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Biomedical subjects

A Thapar

Publications and source records attributed to A Thapar.

At least 37 records · Page 2Linked to original sources
PubMed2001

Examining for association between candidate gene polymorphisms in the dopamine pathway and attention-deficit hyperactivity disorder: a family-based study.

Attention-deficit hyperactivity disorder (ADHD) is a highly heritable childhood-onset psychiatric condition characterized by developmentally inappropriate inattention, hyperactivity, and impulsiveness. The pathophysiology of ADHD is currently unknown. However, the therapeutic effects of stimulant medication together with findings from animal and neuroimaging studies as well as from several molecular genetic studies of the dopamine receptor D4 gene and dopamine transporter gene have implicated involvement of the dopaminergic system. To test the dopaminergic hypothesis further, we have looked for association between ADHD and alleles of seven dopamine-related candidate genes using a family-based association approach in a sample of 150 children diagnosed with ADHD. We tested polymorphisms in genes encoding three dopamine receptors (DRD3, DRD4, and DRD5) and four dopamine-relevant enzymes: tyrosine hydroxylase [tyrosine hydroxylase (TH)], dopamine beta hydroxylase (DbetaH), catechol-O-methyltransferase (COMT), and monoamine oxidase A (MAOA). We were unable to detect a significant association with any of the polymorphisms genotyped, although there was a trend for preferential transmission of the DRD5 148 bp marker allele and the MAOA 122 bp marker allele. We conclude that none of the alleles we have tested makes a major contribution to ADHD, although much larger samples are required to exclude small effects.

Adolescent↗
PubMed2001

Are serum anticonvulsant levels in people with epilepsy appropriately monitored?

The medical care of people with epilepsy has often been described as being poor, although objective markers for the quality of epilepsy care are lacking. This paper describes the results of using a simple quality marker, appropriate measuring of serum anticonvulsant levels, in assessing the quality of epilepsy care. The checking of serum phenytoin levels in certain clinical circumstances is advocated, whereas the checking of serum sodium valproate levels is not generally supported. A total of 1254 people with epilepsy in the community had their medical records examined for evidence of checking of anticonvulsant levels and 1204 of these individuals completed questionnaires about their epilepsy and its treatment. Of those on phenytoin, only 26% to 47% had phenytoin levels checked appropriately; 23% of patients on sodium valproate were inappropriately having their serum levels checked. The only clinical or organizational factor that predicted whether checking of serum phenytoin levels was performed was whether or not patients reported three common phenytoin side-effects but this still showed a small effect size (odds ratio 2.4).

Anticonvulsants↗
PubMed2001

Examining the comorbidity of ADHD-related behaviours and conduct problems using a twin study design.

BACKGROUND: Although attention-deficit hyperactivity disorder (ADHD) and conduct disorder (CD) frequently co-occur, the underlying mechanisms for this comorbidity are not well understood. AIMS: To examine whether ADHD and conduct problems share common risk factors and whether ADHD+CD is a more heritable variant of ADHD. METHOD: Questionnaires were sent to 2846 families. Parent-rated data were obtained for 2082 twin pairs and analysed using bivariate genetic analysis and a liability threshold model approach. RESULTS: The overlap of ADHD and conduct problems was explained by common genetic and non-shared environmental factors influencing both categories. Nevertheless, the two categories appeared to be partly distinct in that additional environmental factors influenced conduct problems. It appeared that ADHD+CD was a genetically more severe variant of ADHD. CONCLUSIONS: Conduct problems and ADHD share a common genetic aetiology; ADHD+CD appears to be a more severe subtype in terms of genetic loading as well as clinical severity.

Adolescent↗
PubMed2001

Bias in conceptual priming.

In recent years, Ratcliff, McKoon, and colleagues have argued that priming in perceptual implicit memory tests is the result of biases in information processing. Three experiments are presented that extend this framework to the conceptual implicit memory domain. Participants studied a list of words before receiving a set of general knowledge questions. For some questions, participants studied the correct answer; for others, they studied a similar but incorrect answer. Although study of a correct answer facilitated performance, study of the similar alternative hurt performance. Costs and benefits of previous study were observed in both production and forced-choice tasks. However, there was no benefit of previous study when participants studied both the correct answer and the similar but incorrect alternative. The pattern of results indicates that participants were biased to respond with previously studied words on the conceptual implicit memory test. This pattern is concordant with the biased information-processing approach to priming.

Bias↗
PubMed2001

False recall and false recognition induced by presentation of associated words: effects of retention interval and level of processing.

The effects of retention interval and level of processing on false recall and false recognition of associates were examined. False recall and false recognition were induced by presenting subjects with words closely associated with a non-studied word. Both level of processing and retention interval affected false recall (Experiment 1) and false recognition (Experiment 2) in the same direction with which they affected accurate recall and accurate recognition. That is, semantically processed lists exhibited higher levels of later false recall and false recognition than did superficially processed lists. Furthermore, a decline in false recall and false recognition occurred across retention intervals of 0, 2, and 7 days. However, the decline in false recall and false recognition was less pronounced than the decline in accurate recall and accurate recognition. Results are consistent with source monitoring and fuzzy trace explanations of false recall and false recognition.

Adult↗
PubMed2001

The effects of aging on reaction time in a signal detection task.

The effects of aging on response time are examined in 2 simple signal detection tasks with young and older subjects (age 60 years and older). Older subjects were generally slower than young subjects, and standard Brinley plot analyses of response times showed typical results: slopes greater than 1 and (mostly) negative intercepts. R. Ratcliff, D. Spieler, and G. McKoon (2000) showed that the slopes of Brinley plots measure the relative standard deviations of the distributions of response times for older versus young subjects. Applying R. Ratcliff's (1978) diffusion model to fit the response times, their distributions, and response accuracy, it was found that the larger spread in older subjects' response times and their slowness relative to young subjects comes from a 50-ms slowing of the nondecision components of response time and more from conservative settings of response criteria.

Adolescent↗
PubMed2000

A family-based and case-control association study of the dopamine D4 receptor gene and dopamine transporter gene in attention deficit hyperactivity disorder.

Attention deficit hyperactivity disorder (ADHD) is a highly heritable psychiatric condition of early childhood onset characterised by marked inattention, hyperactivity and impulsiveness. Molecular genetic investigations of ADHD have found positive associations with the 480-bp allele of a VNTR situated in the 3' untranslated region of DAT1 and allele 7 of a VNTR in exon 3 of DRD4. A number of independent studies have attempted to replicate these findings but the results have been inconsistent. We used both family-based and case control approaches to examine these polymorphisms in a sample of 137 children diagnosed with ICD-10, DSM-IV or DSM-III-R ADHD. We found no evidence of association with the DAT1 polymorphism, despite a sample size that has up to 80% power to detect a previously reported effect size. We observed a significant increase in the DRD4 7 repeat allele amongst ADHD probands (21.7%) and their parents (18.9% in mothers, 22.3% in fathers), compared to ethnically matched controls (12.8%). However TDT analysis showed no preferential transmission of allele 7 to ADHD probands.

Adult↗
PubMed2000

Does the definition of ADHD affect heritability?

OBJECTIVE: A twin study design was used to examine the genetic validity of attention-deficit hyperactivity disorder (ADHD)-related phenotypes. METHOD: Questionnaires covering ADHD symptoms were sent to the families of 2,846 school-age twins. Parent-rated symptoms were obtained for 2,082 twin pairs and teacher-rated symptoms were available for 1,470 twin pairs. RESULTS: Broadly defined parent-rated, teacher-rated, and "pervasive" (both parent- and teacher-rated) ADHD categories were found to be highly heritable. Significant shared environmental effects were also detected for teacher-rated ADHD. A common genetic factor was found to have a modest influence on both parent- and teacher-rated symptom scores and categories, but additional genetic and environmental influences were also found forteacher-rated ADHD. Consistent with previous findings, ADHD symptom scores were again found to be highly heritable. Maternal contrast effects were found for the Rutter A scale items but could not be detected for the DuPaul ADHD rating scale. CONCLUSIONS: Broadly defined pervasive ADHD appears to be as heritable as ADHD behaviors defined by maternal reports alone. A common genetic factor influences maternally rated and teacher-rated ADHD but does not account for all of the genetic variance for teacher-rated ADHD. ADHD symptom scores are highly heritable, and maternal contrast effects appear to vary for different measures.

Adolescent↗
PubMed1999

Genetic basis of attention deficit and hyperactivity.

BACKGROUND: Hyperkinetic disorder or attention-deficit hyperactivity disorder (ADHD) is an important clinical condition. AIMS: The research evidence for a genetic contribution to ADHD is reviewed. METHOD: Measurement of the phenotype, the extent to which attention deficit and hyperactivity are heritable and molecular genetic findings are discussed. Future research directions are also considered. RESULTS: ADHD is a familial disorder. Available adoption evidence suggests genetic influences are important. Twin studies have primarily focused on trait measures which have consistently been found to be highly heritable Molecular genetic studies of clinical disorder so far have suggested the involvement of the dopamine DRD-4 receptor gene and dopamine transporter gene (DAT1). However, these findings await further replication. CONCLUSIONS: Advances in psychiatric genetics and current research interest in the genetics of ADHD should improve our understanding of aetiological factors and have an impact on treatment.

Attention Deficit Disorder with Hyperactivity↗
PubMed1998

Validity of the shortened Mood and Feelings Questionnaire in a community sample of children and adolescents: a preliminary research note.

The Mood and Feelings Questionnaire (MFQ) was designed to detect clinical depression in children and adolescents. Our aim was to investigate the relationship between symptom scores obtained using the short-version MFQ and psychiatric disorders in a non-clinical sample. Seventy-eight parents and 71 twins, who had completed the MFQ, were interviewed separately using a semistructured diagnostic interview, the Child and Adolescent Psychiatric Assessment. Parent-rated MFQ scores (MFQ-P) were found to distinguish those with ICD-10 (point biserial correlation = 0.345) and DSM-III-R depression (point biserial correlation = 0.369) from non-depressed cases. MFQ-P scores also differentiated depressed cases from those with 'other psychiatric diagnoses' (any anxiety disorder, oppositional defiant disorder and conduct disorder, hyperkinetic disorder/attention deficit hyperactivity disorder and adjustment disorder/post-traumatic disorder). The MFQ-P at the chosen cut-off point showed a sensitivity of 0.75 and specificity of 0.73 for an ICD-10 diagnosis of depression and a sensitivity of 0.86 and specificity of 0.87 for DSM-III-R depression. The number of self-rated reports (MFQ-C) was small, but overall the results suggest that self-rated MFQ scores may show less specificity. The MFQ-C at the selected cut-off point showed a sensitivity of 0.6 and specificity of 0.61 for ICD-10 depression, and a sensitivity of 0.75 and specificity of 0.74 for DSM-III-R depression.

Adolescent↗
PubMed1998

Life events and depressive symptoms in childhood--shared genes or shared adversity? A research note.

A twin study design was used to examine to what extent genetic and environmental factors mediate the association between life events and depressive symptoms. Questionnaire measures (maternally rated) of depressive symptoms and life events were obtained for a systematically ascertained sample of 270 twin pairs aged 8 to 17 years. Bivariate genetic model fitting showed that depressive symptoms and some life events (total events, negative impact) share a common genetic influence. The covariation of independent life events and depressive symptoms was explained by a shared environmental influence common to both. At least part of the association between life events and depressive symptoms is mediated by familial factors that include both genes and shared environment.

Adaptation, Psychological↗
PubMed1997

Genes and social skills.

Evidence for one or more loci on the human X chromosome influencing social cognition was recently presented by Skuse et al. The imprinted locus is only expressed from a paternally inherited X chromosome, which means that boys do not express it because their only X chromosome comes from their mother. This raises the possibility of genetic as well as cultural influences on sex differences in behaviour and cognition. It may also offer some explanation for why boys are more vulnerable to developmental disorders that affect social behaviour, such as autism.

Autistic Disorder↗
PubMed1997

Attitudes of general practitioners towards health care for people with intellectual disability and the factors underlying these attitudes.

An intellectual disability attitude questionnaire was used to explore the attitudes of general practitioners (GPs) towards primary health care, organizing health promotion and the role of specialist services for people with intellectual disability. The results of this questionnaire from GPs in Gwent (Wales) and GPs in west Gloucestershire (England) were compared. The GPs in both areas responded similarly and tended to agree that they were responsible for the medical care of people with intellectual disability in the community. They also tended to feel that the move from hospitals to the community of people with intellectual disability would greatly increase their workload. The GPs in both areas were generally against a responsibility on their part for health promotion and health screening initiatives for people with intellectual disability. However, GPs in west Gloucestershire felt more strongly against these issues. Further analysis of the data revealed factors which influenced the response of GPs to the questionnaire, including their position regarding health promotion and screening, and their view of the role of specialist health services. The GPs generally felt that community learning disability teams provided useful support, and there is clearly scope for team members to liaise more closely with GP practices and to provide helpful information to GPs about intellectual disability and the specialist health services available. Professionals seeking to work collaboratively with GPs should be sensitive to their workload pressures and to their attitudes towards health promotion initiatives and health screening.

Adult↗
PubMed1997

Anxiety and depressive symptoms in childhood--a genetic study of comorbidity.

Anxiety and depressive symptoms commonly co-occur yet the underlying mechanisms for this covariation remain poorly understood. Genetic strategies are a useful means of investigating whether the comorbidity of two sets of symptoms or disorders can be explained by the same aetiological factors. In this paper we use a systematically ascertained sample of 172 twin pairs aged 8 to 16 years to examine the causes of covariation of maternally rated anxiety and depressive symptoms. The results suggest that most of the covariation can be explained by a common set of genes that influence anxiety and depressive symptoms. Some covariation between anxiety and depressive symptoms is also explained by environmental influences of the non-shared type. In addition, depressive symptoms also appear to be influenced by specific genetic factors.

Adolescent↗