Levels Between Children with ADHD and Healthy Subjects
Added on 2020-04-15
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Key findingsSignificant differences were observed in anti-Yo levels between children with ADHD andhealthy subjects.No significant differences were observed in GAD and anti-Yo levels between children withADHD and those with ASD.Probable associations were found between cerebellar antibodies and ADHD.Cerebellar antibodies in autism spectrum disorder and attention deficit hyperactivity disorder(ADHD)AbstractCompelling evidences suggest that dysfunction in the cerebellar region of the brain plays asignificiant role in the etiology of autism spectrum disorders (ASD) and attention deficit hyperactivitydisorders (ADHD). The study aims to investigate the association between degeneration of thecerebellum and the etiologies of ASD and ADHD. The study recruited participants comprising of 40children with ASD and 39 children with ADHD. 40 healthy children were recruited as the controlgroup. The participants were analysed for an increase in anti-Yo antibodies and anti-glutamic aciddecarboxylase (GAD) levels during cerebellar damage. Each child with ASD was evaluated using theautism behavior checklist (ABC), aberrant behavior checklist (AbBC) and childhood autism rating scale(CARS). The Conners’ Parent and Teacher Rating Scales-Revised Long Form (CPRS and CTRS) screeningquestionnaires were completed by the parents and teachers of children with ADHD. The anti-Yo andanti-GAD levels were determined using 10 cc venous samples from the participants. No significantsociodemographical difference was observed between the groups. Significant differences were foundin the anti-Yo levels between children with ADHD and healthy subjects (p=0.002). Additionally, apositive correlation was observed between GAD levels and children age. Furthermore, a negativecorrelation was found between their age and ABC scores. This was the first study to evaluate levels ofcerebellar antibodies in ADHD and ASD, and compare it to a control group. It found significant
association between cerebellar antibodies and ADHD. Further studies with larger samples and follow-up periods are necessary in order to investigate possible etiological factors among subjects withneuropsychiatric disorders.Key words: Attention deficit-hyperactivity disorder (ADHD); autism (ASD); cerebellar antibodies; anti-Yo; anti-GAD1. Introduction Autism spectrum disorder (ASD) is an umbrella term that encompasses a group ofneurodevelopmental disorders, characterized by developmental delay, abnormalities in langugagecomprehension, social interaction, reciprocity, communication, and repetitive stereotypicalbehaviors and interests [1]. Although previoius studies provided evidences for the underlyinggenetic, prenatal, early postnatal, and biochemical pathways that are responsible for the disorder,the etiology and pathogenesis are still unclear. Epidemiological studies suggest that there is not asingle reason that leads to the occurrence of ASD. Mulitfactorial conditions (genetic andenvironmental) contribute to the development of autism [2,3]. Recent studies have focused on thepossible role of cerebellar atrophy and loss of Purkinje cells in these neuropsychiatric disorders [4-6].The most widely known abnormalities associated with ASD are atrophy of the cerebellum andselective loss of Purkinje cells [7]. ASD appears to decrease the volume of neocerebellar vermis andresults in loss of Purkinje cells in the cerebellar hemispheres. These factors are thought to contributeto impaired attention, vigilance, and sensorial processes in children with ASD [8-10]. Developmentalabnormalities and damage to the cerebellum result in impaired cognitive functions, poor verbal skillsand increased stereotypical behaviors [11-12]. These findings support the idea that abnormal densityof Purkinje cells could contribute to development of autism phenotype [13]. Attention Deficit Hyperactivity Disorder (ADHD) is another common child neuropsychiatric disorderthat persisits into adulthood. A meta-analysis study showed a frequency of 5-29% among children[14]. ADHD and ASD have similar biological features and are likely to be found together [15-16].Although, the etiology of ADHD is unclear, both neurobiological and psychosocial factors are thought
to play a role. Recent studies have mostly evaluated cerebellar atrophy and loss of Purkinje cells [17].Cerebellar abnormalities are consistently found in ADHD structural neuroimaging studies [18,19].Additionally, many studies have reported impaired developmental differentiation and decreasedcerebellar volume among ADHD children [20-23]. Studies that investigated the pathophysiology ofboth ASD and ADHD pointed out common structural differences in cerebellum [8,9,18,19]. However,previous studies failed to compare the disorders in terms of cerebellar degeneration. Presence ofAnti-Yo antibodies is the most common and well defined characteristic of cerebellar degeneration[24]. Additionally, distribution of glutamic acid decarboxylase (GAD) in the neuroendocrine tissuesand antibodies against GAD act on the cerebellar pathways [25]. These findings highlight the need to(1) compare anti-Yo and anti-GAD serum levels between children with ADHD, ASD, and healthycontrol group, and (2) investigate the association between antibody levels, sociodemographicalfeatures and symptom severity among children with ASD. 2. Methods A total of 119 Caucasian children aged 4 to 12 years of age, who were admitted to the AnkaraPediatric Hematology Oncology Training and Research Hospital between July 2015 and July 2016,were included in this study. The children were gender matched and belonged to the same gradelevel. They were also matched for their intelligent levels. The sample population consisted of 40children diagnosed with ASD and 39 children diagnosed with ADHD, according to DSM-5 criteria. Astratified sampling method was used to select 40 healthy children belonging to the same age groupfrom three different pre-school institutions and three primary schools. They formed the controlgroup. Children with comorbid psychiatric disorders, chronic medical illnesses, mental retardation(intelligence quotient <70) and developmental delays were excluded from the study. Additionally,patients with pure ASD or ADHD were included in the appropriate groups. The parents and childrenwere informed about the study. Verbal and written consent was obtained from the parents. Thestudy was financed by the Ankara Pediatric Hematology Oncology Training and Research Hospital
Scientific Research Support Commission. It followed the principles of the Declaration of Helsinki, andwas approved by the Ethical Committee of Ankara Pediatric Hematology Oncology Training andResearch Hospital. Researchers determined the socio-demographical features and clinical features of all participants.The children were assessed by child and adolescent psychiatrists. They were diagnosed with ADHD orASD according to the DSM-5 criteria. The Schedule for Affective Disorders and Schizophrenia forSchool-Age Children-Present and Lifetime Version (K-SADS PL) was applied to the clinical sample toevaluate the differential diagnosis of each symptom. The reliability and validity of K-SADS-PL wasassessed by Gökler [26]. An assessment of the children aged between 4-6 years was done using theDenver-II (Denver Developmental Screening Test) or Stanford Binet test, to exclude developmentaldelays from consideration. The revised edition of Wechsler Intelligence Scale for Children was usedto exclude mental retardation among the participants aged between 6-12 years. The Conners’ ParentRating Scale-Revised Long Form (CPRS) and Conners’ Teacher Rating Scale-Revised Long Form (CTRS)were completed by parents and teachers of children diagnosed with ADHD. The Autism BehaviorChecklist (ABC) and Aberrant Behavior Checklist (AbBC) were completed by parents of autisticchildren. Researchers applied the Childhood Autism Checklist Scale (CARS) to all participants withautism. The serum anti-Yo and anti-GAD levels were analysed from all participants via the Enzyme-Linked ImmunoSorbent Assay (ELISA) method, in a laboratory at the hospital. The method was usedas a quantitative measurement to investigate the antigen-antibody relationship, and the activity ofan enzyme bound to an anti-core antibody.2.1. Instruments 2.1.1. Conners’ Parent Rating Scale-Revised Long Form (CPRS): It is an assessment tool used byparents to report behavioral problems and severity of ADHD symptoms in their children aged 3-17years [27]. This four-point Likert scale consists of 80-items. The translation, validity and reliability ofthe Turkish version of the scale were done by Kaner [28].
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