Epidemiology of Pervasive Developmental Disorders

Fombonne, Éric; Quirke, Sara; Hagen, Arlene

doi:10.1093/med/9780195371826.003.0007

Cited by 459 publications

(547 citation statements)

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“…The prospective follow-up of these siblings later diagnosed with ASD has led to the observation that some behavioral abnormalities can appear very early on (e.g.,, sensory issues [e.g., extreme responses to certain sounds/textures, fascination with lights/spinning objects] are already present at 7 months of age), others emerge at 12-14 months (e.g., disengagement of visual attention), while the bulk of more typical autistic abnormalities has an onset between 14 and 24 months [45][46][47][48]. Frequently, comorbid conditions include intellectual disability (65 %), seizures (30 %), and different forms of sleep problems [49][50][51]; less recognized, but equally impairing, are frequent psychiatric comorbidities, that include anxiety disorders, obsessive-compulsive disorders, and depression [52]. Altered neurodevelopment during early pregnancy represents the neuropathological cause of ASD [53,54].…”

Section: Autism Spectrum Disorder: Clinical Traits Neuropsychologicamentioning

confidence: 99%

Endocannabinoid Signaling in Autism

et al. 2015

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Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the Bendocannabinoid (eCB) system^, a rather complex ensemble of lipid signals (Bendocannabinoids^), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.Key Words Autism spectrum disorder . endocannabinoid system . fragile X syndrome . metabolic regulation . reward system The Endocannabinoid SystemTwenty-five years after the cloning and expression of a complementary DNA that encoded a G protein-coupled receptor, named type-1 cannabinoid (CB 1 ) receptor [1], there is a good deal of information on the main components of the so-called Bendocannabinoid (eCB) system^, as well as on its role in controlling cannabinergic signaling in human health and disease [2][3][4]. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most active eCBs as yet identified, although this family of bioactive lipids includes other arachidonic acid (AA) derivatives with cannabimimetic properties (i.e., noladin ether, virodhamine, N-arachidonoyldopamine, to name but a few). The classical dogma that eCBs are synthesized and released Bon demand^upon (patho)physiological stimuli has been recently revisited on the basis of unexpected evidence for intracellular reservoirs and transporters of eCBs. These new entities have been shown to drive intracellular trafficking of eCBs, adding a new dimension to the regulation of their biological activity [5]. To date, several metabolic routes have B. Chakrabarti, A. Persico and N. Battista are equal first authors.

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Section: Autism Spectrum Disorder: Clinical Traits Neuropsychologicamentioning

confidence: 99%

Endocannabinoid Signaling in Autism

et al. 2015

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“…The ASD prevalence rate increased from an average of 4 per 10,000 children in the mid-60s and 70s (Fombonne 2005) to 1 per 88 in 2008 (Centers for Disease Control and Prevention 2012). Understanding the extent to which this reflects changes in awareness and clinical practice and/or a true increase in the incidence of the disorder has important clinical and research implications.…”

Section: Introductionmentioning

confidence: 99%

Autism Spectrum Disorder Reclassified: A Second Look at the 1980s Utah/UCLA Autism Epidemiologic Study

Miller

Bilder

Farley

et al. 2012

J Autism Dev Disord

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The purpose of the present study was to re-examine diagnostic data from a state-wide autism prevalence study (n = 489) conducted in the 1980s to investigate the impact of broader diagnostic criteria on autism spectrum disorder (ASD) case status. Sixty-four (59 %) of the 108 originally "Diagnosed Not Autistic" met the current ASD case definition. The average IQ estimate in the newly identified group (IQ = 35.58; SD = 23.01) was significantly lower than in the original group (IQ = 56.19 SD = 21.21; t = 5.75; p < .0001). Today's diagnostic criteria applied to participants ascertained in the 1980s identified more cases of autism with intellectual disability. The current analysis puts this historic work into context and highlights differences in ascertainment between epidemiological studies performed decades ago and those of today.

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“…Comorbidity is high in ASD and ADHD individuals. For example, the overlap of ASD and intellectual developmental disorders is in the range of 50% (Fombonne, 2009). Simonoff et al (2008) found that ß28% of school-aged children with ASD also fulfill DSM-IV criteria for ADHD and 9% for chronic tic disorder.…”

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The Roots of Autism and ADHD Twin Study in Sweden (RATSS)

et al. 2014

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Neurodevelopmental disorders affect a substantial minority of the general population. Their origins are still largely unknown, but a complex interplay of genetic and environmental factors causing disturbances of the central nervous system's maturation and a variety of higher cognitive skills is presumed. Only limited research of rather small sample size and narrow scope has been conducted in neurodevelopmental disorders using a twin-differences design. The Roots of Autism and ADHD Twin Study in Sweden (RATSS) is an ongoing project targeting monozygotic twins discordant for categorical or dimensional autistic and inattentive/hyperactive-impulsive phenotypes as well as other neurodevelopmental disorders, and typically developing twin controls. Included pairs are 9 years of age or older, and comprehensively assessed for psychopathology, medical history, neuropsychology, and dysmorphology, as well as structural, functional, and molecular brain imaging. Specimens are collected for induced pluripotent (iPS) and neuroepithelial stem cells, genetic, gut bacteria, protein-/monoamine, and electron microscopy analyses. RATSS's objective is to generate a launch pad for novel surveys to understand the complexity of genotype-environment-phenotype interactions in autism spectrum disorder and attention-deficit hyperactivity disorder (ADHD). By October 2013, RATSS had collected data from 55 twin pairs, among them 10 monozygotic pairs discordant for autism spectrum disorder, seven for ADHD, and four for other neurodevelopmental disorders. This article describes the design, recruitment, data collection, measures, collected pairs’ characteristics, as well as ongoing and planned analyses in RATSS. Potential gains of the study comprise the identification of environmentally mediated biomarkers, the emergence of candidates for drug development, translational modeling, and new leads for prevention of incapacitating outcomes.

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Epidemiology of Pervasive Developmental Disorders

Cited by 459 publications

References 0 publications

Endocannabinoid Signaling in Autism

Endocannabinoid Signaling in Autism

Autism Spectrum Disorder Reclassified: A Second Look at the 1980s Utah/UCLA Autism Epidemiologic Study

The Roots of Autism and ADHD Twin Study in Sweden (RATSS)

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