Manually analyzing neural histopathology is a tedious process, and while there are reference sources available such as the Allen Brain Atlas, one of the primary challenges of using image analysis software to compare neural pathology between animals is the alignment of the rostral-caudal axis. The current study aims to investigate the use of Visiopharm, an image analysis software, and supervised machine learning to automate the assignment of brain sections along the rostral-caudal axis.This research is a part of a larger study conducted to analyze potential neuropathological changes in male mice that have undergone blast-induced mild traumatic brain injuries. Glial fibrillary acidic protein (GFAP), Tyrosine hydroxylase (TH), Tryptophan hydroxylase (TPH), Kappa Opioid Receptor (KOR) and Ionized Calcium-Binding Adapter (IBA) were used to identify histopathology. First, we manually labeled sections in Visiopharm and trained a deep learning algorithm to outline the sections and compute section parameters (e.g., circumference, diameter, convexity). In parallel, we manually assigned each labeled section according to the Allen Brain Atlas (ABA) rostral-caudal axis. Finally, we used python to train a supervised machine learning regressor to predict the assigned ABA slide number based on the section parameters generated by Visiopharm. We have successfully completed workflow for TH labeled sections and are currently working to generalize the algorithms to the other stains. We expect that with additional labeling and training, we will be able to successfully develop an automated process for classifying sections on the rostral-caudal axis.The goal is that after training the app further through the labeling of sections, the app will be able to create parameters for future stains, thus creating a general classification framework.This framework will increase consistency across future labeling, which allows for more reliable and faster classification. This additional time can be devoted to analyzing specific stains and other research questions.

Despite research supporting the efficacy of certain mental health practices, many mental health care providers in community mental health clinics are not utilizing evidence-based practices (EBPs) consistently when treating patients with mental health needs. Clinical supervisors play a critical role in EBP implementation given that they have regular oversight with clinicians and can gauge how often clinicians use EBPs and how effective they are at delivering them. The purpose of our project is to examine the feasibility and self-reported usefulness of case-based consultation for clinical supervisors at child-serving community mental health clinics to support the implementation of EBPs. In our pilot study, nine clinical supervisors and two supervisor consultants were recruited from community mental health clinics to participate in supervisor consultation calls. The purpose of these calls was to improve clinical supervision skills and perceived competencies for clinical supervisors. These calls consisted of: (1) a brief 15-minute didactic lead by the supervisor consultant that covered various content areas relevant to their roles as supervisors; and (2) 45 minutes of case-based consultation among the consultant and the clinical supervisors where they discussed real-life supervision scenarios, barriers and challenges that they faced, and proposed solutions or strategies. Pre and post surveys with clinical supervisor participants showed the consultation calls resulted in greater self-reported supervision competency. To build on the quantitative analyses, my mentors and I have been conducting a qualitative thematic analysis of eleven of the case-based consultation calls, which were recorded and transcribed. We will analyze the qualitative data to identify reoccurring themes discussed on the calls coded as barriers or solutions to supervision and clinical challenges to EBP implementation. This thematic analysis will help us gain insight into one potential support strategy to improve EBP implementation and sustainment to increase the quality of behavioral health care for youth.

As high levels of drug use account for thousands of drug related deaths every week, it’s important to investigate the neural mechanisms behind drug escalation as well as develop possible harm reduction strategies for drug taking. Therefore, the purpose of this experiment was to examine the effects of the Kappa Opioid receptor (KOR) on cocaine escalation in the mesolimbic system. Using a preclinical model to examine this hypothesis, CRISPR/SaCas9 was utilized in the ventral tegmental area (VTA) to selectively repress expression of KOR. After four weeks, the rats underwent cocaine self-administration during short access periods and then escalation was tested in long access periods. Lastly we utilized immunohistochemistry to confirm CRISPR/SaCas9 transduction in dopaminergic neurons. We found that decreased expression of the KOR decreased escalation during long access periods. Future research will examine the role of KOR from and in specific brain regions such that KOR expression will be decreased only in dopaminergic projections from the VTA into the NAc.

The ability to selectively and efficiently insert DNA into the genome has been a long-standing goal to potentially fix disease associated variations and add tags to proteins for biochemical assays. The advent of CRISPR-Cas9 technology has allowed for the ability to specifically target any region of the genome with a single guide RNA (sgRNA) and lead to DNA cleavage. This double stranded break by Cas9 can be repaired either through nonhomologous end joining (NHEJ), which creates insertions or deletions, or homologous recombination (HR), which requires DNA that matches the region where the break occurred. The goal of this project is to create a tool that favors HR repair over NHEJ repair after cleaving with CRISPR-Cas9 to allow for targeted gene insertion. One way to do this is to generate large amounts of multicopy single-stranded DNA (msDNA), an RNA-DNA generated by a reverse transcriptase, which transcribes RNA back into DNA. We want to determine if combining CRISPR-Cas9 technology with a reverse transcriptase to generate msDNA will produce enough homologous DNA strands to drive HR repair over NHEJ repair in vivo. To test this method, we have replaced the tyrosine hydroxylase (TH) gene, the rate limiting enzyme that produces dopamine, with green fluorescent protein (GFP). We have generated a virus containing a reverse transcriptase with a sgRNA targeted to TH and msDNA containing homology arms flanking GFP. Four weeks after co-injection of this virus with a virus containing Cas9 into the ventral tegmental area of adult mice, we analyzed brain slices to determine the loss of TH and expression of GFP. Future studies will aim to quantify gene insertion and target other genes to insert point mutations. The findings of this study may further research in the repairment of disease associated variations in genes. 

Sleep problems in adolescents are commonly associated with bedtime media use due to subsequent psychological and cognitive arousal. The purpose of Sleepazoid is to better understand the impact of mind-body interventions on mitigating the effects of media use on sleep in adolescents. Participants virtually attended assessment visits and played pre-selected mobile video games while we conducted arousal level measurements during varied time intervals. We conducted assessment visits at baseline and follow-up to establish arousal levels through Heart Rate Variability (HRV) and Electrodermal Activity (EDA) at rest, and during the gameplay and recovery phases. The Actiheart device measures HRV through heart rhythms and variability in time between each individual heartbeat while the Empatica E4 Wristband measures EDA through the degree to which skin conducts electricity. We monitored the participants during the various phases and tracked their activity for media-induced arousal task compliance. After the remote assessment visit, participants continued to track media use, sleep, and their arousal responses on designated study nights. The pandemic necessitated major protocol changes such as mailing the measurement devices, remotely downloading games, and conducting Microsoft Teams sessions in comparison to the original in-person design. This created barriers such as unstable internet connection and improper camera positioning which hindered our ability to obtain reliable data during assessment tracking. Despite the challenges of implementing virtual assessments, it is possible to transition a psychophysiological experimental protocol to remote administration by revising participant instructions, introducing instructional videos for visual reference, and ensuring a more robust protocol with closer collaboration with the participants. Ultimately, state arousal levels are predicted to return more quickly to baseline in the mind-body intervention group (e.g: bedtime yoga, breathing exercises) during follow-up assessments, during and after ceasing evening media use, and at bed time in comparison to the control group.

The lifetime prevalence of PTSD is approximately 6.8% among adults in the United States, with an estimated 36.6% experiencing serious impairment. While increased reactivity to trauma stimuli, or hyperarousal, is heavily researched and well-understood, differences in the appraisal of neutral stimuli are minimally studied. Hostile Assessment Bias (HAB) is a measure of the extent to which a person views others’ actions as hostile or threatening towards them. People with higher levels of Hostile Assessment Bias may be at greater risk of decreased functionality and increased emotional distress due to their disproportionately negative reaction to neutral stimuli. Utilizing one of our existing studies which investigate the use of Prazosin, an alpha-1 adrenergic receptor antagonist, in treating subjective symptoms and functional distress in veterans diagnosed with post traumatic stress disorder (PTSD), we investigated the relationship between PTSD severity and increased Hostile Assessment Bias while a participant is not receiving treatment for PTSD, examine the role trauma type and substance abuse play in hostile cognition, and evaluate functional impairment in veterans with both PTSD and increased HAB.We also evaluated if medication (prazosin) improves HAB and if the improvement is associated with biomarkers of noradrenergic signaling. With a positive relationship established and prazosin effectively normalizing hostile assessment patterns, it could provide a new way to target functionally impairing symptoms. We expect this research to have applications in understanding and preventing police brutality, given police officers’ repeated exposure to trauma. The next steps would include participating in the design of a clinical trial based on first responders, including the police.

Adolescence is a critical developmental period for many with regard to initiation of marijuana use. With increasing nationwide trends toward legalization of marijuana and known negative consequences associated with an earlier age of marijuana use onset, it is imperative to identify adolescent risk factors associated with motives for using marijuana. Previous research among adults has found that motives for marijuana use vary based on personality dimensions, with higher levels of neuroticism being significantly associated with greater coping motives. Despite these findings, little research has been done on this topic with late adolescents. The overarching aim of this study was to examine associations between personality risk factors and motives for marijuana use among late adolescents. The current study included 170 late adolescents (15-18 years old, M_age = 16.86, 50% female) recruited from Washington State with stratified sampling to enroll participants who ranged from never having used marijuana to those who report heavy, regular marijuana use. Participants completed online assessments that included the Mini-IPIP Big Five Factors of Personality Scale and the Comprehensive Marijuana Motives Questionnaire to assess personality and marijuana use motives, respectively. We examined associations between personality dimensions (extraversion, agreeableness, conscientiousness, neuroticism, imagination) and marijuana use motives (enjoyment, conformity, coping, celebration, perceptions, anxiety, risk, sleep) using correlational and regression analyses. We hypothesized several positive associations between personality and motives including between 1) neuroticism and using to cope with depression/anxiety, 2) imagination and using to alter perceptions, and 3) agreeableness and using to conform to peers. Further, we predicted that late adolescents high in neuroticism that use marijuana to cope would report more marijuana-related consequences. The results inform whether screening for personality dimensions in adolescents could help predict future motives for marijuana use and thus be beneficial in preventing negative marijuana consequences and providing early interventions for marijuana misuse.

Disruptive mutations to DYRK1A, located in the Down Syndrome critical region of chromosome 21, are associated with autism spectrum disorder and medical comorbidities. Previous literature suggests facial anomalies in children with DYRK1A mutations, and studies of DYRK1A’s regulatory functions confirm its role in the expression of several morphology-affecting genes, particularly DCAF7. This study attempted to determine if quantitative differences in facial features exist between children with DYRK1A mutations and the general population, including unaffected parents. From a sample of 28 children with de novo DYRK1A mutations, analyses focused on nine white non-Hispanic children (M age = 11.33 years, 77.78% male) whose data were collected using a 3dMDhead System through an ongoing genetics-first study. Measurements between facial landmarks were later calculated using 3dMDvultus. FaceBase’s 3D Facial Norms for European Caucasians were used as a control group, and Z-scores were calculated for all complete measures. Six measures—intercanthal width, outercanthal width, palpebral fissure lengths, cranial base width, and philtrum width–were selected for analysis based on previous clinical findings. Wilcoxon sign-rank tests compared Z-scores between probands and each biological parent, assessing familial genetic influence on observed dysmorphologies. Outercanthal width in probands significantly differed from both biological parents and was significantly below population average. Additionally, palpebral fissure lengths significantly differed between probands and fathers and fell below population averages for probands. These findings bolster the link between DYRK1A and genes that code for craniofacial development and suggest the facial phenotype associated with DYRK1A mutations may be more variable and nuanced than expected, presenting challenges for clinical assessment. Additional research should examine how DYRK1A interacts with genes that code for eye regions, facial phenotypes in non-white participants, and possible differences in dysmorphology between sexes.

The nucleus accumbens (NAc) is a midbrain region associated with addiction-related behaviors. The NAc consists of medium spiny neurons (MSNs) that project to the substantia nigra (SN) or the ventral pallidum (VP) forming the direct (Go) and indirect (No-Go) pathways, respectively. The Go and No-Go pathways are mostly dichotomous in their expression of distinct receptors and neuropeptides. Dopamine receptor (D1) and adenosine receptor (A2a) expression corresponds to the Go and No-Go pathways, respectively. My goal is to investigate whether collateralization exists (i.e., single neuron projecting to both the VP and SN). This will be assessed by injecting retrograde tracers into the output regions and quantifying expression in MSNs. I used D1-iCre and A2a-iCre transgenic rats that express codon-improved Cre recombinase (iCre) in neurons expressing D1 or A2a, respectively. When the iCre expressing neurons are infected with a canine adeno-associated virus (CAV) containing a double-floxed and inverted (DIO) copy of a fluorescent protein, this anatomical marker protein is inverted and expressed specifically in these cells. I bilaterally injected four D1-iCre and four A2a-iCre males with CAV-DIO-TdTomato into the VP and CAV-DIO-ZsGreen into the SN. D1 and A2a neurons projecting to the viral injection site will uptake the virus and retrogradely label D1- or A2a-expressing MSNs in the NAc. The expression of these fluorescent proteins within the NAc will be quantified to investigate the projections’ dichotomy and collateralization. The dichotomy could be validated if the tracers expressed in exclusive populations of the NAc. Based on mouse studies, I hypothesize D1-Cre rats may have minimal colocalization in NAc MSNs but A2a-Cre rats may only express TdTomato in the NAc. Addiction continues to affect millions of individuals. We aim to elucidate anatomical differences to gain a better understanding of these midbrain pathways, which could be critical for the future of clinical treatment.

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide and has been established as a risk factor for neurodegenerative diseases such as Alzheimer’s disease (AD). The progression of AD is characterized by intracellular aggregates of phosphorylated tau protein, which is mainly found in neurons and plays an important role in the stabilization of microtubules. One of the mechanisms that may contribute to tau aggregation is decreased tau clearance by the glymphatic system, a pathway that clears solutes from the brain. This fluid movement is facilitated by the astrocytic water channel aquaporin-4 (AQP4) which is primarily localized to the astrocytic endfeet that line perivascular channels surrounding the brain vasculature. Prior studies demonstrate that solute clearance along these pathways is slowed following TBI, and that there is a loss of perivascular localization of AQP4. Based on these findings we hypothesized the loss of perivascular localization of AQP4 may impair interstitial tau clearance and promote neurodegeneration. We first tested this hypothesis by examining whether loss of perivascular AQP4 following TBI promotes tau pathology in a transgenic PS19 mouse that spontaneously develops tau pathology. We then evaluated whether deletion of perivascular AQP4 in an alpha-syntrophin knock-out mouse promotes tau pathology both in the presence and absence of TBI, and when crossed with a PS19 tauopathy mouse. Alpha-syntrophin is a protein that anchors AQP4 and is important in perivascular localization; therefore, deletion of alpha-syntrophin results in loss of localization of AQP4 and impairment of clearance. We assessed levels of pathological tau using histology on the transgenic mice and crosses both with and without TBI. If validated, our findings may suggest that loss of perivascular AQP4 may increase the brain’s vulnerability to tau aggregation and neurodegeneration following TBI and provide the basis for potential treatment to prevent the development of post-traumatic neurodegeneration.

Amyloid β (Aβ) plaques are a hallmark of Alzheimer’s disease (AD), the most common form of dementia that afflicts over 5 million Americans. Soluble proteins, including Aβ, are cleared from the brain by the glymphatic system, a brain wide network of perivascular spaces that facilitates the intermixing of cerebrospinal fluid and interstitial fluid. Prior studies report that aquaporin-4 (AQP4), a water channel polarized to perivascular astrocyte endfeet, supports glymphatic clearance of soluble proteins from the brain. In the aging brain, glymphatic clearance becomes impaired and AQP4 becomes depolarized from astrocytic endfeet. Such loss of perivascular AQP4 localization is correlated with AD status and Aβ plaque burden in the human brain. In the present study, we test whether such AQP4 depolarization promotes Aβ plaque formation. AQP4 is anchored to astrocytic endfeet via the dystrophin protein complex that includes the adaptor protein α-syntrophin (α-Syn). We crossed the α-Syn knockout mouse, which lacks perivascular AQP4 localization, with the 5XFAD mouse line which spontaneously develops Aβ plaques. Our preliminary analysis suggests that loss of perivascular AQP4 localization with α-Syn knockout increases Aβ burden relative to controls. These findings demonstrate that loss of perivascular AQP4 localization, such as occurs in the human brain in the setting of AD, contributes to the development of Aβ pathology. In the future, it may be possible that targeting the localization of AQP4 may be the basis for new therapeutics that can slow or even reverse AD pathology.

Alzheimer’s Disease (AD) is a neurodegenerative disease, characterized by amyloid-ß plaque deposition in the brain, that affects more than 5 million Americans. The glymphatic system is a network of perivascular spaces that facilitates fluid movement and solute clearance from the brain, and its dysfunction in aging has been implicated in the development of AD. The water channel aquaporin-4 (AQP4), located in astrocytic endfeet bordering the perivascular spaces, supports glymphatic function. In the aging rodent and human AD brain, loss of perivascular AQP4 localization is associated with impaired glymphatic function and increased amyloid-ß deposition. Yet the molecular basis for this loss of perivascular AQP4 localization is unknown. Aquaporin-4ex (AQP4ex) is a novel translational readthrough variant of AQP4. Selective deletion of AQP4ex results in the mislocalization of AQP4 all over the astrocytic membrane, indicating that AQP4ex is a crucial element in the perivascular localization of AQP4. In this study, we quantitatively analyze the expression and localization of AQP4ex to determine whether changes in AQP4ex associate with aging, AD status, or AD pathology. Using immunofluorescent double-labeling, confocal microscopy, and custom digital image analysis techniques, we define AQP4ex expression and localization between young and aged mice, and compare these changes between wild-type animals and transgenic animals that spontaneously form amyloid-ß plaques. Using a case series of post mortem human frontal cortical tissue, we compare AQP4ex expression between healthy young adults, cognitively intact aged subjects, and aged subjects with an AD diagnosis. This is the first characterization of AQP4ex expression in the murine brain and in a human case series, and these data will contribute to the small but growing body of research on AQP4ex and its relationship with AQP4 localization, creating opportunities to identify a new novel mechanism and novel target in AD pathology.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication, restricted interests, and repetitive behaviors. Symptoms can vary widely in type and severity between individuals, but approximately 23% of children show clinical levels of aggression. Considering evidence for other racial disparities in healthcare, race/ethnicity is also a factor of interest in ASD research on disparities in diagnosis rates and severity. Previous studies have found ASD symptom severity, but not race, to be a significant predictor of physical aggression, though they investigated race alone and not as a moderator. This project aims to look at the relationship between measures of aggression and symptom severity, and the moderating effect of race/ethnicity on that relationship. 145 participants between the ages of 8-17 years with an autism diagnosis from an NIH-funded study were included in the analysis. Symptom severity was determined based on clinician observation of and interaction with the participant using the Autism Diagnostic Observation Schedule Calibrated Severity Score (ADOS CSS). Parents of the participants completed the Child Behavior Checklist (CBCL), rating their child’s level of emotional/behavioral problems. Questions were grouped together to yield scores in different “syndrome scale” categories, including aggressive behaviors. We will use multiple linear regressions to do predictive analysis on the relationships between symptom severity, aggression, and race. We expect that children with greater ASD symptom severity will display more aggressive behaviors. We also predict that there will be a moderating effect of race/ethnicity, with this relationship being stronger in white, non-Hispanic children than others. This study will provide insight into the diversity of ASD presentation, and it may help illuminate (biological or socially constructed) differences in ASD presentation between races/ethnicities and further efforts for equitable treatment.

Autism Spectrum Disorder is a neurodevelopmental disorder that is characterized by deficits in communication and social skills, and increased repetitive behaviors. These deficits also have the potential to impact executive functioning (EF). EF refers to the important mental processes of working memory, flexible thinking, and inhibitory control in order to reach a goal or complete a task. Language development centers around the ability to communicate, understand, and problem solve through verbal communication. Previous studies in typically developing (TD) children have found a moderately strong relationship between language ability and EF in children, as language allows for individuals to communicate more effectively, leading to higher EF ability when it comes to completing a task. The aim of this study is to analyze the correlation between language development and EF in individuals with and without ASD. As language and verbal communication requires recall and focus, it is likely that the two areas of EF most impacted by language development will be working memory and the ability to shift between tasks. Participants (ASD= 60, TD = 60) ages 8-17 years participated in a four-site study looking at sex differences in autism and completed the CELF-4, a clinician administered language measure. Parents of children completed the Behavior Rating Inventory of Executive Functioning Questionnaire (BRIEF), an 86 item EF questionnaire that results in a global executive composite score. We expect (1) that ASD youth will have greater impairments in language and EF compared to TD youth, (2) to see correlations between EF and language across both groups. Additionally, we predict higher EF and language scores for females than males. This study will provide a better understanding of language and EF that may be used to guide treatments, such as speech therapy for EF improvement.

Autism Spectrum Disorder (ASD) is a neurological disorder that causes developmental delays and difficulty in communication. Previous research shows children's communication skills may vary with parents' level of education. Children with parents who completed college are more verbal and show stronger communication skills in comparison to children with parents who have not completed college. This could potentially be due to an increased awareness of the importance of communicative skills among parents who have a higher education. Our goal is to explore this relationship in the GENDAAR sample, a four-site NIH funded study looking at sex and gender differences in autism. In addition to parental education, other socioeconomic factors (SES) such as household income and household structure and their relation to language skills will be explored in order to investigate the impact of SES on language development. Participants included 125 youth, ages 8-17 years with and without ASD. ASD diagnosis was confirmed via standardized assesments such as ADOS-2 and ADI-R and all participants included had a verbal IQ>70. Participants completed the Clinical Evaluation of Language Fundamentals (CELF-4) measure that focused on language skills in areas including word structure and recalling sentences. Parents completed the ACE Demographic questionnaire containing questions about SES. Based on previous data, we hyothesize that children with parents of higher education will have stronger language skills that children with parents of lower education levels. We also expect to see children in multimember households and children with higher family income to have better language outcomes. Knowledge of this information could lead to a deeper understanding of language skills in children, which would allow care to be directed towards individuals who are not recieving access to resources necessary to imporove language skills. 

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by deficits in communication, cognitive, and social impairments (Morgan et al., 2019). Earlier diagnosis has been shown to have a positive language trajectory for children with ASD. Delays in language development is one of the earliest signs of autism, and the more severe the child's early language delays are, the more likely they will have impaired language functioning (Mody & Belliveau, 2013). This project aims to evaluate if early language behavioral concerns raised by parents (age at first concerns of language) predict later language ability in youth with and without ASD. Participants included 68 children with ASD (males=34) between the ages of 8 and 17 years from the four site NIH funded study looking at sex differences in autism. All participants included met ASD criteria via standardized measures and had a verbal IQ >70. Parents of participants completed the Autism Diagnostic Interview (ADI-R), including questions related to when they observed the first signs of language and behavioral concerns and if concerns started at certain milestone ages (before 12 months, 18 months). Child participants completed a clinician-administered language task (CELF-IV), including answering questions related to recalling and formulating sentences. We predict that ASD children, whose parents identified concerns at an earlier age, have better language skills later in childhood. Previous research has indicated that females with ASD have a better language trajectory and have more vital verbal skills (Banks, 2020). Considering this research, we will explore sex differences, age of concerns, and later language development. This research can shed light on the importance of providing training to parents to recognize language delays early in children.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by social, communicative, and behavioral impairments. Some individuals with ASD attempt to conceal their social impairments in a coping strategy known as camouflaging. Camouflaging includes (1) masking or suppressing instinctive autistic behaviors, and (2) compensating by memorizing and following social-communication norms. Even though camouflaging can help individuals with ASD secure jobs, avoid rejection, and form meaningful relationships, individuals with ASD qualitatively report that camouflaging is socially exhausting and can cause undue stress, anxiety, and feelings of inauthenticity. Given the qualitative reports of anxiety related to camouflaging, this study includes a quantitative investigation of the correlations between social camouflaging, mental health, and autistic traits across ASD and typically developing (TD) youth and young adults. Twenty ASD participants (Male=11) and 30 TD participants (Male=12) from the ACE GENDAAR network, a five site NIH funded project investigating gender differences in individuals with autism are included in the study. ASD diagnosis was confirmed via gold-standard diagnostic measures. Camouflaging was assessed using the Camouflaging Autistic Traits Questionnaire, a self-report measure of camouflaging behaviors. Mental health was assessed via the Adult Self Report or Youth Self Report, self-report behavioral checklists of co-morbid mental health symptoms. Social impairments associated with ASD were measured using the Social Responsiveness Scale, a parent-report questionnaire on their child's autistic traits. We hypothesize a positive correlation between the degree of camouflaging and the severity of depression/anxiety for both ASD and TD participants. We also predict camouflaging to be a better predictor of depression/anxiety severity than autistic traits. Data from this study can provide a better understanding of the prevalence of camouflaging in ASD and TD participants. It can also help create earlier mental health interventions for participants who camouflage their autistic traits.

Autism Spectrum Disorder (ASD) is a complex developmental disorder that is characterized by persistent challenges in social, behavioral, and communication functioning. The various challenges posed by ASD-related symptoms may result in lower quality of life (QoL) (Burgess & Gutstein, 2007). Previous research has focused on the relationship between others’ reports of autism traits (parent or clinician) and self- report of QoL for individuals with ASD (Mason et al., 2018), and only few reports have used self-report of autism traits and self-report of QoL. Self-report measures provide direct self-assessment rather than other’s interpreting a behavior from observation. The use of self-report provides a better understanding of how individuals with ASD evaluate autism traits and QoL without others’ bias. The present study aims to evaluate the relationship between self-reported autism traits and self-reported QoL in youth with and without ASD. Participants (ASD = 35, TD= 56) ages 16-34 year from a four-site NIH funded study on gender differences in autism were included. All participants met inclusionary criteria on standardized measures and had an IQ>70. Participants completed self-report assessment of autism traits (SAAT), a 58 item questionnaire on autism traits, and quality of life (Peds-QL) questionnaire, where questions about physical health, functioning, and emotional health were answered. We expect individuals with autism to report a lower QoL than TD peers replicating previous findings, and self-report of autism severity to be a predictor of QoL. We will additionally explore gender differences across these relationships to evaluate if females report lower autism traits considering more males are clinically diagnosed with ASD than females. These results will provide insight into the importance of timely recognition of QoL challenges in individuals with autism so supports can be developed and provided to young adults with autism.

Autism Spectrum Disorder (ASD) is a developmental disorder that is characterized by impairments in social, communication, and behavioral skills. One particular characteristic commonly seen in individuals with ASD is the presence of repetitive behaviors which include motor movements such as hand flapping or more ritualistic behaviors such as needing to touch objects in a particular order. Repetitive behaviors in ASD are similar to those seen in certain anxiety disorders, and the presence of a comorbid anxiety disorder in an individual with ASD has been shown to increase symptom severity, such as in social and communication impairments. Given the similarity between repetitive behaviors seen in ASD and anxiety disorders and the tendency for anxiety disorders to exacerbate ASD symptoms, this research aimed to assess the severity of repetitive behaviors between those with ASD and those with ASD + anxiety. Children between the ages of 8 and 17 participated in an NIH funded study (ASD only = 145) (ASD + anxiety = 67). Parents completed the ACE Medical History interview about their child and completed the Repetitive Behavior Scale - Revised (RBS-R) which is a 44-item questionnaire that assesses repetitive behaviors on 6 different subscales. We predict that the ASD + anxiety group will have a higher severity score (total and subscales) when compared to the ASD only group. Additionally, we will explore sex differences across these relationships. Overall, the information gained in this study will shed further light on symptom severity in subsets of the ASD population, thus better informing the development of treatment for individuals.