Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The core symptoms of Autistic Spectrum Disorder (ASD) are impairment in reciprocal social interaction, communication, narrow interests, and stereotyped behaviour. These are frequently severe and persistent, although their severity may change over the course of life. Furthermore, the frequently associated symptoms of self-injury, aggressive behaviour, impulsivity, poor attention, anxiety, depression, and sleep disruption, can become a major source of additional distress and interference in functioning. The causes of autism are not yet known, but there is a general consensus that ASDs are highly heritable. Comprehension of the neurobiological basis for autism-spectrum disorders is still in its initial stages: a large body of research, however, has established ASD signs and symptoms are of neurological origin, and suggest that autism is a distributed neural system disorder, which disproportionately impairs many higher order abilities. Currently available medical treatments, primarily address co-morbid symptoms, rather than core symptoms. Thus, in spite of recent advances in psychopharmacology, the treatment approach still has important limits and shows poor efficacy on global outcomes. A potential pathway for improving clinical outcomes is that of the personalised treatment for autism, by using therapeutic drug monitoring (TDM) - a valuable tool for drugs with narrow therapeutic index - as well as systematic genetic background assessment, foreseen in future applications. However, it is already possible to implement an active surveillance programme to address safety concerns and to optimise therapeutic drug interventions in ASD.
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PMID:Potential benefits and limits of psychopharmacological therapies in pervasive developmental disorders. 2405 Jul 44

Autism spectrum and schizophrenia spectrum disorders are classified separately in the DSM-5, yet research indicates that these two disorders share overlapping features. The aim of the present study was to examine the overlap between autistic and schizotypal personality traits and whether anxiety and depression act as confounding variables in this relationship within a non-clinical population. One hundred and forty-four adults completed the Autism Spectrum Quotient and the Schizotypal Personality Questionnaire and the Depression Anxiety Stress Scales-21. A number of associations were seen between autistic and schizotypal personality traits. However, negative traits were the only schizotypal feature to uniquely predict global autistic traits, thus highlighting the importance of interpersonal qualities in the overlap of autistic and schizotypal characteristics. The inclusion of anxiety and depression did not alter relationships between autistic and schizotypal traits, indicating that anxiety and depression are not confounders of this relationship. These findings have important implications for the conceptualisation of both disorders.
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PMID:Overlap between autistic and schizotypal personality traits is not accounted for by anxiety and depression. 2493 May 76

Previous studies suggested that risk for Autism Spectrum Disorder (ASD) may be increased in children exposed to antidepressants during the prenatal period. The disease specificity of this risk has not been addressed and the possibility of confounding has not been excluded. Children with ASD or attention-deficit hyperactivity disorder (ADHD) delivered in a large New England health-care system were identified from electronic health records (EHR), and each diagnostic group was matched 1:3 with children without ASD or ADHD. All children were linked with maternal health data using birth certificates and EHRs to determine prenatal medication exposures. Multiple logistic regression was used to examine association between prenatal antidepressant exposures and ASD or ADHD risk. A total of 1377 children diagnosed with ASD and 2243 with ADHD were matched with healthy controls. In models adjusted for sociodemographic features, antidepressant exposure prior to and during pregnancy was associated with ASD risk, but risk associated with exposure during pregnancy was no longer significant after controlling for maternal major depression (odds ratio (OR) 1.10 (0.70-1.70)). Conversely, antidepressant exposure during but not prior to pregnancy was associated with ADHD risk, even after adjustment for maternal depression (OR 1.81 (1.22-2.70)). These results suggest that the risk of autism observed with prenatal antidepressant exposure is likely confounded by severity of maternal illness, but further indicate that such exposure may still be associated with ADHD risk. This risk, modest in absolute terms, may still be a result of residual confounding and must be balanced against the substantial consequences of untreated maternal depression.
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PMID:Prenatal antidepressant exposure is associated with risk for attention-deficit hyperactivity disorder but not autism spectrum disorder in a large health system. 2515 80

Previous research provides disparate accounts of the putative association between creativity and psychopathology, including schizotypy, psychoticism, hypomania, bipolar disorder, ADHD, and autism spectrum disorders. To examine these association, healthy, non-clinical participants completed several psychopathology-spectrum measures, often postulated to associate with creativity: the Schizotypal Personality Questionnaire, the Psychoticism scale, the Personality Inventory for DSM-5, the Hypomanic Personality Scale, the Attention Deficit/Hyperactivity Disorder scale, the Beck Depression Inventory, and the Autism-Spectrum Quotient. The goal of Study 1 was to evaluate the factor structure of these dimensional psychopathology measures and, in particular, to evaluate the case for a strong general factor(s). None of the factor solutions between 1 and 10 factors provided a strong fit with the data based on the most commonly used metrics. The goal of Study 2 was to determine whether these psychopathology scales predict, independently, two measures of creativity: 1. a measure of participants' real-world creative achievements, and 2. divergent thinking, a laboratory measure of creative cognition. After controlling for academic achievement, psychoticism and hypomania reliably predicted real-world creative achievement and divergent thinking scored with the consensual assessment technique. None of the psychopathology-spectrum scales reliably predicted divergent thinking scored with the manual scoring method. Implications for the potential links between several putative creative processes and risk factors for psychopathology are discussed.
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PMID:Do dimensional psychopathology measures relate to creative achievement or divergent thinking? 2527 19

The Research Domain Criteria (RDoC) adopts a dimensional approach for examining pathophysiological processes underlying categorically defined psychiatric diagnoses. We used this framework to examine relationships among symptom dimensions, diagnostic categories, and resting state connectivity in behaviorally and emotionally dysregulated youth selected from the Longitudinal Assessment of Manic Symptoms study (n=42) and healthy control youth (n=18). Region of interest analyses examined relationships among resting state connectivity, symptom dimensions (behavioral and emotional dysregulation measured with the Parent General Behavior Inventory-10 Item Mania Scale [PGBI-10M]; dimensional severity measures of mania, depression, anxiety), and diagnostic categories (Bipolar Spectrum Disorders, Attention Deficit Hyperactivity Disorder, Anxiety Disorders, and Disruptive Behavior Disorders). After adjusting for demographic variables, two dimensional measures showed significant inverse relationships with resting state connectivity, regardless of diagnosis: 1) PGBI-10M with amygdala-left posterior insula/bilateral putamen; and 2) depressive symptoms with amygdala-right posterior insula connectivity. Diagnostic categories showed no significant relationships with resting state connectivity. Resting state connectivity between amygdala and posterior insula decreased with increasing severity of behavioral and emotional dysregulation and depression; this suggests an intrinsic functional uncoupling of key neural regions supporting emotion processing and regulation. These findings support the RDoC dimensional approach for characterizing pathophysiologic processes that cut across different psychiatric disorders.
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PMID:Decreased amygdala-insula resting state connectivity in behaviorally and emotionally dysregulated youth. 2543 24

The fragile X mental retardation 1 gene (FMR1), which codes for the fragile X mental retardation 1 protein (FMRP), is located at Xp27.3. The normal allele of the FMR1 gene typically has 5 to 40 CGG repeats in the 5' untranslated region; abnormal alleles of dynamic mutations include the full mutation (> 200 CGG repeats), premutation (55-200 CGG repeats) and the gray zone mutation (45-54 CGG repeats). Premutation carriers are common in the general population with approximately 1 in 130-250 females and 1 in 250-810 males, whereas the full mutation and Fragile X syndrome (FXS) occur in approximately 1 in 4000 to 1 in 7000. FMR1 mutations account for a variety of phenotypes including the most common monogenetic cause of inherited intellectual disability (ID) and autism (FXS), the most common genetic form of ovarian failure, the fragile X-associated primary ovarian insufficiency (FXPOI, premutation); and fragile X-associated tremor/ataxia syndrome (FXTAS, premutation). The premutation can also cause developmental problems including ASD and ADHD especially in boys and psychopathology including anxiety and depression in children and adults. Some premutation carriers can have a deficit of FMRP and some unmethylated full mutation individuals can have elevated FMR1 mRNA that is considered a premutation problem. Therefore the term "Fragile X Spectrum Disorder" (FXSD) should be used to include the wide range of overlapping phenotypes observed in affected individuals with FMR1 mutations. In this review we focus on the phenotypes and genotypes of children with FXSD.
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PMID:Fragile X spectrum disorders. 2560 63

Researchers and clinical practitioners have found that hoarding appears in many autism patients and that most of these patients show high anxiety and depression. There is no consensus on the relationship between autistic traits and hoarding, and little research concerning the role of negative emotions. This study investigated the relationship between autistic traits and hoarding in a large non-clinical Chinese sample. Participants were 3,229 university students (M age = 20.5 yr., SD = 1.6; 1,839 men) who were recruited in classroom. They completed measures of hoarding, autistic symptomology, anxiety, and depression: specifically the Saving Inventory-Revised, the Autism-Spectrum Quotient, the Zung Self-Rating Anxiety Scale, and The Center for Epidemiological Studies Depression Scale. Mediating effects of anxiety and depression in the correlation between autistic traits and hoarding were also explored. There was a weak but significant correlation between autistic traits and hoarding. Significant mediating effects of anxiety and depression were observed. Hoarding in people with high autistic traits could be influenced by anxiety and depression.
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PMID:Relationship between autistic traits and hoarding in a large non-clinical Chinese sample: mediating effect of anxiety and depression. 2565 Jun 39

The Autism-Spectrum Quotient (AQ) is a self-report measure of autistic traits. It is frequently cited in diverse fields and has been administered to adults of at least average intelligence with autism and to nonclinical controls, as well as to clinical control groups such as those with schizophrenia, prosopagnosia, anorexia, and depression. However, there has been no empirical systematic review of the AQ since its inception in 2001. The present study reports a comprehensive systematic review of the literature to estimate a reliable mean AQ score in individuals without a diagnosis of an autism spectrum condition (ASC), in order to establish a reference norm for future studies. A systematic search of computerized databases was performed to identify studies that administered the AQ to nonclinical participant samples representing the adult male and female general population. Inclusion was based on a set of formalized criteria that evaluated the quality of the study, the usage of the AQ, and the population being assessed. After selection, 73 articles, detailing 6,934 nonclinical participants, as well as 1,963 matched clinical cases of ASC (from available cohorts within each individual study), were analyzed. Mean AQ score for the nonclinical population was 16.94 (95% CI 11.6, 20.0), while mean AQ score for the clinical population with ASC was found to be 35.19 (95% CI 27.6, 41.1). In addition, in the nonclinical population, a sex difference in autistic traits was found, although no sex difference in AQ score was seen in the clinical ASC population. These findings have implications for the study of autistic traits in the general population. Here, we confirm previous norms with more rigorous data and for the first time establish average AQ scores based on a systematic review, for populations of adult males and females with and without ASC. Finally, we advise future researchers to avoid risk of bias by carefully considering the recruitment strategy for both clinical and nonclinical groups and to demonstrate transparency by reporting recruitment methods for all participants.
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PMID:Measuring autistic traits in the general population: a systematic review of the Autism-Spectrum Quotient (AQ) in a nonclinical population sample of 6,900 typical adult males and females. 2626 38

Once a molecule has been characterized as engaging an identified target at the appropriate location (affinity and potency), the next step involves designing experiments that will determine its pharmacodynamic activities both for efficacy (on target) and safety-tolerability (on/off target). Two expert presentations focused on looking back at completed programs and two concentrated on looking forward at ongoing programs. Specific discussions pertain to assessment of pharmacologic agonists (mGluR2/3, k-opiate, peroxisome proliferator-activated receptor gamma) and antagonists (orexin and cannabinoid) in disorders of cognition, mood, and anxiety. Advanced experimental study designs using genetics to guide a treatment trial in Alzheimer's disease and neural target-based approaches as the primary outcome measure in the National Institute of Mental Health-sponsored Fast-Fail Trials (FAST)-Mood and Anxiety Spectrum Disorders (MAS) initiative for depression showcases novel methodological approaches. Of interest, some of these initiatives were successful, while others were not, and two are currently ongoing. In conclusion, methodologies that were utilized and are currently employed to reach a successful clinical drug trial outcome are appreciated, and in case of failure, approaches to reviewing programs to enable learning that would be helpful to future programs are brought forth. This article is based on proceedings from the "Designing the Right Series of Experiments" session, which was held during the International Society for Clinical Trials Meeting (ISCTM) in Philadelphia, Pennsylvania, September 30 to October 2, 2013.
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PMID:Lessons Learned and Potentials for Improvement in CNS Drug Development: ISCTM Section on Designing the Right Series of Experiments. 2597 37

In recent studies it has been suggested that Cognitive Behavior Therapy (CBT) is beneficial to people with Autism Spectrum Disorder (ASD) but that the method needs to be modified in relation to their cognitive profile. The aim of this study is to measure the effect of modified CBT, that is, using visualized language throughout the entire session for clients with ASD and anxiety and avoidance behavior. The modification of CBT in this study consists of focusing on CBT protocols for anxiety disorders and depression, while visualizing and systematizing "the invisible" in the conversation, in order for the clients to understand the social, cognitive and emotional context of self and others and how they should interact to avoid misunderstandings. ASD clients may need help to detect the invisible code of social interaction and communication. The level of anxiety and the frequency of target behavior were measured. Four assessments were made, two at the pre-assessment, and one in mid-therapy and end of therapy respectively. Generally, results suggest no improvement during pre-treatment period but a significant improvement during treatment. The values of the clients' psychological, social and occupational ability to function improved on the Global Function Rating scale. The preliminary conclusion of this pilot study indicates that the use of visualized language throughout the CBT therapy sessions is a promising modification of current CBT protocols for individuals with ASD. After manualization, larger studies with randomized controlled study designs can replicate or challenge these results.
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PMID:Modified CBT using visualization for Autism Spectrum Disorder (ASD), anxiety and avoidance behavior--a quasi-experimental open pilot study. 2656 32


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