telephone interview and from several maternal and paternal relatives by questionnaire. RESULTS: All components of the lesser variant were more common in biological relatives (BR) than nonbiological relatives (NBR), confirming the familial aggregation of the traits. Proband characteristics associated with an increased risk of the lesser variant in relatives were a higher level of functioning and coming from a MPX family. CONCLUSIONS: These findings on the familial aggregation of the lesser variant suggest that the genes for PDD also confer susceptibility to the lesser variant and that PDD may be a genetically heterogeneous disorder.