Outcomes of an emotion regulation intervention group in young adults with autism spectrum disorder.

Individuals on the autism spectrum experience difficulties in social relationships and emotion regulation. The aim of the present exploratory research study was to develop and explore the effectiveness of a manualized emotion regulation group intervention for autistic adults to improve emotion regulation and social communication. The group participants included seven young adults (age > 18 years) on the autism spectrum. Primary outcome measures were the Social Responsiveness Scale (SRS-2) and the Emotion Regulation Questionnaire (ERQ). Group participants reported significant improvements on the Social Communication and Interaction subscale (SCI; t = 2.601, p = .041), the Social Awareness (AWR; t = 3.163, p = .019), and the Social Cognition (COG; t = 4.861, p = .003) subscales of the SRS-2: Self Report. Overall, this study provides preliminary evidence of the effectiveness of a group treatment approach that focuses on emotion regulation to improve social interactions for young adults on the autism spectrum.

Sexuality in the Autism Spectrum Study (SASS): Reports from Young Adults and Parents.

Previous research indicates that although those with ASD desire sexual relationships, they may not effectively engage in romantic and intimate interactions. The purpose of this study was to compare reports from young adults with ASD and parents from the same families on the young adult's sexual behavior, experiences, knowledge, and communication. 100 young adults (18-30 years) and parents completed an online survey. Results indicated that young adults reported more typical privacy and sexual behaviors, and higher sexual victimization than their parents reported on their behalf. Our findings indicated that individuals with ASD desire and pursue sexual relationships typical of most people and suggest the need for sex education and communication about topics generally covered for neurotypically developing young adults.

Clinical considerations for the inclusion of individuals with autism spectrum disorder in clinical trials.

Diagnoses of autism spectrum disorder (ASD) have increased considerably over the past 20 years. Because of this rise and the inherent complexity of ASD, there is a need for an increased number of scientifically valid basic and clinical research studies addressing this disorder. This manuscript serves as an introduction to the clinical presentation of ASD as well as the unique challenges and modifications required to conduct clinical research with this population. This includes detailing the current diagnostic criteria, process of receiving an ASD diagnosis, information on assessment measures, and special considerations when developing research. It is the hope that this information will provide researchers interested in conducting clinical trials with those with ASD with baseline information and considerations when developing their research topics and methodology.

Life After an Autism Spectrum Disorder Diagnosis: A Comparison of Stress and Coping Profiles of African American and Euro-American Caregivers.

The purpose of the present study was to understand how caregiver stress and coping behaviors impact African American and Euro-American families differently when caring for a child with autism. This study used discriminate function analysis to contrast the stress and coping profiles of Euro-American caregivers who are more acculturated with the majority culture with African American caregivers who ascribe to more traditional values. A sample of 103 families was recruited (52 Euro-American, 51 African American). African American families reported significantly more stress and utilizing more varied coping strategies than their Euro-American counterparts. Additional differences were found between the high and low acculturated African American groups such that low acculturated African Americans were more likely to engage in religious coping.

Neuromotor and cognitive responses of adults with autism spectrum disorder compared to neurotypical adults.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder, whose core symptom domains include impaired social communication and narrowed interests and/or repetitive behaviors; in addition, deficits of general cognition, neuromotor function, and movement ability can be observed. This study was designed to examine differences in neuromotor and cognitive functions for a group of young adults with ASD and age-matched controls. It was also of interest to assess whether changes in the intra-individual variability (IIV) of these selected neuromotor and cognitive tasks also occurred. Increased IIV in persons with ASD may reveal important organizational features of their neuromotor system that differ from neurotypical controls. Twenty neurotypical adult individuals (24.3 ± 2.8 years) and twenty adults with a clinician-assigned diagnosis of ASD (21.2 ± 4.4 years) participated in this study. Specific cognitive and motor assessments included Trails Making Tests A&B, Symbol Digit Modalities Test, Purdue Pegboard Test, simple reaction time, finger tapping, hand grip strength, balance, and gait. Results revealed that the ASD adults exhibited decreased upper limb strength and slower responses for finger tapping, hand dexterity, reaction times, and gait compared to the non-ASD controls. The general slowing of motor responses for the persons with ASD was also associated with increased within-subject variability during the reaction time, finger tapping, hand grip, and gait assessments compared to neurotypical adults, illustrating that IIV measures may be a useful marker of widespread neuromotor dysfunction for adults with ASD. Overall, these findings are consistent with clinical observations that abnormalities of movement performance and cognitive performance are an associated feature of ASD in young adults.

Autism spectrum disorder in Latin American families: Experiences in Chile.

INTRODUCTION: The present study provides pilot data investigating relationships between severity of autism spectrum disorder (ASD) traits, community supports, and other family variables as reported by caregivers of children with ASD in Chile. METHOD: An anonymous caregiver survey was developed based on previous ASD survey studies conducted in the United States and direct input from collaborators residing in Chile. Participants included Chilean caregivers of individuals with ASD (N = 50; Mchild age = 6.98). The survey addressed topics regarding the child's ASD traits, the caregiver's beliefs and perceptions of ASD, and community supports and engagement. RESULTS: Correlational analyses indicated associations between ASD traits, physician support, family stress, stigma, and community engagement. DISCUSSION: Results from this study highlight the importance of future research to better understand and treat Latin American children with ASD and their families. (PsycINFO Database Record

Sugarcoated Perineuronal Nets Regulate "GABAergic" Transmission: Bittersweet Hypothesis in Autism Spectrum Disorder.

Fast-spiking, parvalbumin-expressing "GABAergic" interneurons regulate synchronous oscillatory output of pyramidal neurons. Metabolic demands of these GABAergic projections are great because local ion concentrations must be optimally maintained; in addition, high rates of mitochondrial respiration necessitate exquisite redox regulation. Interestingly, only fast-spiking, parvalbumin-expressing basket cells coexpressing 3 metalloproteinases seem to be preferentially enwrapped in perineuronal nets (PNNs), a specialized lattice-like structure of the extracellular matrix. The PNNs maintain optimal local concentrations of ions, protect against oxidative stress, and concentrate transcription factors and chemorepulsive axon guidance cues. The PNNs mediate opening and closing of periods of heightened plasticity. Therapeutic strategies in autism spectrum disorders include promoting both maintenance and deliberate disruption of PNNs to promote new learning and cognitive flexibility.

The 15q13.3 deletion syndrome: Deficient α(7)-containing nicotinic acetylcholine receptor-mediated neurotransmission in the pathogenesis of neurodevelopmental disorders.

Array comparative genomic hybridization (array CGH) has led to the identification of microdeletions of the proximal region of chromosome 15q between breakpoints (BP) 3 or BP4 and BP5 encompassing CHRNA7, the gene encoding the α7-nicotinic acetylcholine receptor (α7nAChR) subunit. Phenotypic manifestations of persons with these microdeletions are variable and some heterozygous carriers are seemingly unaffected, consistent with their variable expressivity and incomplete penetrance. Nonetheless, the 15q13.3 deletion syndrome is associated with several neuropsychiatric disorders, including idiopathic generalized epilepsy, intellectual disability, autism spectrum disorders (ASDs) and schizophrenia. Haploinsufficient expression of CHRNA7 in this syndrome has highlighted important roles the α7nAChR plays in the developing brain and normal processes of attention, cognition, memory and behavior throughout life. Importantly, the existence of the 15q13.3 deletion syndrome contributes to an emerging literature supporting clinical trials therapeutically targeting the α7nAChR in disorders such as ASDs and schizophrenia, including the larger population of patients with no evidence of haploinsufficient expression of CHRNA7. Translational clinical trials will be facilitated by the existence of positive allosteric modulators (PAMs) of the α7nAChR that act at sites on the receptor distinct from the orthosteric site that binds acetylcholine and choline, the receptor's endogenous ligands. PAMs lack intrinsic efficacy by themselves, but act where and when the endogenous ligands are released in response to relevant social and cognitive provocations to increase the likelihood they will result in α7nAChR ion channel activation.

The α7 nicotinic acetylcholine receptor: A mediator of pathogenesis and therapeutic target in autism spectrum disorders and Down syndrome.

Currently, there are no medications that target core deficits of social communication and restrictive, repetitive patterns of behavior in persons with autism spectrum disorders (ASDs). Adults with Down syndrome (DS) display a progressive worsening of adaptive functioning, which is associated with Alzheimer's disease (AD)-like histopathological changes in brain. Similar to persons with ASDs, there are no effective medication strategies to prevent or retard the progressive worsening of adaptive functions in adults with DS. Data suggest that the α7-subunit containing nicotinic acetylcholine receptor (α7nAChR) is implicated in the pathophysiology and serves as a promising therapeutic target of these disorders. In DS, production of the amyloidogenic Aß1-42 peptide is increased and binds to the α7nAChR or the lipid milieu associated with this receptor, causing a cascade that results in cytotoxicity and deposition of amyloid plaques. Independently of their ability to inhibit the complexing of Aß1-42 with the α7nAChR, α7nAChR agonists and positive allosteric modulators (PAMs) also possess procognitive and neuroprotective effects in relevant in vivo and in vitro models. The procognitive and neuroprotective effects of α7nAChR agonist interventions may be due, at least in part, to stimulation of the PI3K/Akt signaling cascade, cross-talk with the Wnt/ß-catenin signaling cascade and both transcriptional and non-transcriptional effects of ß-catenin, and effects of transiently increased intraneuronal concentrations of Ca(2+) on metabolism and the membrane potential. Importantly, α7nAChR PAMs are particularly attractive medication candidates because they lack intrinsic efficacy and act only when and where endogenous acetylcholine is released or choline is generated.

Pharmacotherapeutic implications of the association between genomic instability at chromosome 15q13.3 and autism spectrum disorders.

Recurrent microdeletions of chromosome 15q13.3 are causally associated with autism spectrum disorders (ASDs), suggesting that haploinsufficiency of CHRNA7, the gene that codes for the α7 nicotinic acetylcholine receptor (α7 nAChR) subunit, is an etiological mechanism. Independent of these genetic data, given the location of α7 nAChRs on γ-aminobutyric acid-inhibitory neurons and their role in maintaining central inhibitory tone, a compelling pharmacological rationale exists for therapeutically targeting the α7 nAChR in persons with ASDs. Given the availability of positive allosteric modulators of nicotinic acetylcholine receptors and selective agonists for the α7 nAChR (eg, choline derived from dietary administration of cytidine 5'diphosphocholine and anabasine derivatives), it is possible to conduct "proof of concept" clinical trials, exploring the effects of α7 nAChR agonist interventional strategies on domains of psychopathology, such as attention, cognition, and memory, in persons with ASDs.

Cholinergic abnormalities in autism: is there a rationale for selective nicotinic agonist interventions?

The core dysfunctions of autism spectrum disorders, which include autistic disorder, Asperger disorder, and pervasive developmental disorder not otherwise specified, include deficits in socialization and communication and a need for the preservation of "sameness;" intellectual impairment and epilepsy are common comorbidities. Data suggest that pathological involvement of cholinergic nuclei and altered expression of acetylcholine receptors, particularly nicotinic acetylcholine receptors, occur in brain of persons with autistic disorder. However, many of these studies involved postmortem tissue from small samples of primarily adult persons. Thus, the findings may reflect compensatory changes and may relate more closely to intellectual impairment and the confounding effects of seizures and medications, as opposed to the core dysfunctions of autism. Nonetheless, because of the roles played by acetylcholine receptors in general, and nicotinic acetylcholine receptors in particular, in normal processes of attention, cognition, and memory, selective cholinergic interventions should be explored for possible therapeutic effects. Additionally, there are electrophysiological data that complement the clinical observations of frequent comorbid seizure disorders in these patients, suggesting a disturbance in the balance of excitatory and inhibitory tone in the brains of persons with autistic disorders. Conceivably, because the alpha7 nicotinic acetylcholine receptor is located on the surface of gamma-aminobutyric acid inhibitory neurons, selective stimulation of this receptor would promote gamma-aminobutyric acid's release and restore diminished inhibitory tone. The development of agonists and partial agonists for nicotinic acetylcholine receptors and positive allosteric modulators that enhance the efficiency of coupling between the binding of agonist and channel opening should facilitate consideration of clinical trials.